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University of Texas – Austin
1.
Pomrenze, Matthew Brian.
Genetic dissection of an amygdala CRF circuit for fear and anxiety.
Degree: PhD, Neuroscience, 2018, University of Texas – Austin
URL: http://dx.doi.org/10.26153/tsw/2172 
► Fear and anxiety are ethological responses to threats and danger in the environment. The central amygdala (CeA) is a brain structure important for fear responses…
(more)
▼ Fear and anxiety are ethological responses to threats and danger in the environment. The central
amygdala (CeA) is a brain structure important for fear responses to discrete cues that predict threat. Recent findings indicate that the CeA also contributes to states of sustained apprehension in the absence of discrete cues that characterize anxiety, although less is known about the neural circuitry involved. The stress neuropeptide corticotropin releasing factor (CRF) is anxiogenic and produced by subpopulations of neurons in the CeA and the dorsolateral bed nucleus of the stria terminalis (dlBNST), a structure with strong connections to the CeA. Early models of the neurobiology of fear and anxiety proposed that the CeA promotes fear behaviors but not anxiety behaviors, and the BNST mediates anxiety but not fear. Furthermore, these models also hypothesized that a CRF pathway from the CeA to the dlBNST could be important for anxiety behavior, but this prediction remained untested. Here, the function of CeA CRF (CeA [superscript CRF]) neurons in fear and anxiety was investigated using Cre-dependent viral-genetic tools and male rats that express Cre recombinase from a Crh promoter. CeA [superscript CRF] neurons mediated both stress-induced anxiety and fear behaviors, both of which were dependent on CRF signaling. Additionally, the neuropeptide dynorphin, but not neurotensin, produced by CeA [superscript CRF] neurons was critical for fear and anxiety behaviors. Neurotensin release had no effect on anxiety but dampened fear learning. GABA release from these neurons played a major role in setting the level of anxiety in the basal state. Finally, the CeA [superscript CRF] pathway to the dlBNST was tested for its role in anxiety and was found to be critical for these behaviors. This pathway also recruited CRF signaling and local CRF neurons in the dlBNST to engage anxiety-like behaviors. Collectively, these findings suggest that CeA [superscript CRF] neurons promote both fear and anxiety via the release of GABA and different neuropeptides and a projection to the dlBNST. The data presented here refine early neuroanatomical models of fear and anxiety and provide mechanistic support for recent human primate data suggesting that the CeA and BNST act together to generate negative emotional states.
Advisors/Committee Members: Messing, Robert O (advisor), Marinelli, Michela (advisor), Drew, Michael R (committee member), Harris, Adron (committee member), Zemelman, Boris V (committee member), Nishiyama, Hiroshi (committee member).
Subjects/Keywords: Amygdala; CRF
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APA (6th Edition):
Pomrenze, M. B. (2018). Genetic dissection of an amygdala CRF circuit for fear and anxiety. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://dx.doi.org/10.26153/tsw/2172
Chicago Manual of Style (16th Edition):
Pomrenze, Matthew Brian. “Genetic dissection of an amygdala CRF circuit for fear and anxiety.” 2018. Doctoral Dissertation, University of Texas – Austin. Accessed March 07, 2021.
http://dx.doi.org/10.26153/tsw/2172.
MLA Handbook (7th Edition):
Pomrenze, Matthew Brian. “Genetic dissection of an amygdala CRF circuit for fear and anxiety.” 2018. Web. 07 Mar 2021.
Vancouver:
Pomrenze MB. Genetic dissection of an amygdala CRF circuit for fear and anxiety. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2018. [cited 2021 Mar 07].
Available from: http://dx.doi.org/10.26153/tsw/2172.
Council of Science Editors:
Pomrenze MB. Genetic dissection of an amygdala CRF circuit for fear and anxiety. [Doctoral Dissertation]. University of Texas – Austin; 2018. Available from: http://dx.doi.org/10.26153/tsw/2172
Boston University
2.
Murati, Anastasia.
The automatic segmentation of the human amygdala in amnestic mild cognitive impairment.
Degree: MS, Anatomy & Neurobiology, 2020, Boston University
URL: http://hdl.handle.net/2144/41309
► BACKGROUND: Mild cognitive impairment (MCI) is a clinical condition that is characterized by mild changes in cognition. The amnestic form of MCI (aMCI) primarily affects…
(more)
▼ BACKGROUND: Mild cognitive impairment (MCI) is a clinical condition that is characterized by mild changes in cognition. The amnestic form of MCI (aMCI) primarily affects memory and is thought to represent a stage between healthy aging and Alzheimer’s disease (AD). The medial temporal lobe (MTL) and the limbic system are two areas of the brain that have been implicated in the amnestic form of MCI. While MCI represents a risk factor for AD, it does not always lead to dementias. Being a carrier of the APOE Ɛ4 allele has also shown to increase chances of progression from MCI to AD.
OBJECTIVE: To determine whether the subnuclei of the
amygdala, along with other specific regions within the MTL, can differentiate between cognitively normal individuals and age-matched subjects with aMCI.
METHODS: T1-weighted magnetic resonance imaging (MRI) data from two sources, the Boston University Alzheimer’s Disease Center (BU-ADC) and the Alzheimer’s Disease Neuroimaging Initiative (ADNI), was compiled for cross-sectional analysis. 95 scans in total from 45 cognitively normal participants and 50 diagnosed with aMCI were analyzed and the volumes of interest were automatically generated by the developmental version of FreeSurfer v6.0. To evaluate how well the volumes could predict either group membership (i.e. control group or MCI group) or APOE Ɛ4 status (i.e. carrier or noncarrier), the variables were assessed by nominal logistic regression models.
RESULTS: Six of the nine nuclei of the
amygdala had significantly reduced volumes in the aMCI group compared to controls. The whole
amygdala and the perirhinal cortex also demonstrated reduced volumes in the aMCI group compared to the control group. The whole
amygdala was a good predictor of group membership (R2 = 0.1386, whole model test chi square = 18.21558, p = 0.0004), but none of the subnuclei were good predictors individually. A model containing the 9 nuclei, the entorhinal cortex, and the perirhinal cortex provided a good fit for predicting APOE Ɛ4 status fit (R2 = 0.3000, whole model test chi square = 36.29563, p = 0.0002) and the best predictor was the corticoamygdaloid transition area of the
amygdala.
CONCLUSIONS: The results of our study confirm previous findings of reduced whole
amygdala volume and add to the limited literature of reduced perirhinal cortex and amygdaloid nuclei volumes in MCI compared to healthy controls. To the best of our knowledge, this was the first time the automatic segmentation atlas was used to analyze the volumes of nine subnuclei of the
amygdala in a population of aMCI. Our model testing the volume of the whole
amygdala accurately predicted aMCI subjects with 58% accuracy and controls with 70% accuracy; the accuracy rose to 69% when the entorhinal cortex and the perirhinal cortex were added to the model to predict aMCI subjects from controls. Additionally, the model for predicting APOE Ɛ4 status identified noncarriers of the allele at 85% accuracy. Future studies should consider increasing the sample size to better assess small ROIs and assess for…
Advisors/Committee Members: Killiany, Ronald J. (advisor), Mian, Asim (advisor).
Subjects/Keywords: Neurosciences; Amnestic mild cognitive impairment; Amygdala; Amygdala nuclei; Amygdala subnuclei; Mild cognitive impairment; Perirhinal cortex
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APA (6th Edition):
Murati, A. (2020). The automatic segmentation of the human amygdala in amnestic mild cognitive impairment. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/41309
Chicago Manual of Style (16th Edition):
Murati, Anastasia. “The automatic segmentation of the human amygdala in amnestic mild cognitive impairment.” 2020. Masters Thesis, Boston University. Accessed March 07, 2021.
http://hdl.handle.net/2144/41309.
MLA Handbook (7th Edition):
Murati, Anastasia. “The automatic segmentation of the human amygdala in amnestic mild cognitive impairment.” 2020. Web. 07 Mar 2021.
Vancouver:
Murati A. The automatic segmentation of the human amygdala in amnestic mild cognitive impairment. [Internet] [Masters thesis]. Boston University; 2020. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2144/41309.
Council of Science Editors:
Murati A. The automatic segmentation of the human amygdala in amnestic mild cognitive impairment. [Masters Thesis]. Boston University; 2020. Available from: http://hdl.handle.net/2144/41309
Vanderbilt University
3.
Ramikie, Teniel Sonya.
Mechanistically Distinct Modes of Endocannabinoid Mobilization at Glutamatergic Synapses of the Lateral Division of the Central Amygdala and Its Regulation by Chronic Stress.
Degree: PhD, Neuroscience, 2014, Vanderbilt University
URL: http://hdl.handle.net/1803/14788
► The lateral division of the central amygdala (CeAL) is a key structure at the limbic-motor interface regulating stress-responses and emotional learning. Endocannabinoid (eCB) signaling is…
(more)
▼ The lateral division of the central
amygdala (CeAL) is a key structure at the limbic-motor interface regulating stress-responses and emotional learning. Endocannabinoid (eCB) signaling is heavily implicated in the regulation of stress-response physiology and emotional learning processes, however, the role of eCBs in the modulation of synaptic efficacy in the CeAL is not well understood. Here we describe the subcellular localization of type 1 cannabinoid receptors (CB1) and the eCB synthetic machinery at glutamatergic synapses in the CeAL and find that CeAL neurons exhibit multiple mechanistically and temporally distinct modes of postsynaptic eCB mobilization. Furthermore, this work demonstrates that following chronic stress exposure, eCB-mediated suppression of CeAL excitatory inputs is enhanced. Collectively, these data identify a prominent role for eCBs in the modulation of excitatory drive to CeAL neurons and provide insight into the mechanisms by which eCB signaling and exogenous cannabinoids could regulate stress-responses and emotional learning.
Advisors/Committee Members: Sachin Patel MD., PhD. (committee member), Karoly Mirnics, MD., PhD. (committee member), Roger Cone, PhD. (committee member), Sean Davies, PhD. (committee member), Danny Winder, PhD. (Committee Chair).
Subjects/Keywords: central amygdala; endocannabinoid; stress
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APA (6th Edition):
Ramikie, T. S. (2014). Mechanistically Distinct Modes of Endocannabinoid Mobilization at Glutamatergic Synapses of the Lateral Division of the Central Amygdala and Its Regulation by Chronic Stress. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14788
Chicago Manual of Style (16th Edition):
Ramikie, Teniel Sonya. “Mechanistically Distinct Modes of Endocannabinoid Mobilization at Glutamatergic Synapses of the Lateral Division of the Central Amygdala and Its Regulation by Chronic Stress.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed March 07, 2021.
http://hdl.handle.net/1803/14788.
MLA Handbook (7th Edition):
Ramikie, Teniel Sonya. “Mechanistically Distinct Modes of Endocannabinoid Mobilization at Glutamatergic Synapses of the Lateral Division of the Central Amygdala and Its Regulation by Chronic Stress.” 2014. Web. 07 Mar 2021.
Vancouver:
Ramikie TS. Mechanistically Distinct Modes of Endocannabinoid Mobilization at Glutamatergic Synapses of the Lateral Division of the Central Amygdala and Its Regulation by Chronic Stress. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1803/14788.
Council of Science Editors:
Ramikie TS. Mechanistically Distinct Modes of Endocannabinoid Mobilization at Glutamatergic Synapses of the Lateral Division of the Central Amygdala and Its Regulation by Chronic Stress. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14788
University of Waikato
4.
Brunton, Chloe.
Social interaction affects acquisition of lithium chloride-induced conditioned taste aversion: identification of underlying changes in neuronal activation in key forebrain areas
.
Degree: 2016, University of Waikato
URL: http://hdl.handle.net/10289/10641
► A conditioned taste aversion (CTA) develops when exposure to a novel tastant is followed by sickness/malaise. Recently, it has been shown that a CTA can…
(more)
▼ A conditioned taste aversion (CTA) develops when exposure to a novel tastant is followed by sickness/malaise. Recently, it has been shown that a CTA can be reduced if the animal is placed in a social environment, i.e., in the presence of a conspecific, during the CTA acquisition phase. The current project was aimed to expand on our understanding of this phenomenon by (a) identifying the magnitude of an aversive response to a saccharin solution induced by lithium chloride (LiCl), a known emetic agent, in mice maintained in the social versus non-social setting; and (b) defining differences in LiCl-induced neuronal activation in the key CTA-related forebrain areas of animals in the social and non-social scenario. In mice lacking social stimulation, LiCl at a dose of 1 mEq induced a mild CTA to saccharin and the 6-mEq dose produced a profound aversive response. On the other hand, 6 mEq was the lowest effective dose in mice kept in the social setting. Immunohistochemical analysis of a neuronal activity marker, c-Fos, showed that alteration of activity in the paraventricular nucleus of the hypothalamus (PVN) and central nucleus of the
amygdala (CEA) is associated with the observed changes. In LiCl-injected mice subjected to social stimulation, also the percentage of Fos-positive oxytocin (OT), but not vasopressin neurons in the PVN was higher than in LiCl-treated single-housed mice. These results are discussed in context of the effects that sociality has on the magnitude of responses to adverse associative stimuli and an involvement of specific elements of brain circuitry in mediating these effects.
Advisors/Committee Members: Olszewski, Pawel K (advisor).
Subjects/Keywords: aversion;
oxytocin;
sociality;
amygdala;
hypothalamus
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APA (6th Edition):
Brunton, C. (2016). Social interaction affects acquisition of lithium chloride-induced conditioned taste aversion: identification of underlying changes in neuronal activation in key forebrain areas
. (Masters Thesis). University of Waikato. Retrieved from http://hdl.handle.net/10289/10641
Chicago Manual of Style (16th Edition):
Brunton, Chloe. “Social interaction affects acquisition of lithium chloride-induced conditioned taste aversion: identification of underlying changes in neuronal activation in key forebrain areas
.” 2016. Masters Thesis, University of Waikato. Accessed March 07, 2021.
http://hdl.handle.net/10289/10641.
MLA Handbook (7th Edition):
Brunton, Chloe. “Social interaction affects acquisition of lithium chloride-induced conditioned taste aversion: identification of underlying changes in neuronal activation in key forebrain areas
.” 2016. Web. 07 Mar 2021.
Vancouver:
Brunton C. Social interaction affects acquisition of lithium chloride-induced conditioned taste aversion: identification of underlying changes in neuronal activation in key forebrain areas
. [Internet] [Masters thesis]. University of Waikato; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10289/10641.
Council of Science Editors:
Brunton C. Social interaction affects acquisition of lithium chloride-induced conditioned taste aversion: identification of underlying changes in neuronal activation in key forebrain areas
. [Masters Thesis]. University of Waikato; 2016. Available from: http://hdl.handle.net/10289/10641
University of Ottawa
5.
Qin, Zhaohong.
The Role of LMO4 in the Regulation of Hippocampal and Amygdalar Synaptic Function
.
Degree: 2013, University of Ottawa
URL: http://hdl.handle.net/10393/26204
► Synaptic activity can encode and store information in the brain through changes in synaptic strength as well as by control of gene expression. One corollary…
(more)
▼ Synaptic activity can encode and store information in the brain through changes in synaptic strength as well as by control of gene expression. One corollary challenge becomes identifying these activity-dependent regulatory proteins and the underlying mechanisms associated with neuronal functions. By using biochemical, electrophysiological and behavioral approaches in combination with genetic and pharmacological manipulation, I report that LIM domain only 4 (LMO4) is a key regulator of calcium induced calcium release (CICR) and protein tyrosine phosphatase 1B (PTP1B) in the hippocampus and amygdala, respectively. Neuronal ablation of LMO4 in the glutamatergic neurons (LMO4KO) was associated with reduced promoter activity, mRNA, and protein expression of ryanodine receptor 2 (RyR2), suggesting the involvement of LMO4 in the transcriptional regulation. CICR function in LMO4KO mice was severely compromised, reflected by inefficient CICR-mediated electrophysiological responses including afterhyperpolarization, calcium rise from internal stores and glutamate release probability. These changes were accompanied with impaired hippocampal long term potentiation (LTP) and hippocampal-dependent spatial learning ability. LMO4 was also shown to exert a cytoplasmic regulation as an endogenous inhibitor for PTP1B that accounts for tyrosine dephosphorylation of mGluR5 in the amygdala. LMO4KO mice had elevated PTP1B activity and decreased mGluR endocannabinoid signaling, resulting in a profound anxiety phenotype. The potential clinical value of PTP1B/LMO4 is promising, given that intra-amygdala injection of the PTP1B inhibitor Trodusquemine or a PTP1B shRNA alleviated anxiety by restoring eCB signal in LMO4KO mice. Thus this study identified PTP1B as a potential therapeutic target for anxiety, besides the previous findings of its association with obesity and diabetes. Moreover, this PTP1B-mediated anxiety may be a general mechanism during chronic stress. Collectively, these findings identify that LMO4 plays an essential role for non-genomic and genomic regulation in central neurons, providing a mechanism for LMO4 to modulate a wide range of neuronal functions and behavior.
Subjects/Keywords: LMO4;
Hippocampus;
Amygdala;
Synaptic function
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APA (6th Edition):
Qin, Z. (2013). The Role of LMO4 in the Regulation of Hippocampal and Amygdalar Synaptic Function
. (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/26204
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Qin, Zhaohong. “The Role of LMO4 in the Regulation of Hippocampal and Amygdalar Synaptic Function
.” 2013. Thesis, University of Ottawa. Accessed March 07, 2021.
http://hdl.handle.net/10393/26204.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Qin, Zhaohong. “The Role of LMO4 in the Regulation of Hippocampal and Amygdalar Synaptic Function
.” 2013. Web. 07 Mar 2021.
Vancouver:
Qin Z. The Role of LMO4 in the Regulation of Hippocampal and Amygdalar Synaptic Function
. [Internet] [Thesis]. University of Ottawa; 2013. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10393/26204.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Qin Z. The Role of LMO4 in the Regulation of Hippocampal and Amygdalar Synaptic Function
. [Thesis]. University of Ottawa; 2013. Available from: http://hdl.handle.net/10393/26204
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
6.
Snow, Matthew.
GABA Cells in the Central Nucleus of the Amygdala Control Cataplexy.
Degree: 2016, University of Toronto
URL: http://hdl.handle.net/1807/72794
► Cataplexy is a hallmark of narcolepsy characterized by the sudden onset of muscle weakness or paralysis during wakefulness. It can occur spontaneously but is typically…
(more)
▼ Cataplexy is a hallmark of narcolepsy characterized by the sudden onset of muscle weakness or paralysis during wakefulness. It can occur spontaneously but is typically triggered by positive emotions like laughter. Although cataplexy was identified over 130 years ago, its neural mechanism remains unclear. Here, we show that a newly identified GABA circuit within the central nucleus of the amygdala (CeA) may play a causal role in promoting cataplexy. We found that, in narcoleptic mice, chemogenetic activation of GABA cells within the CeA triggered a 253% increase in the number of cataplexy attacks without affecting their duration. We also show that GABA cell activation only promotes cataplexy attacks associated with emotionally rewarding stimuli such as wheel running, without impacting spontaneous attacks. Our results indicate that the CeA plays a pivotal role in controlling cataplexy onset, and that emotionally rewarding stimuli may trigger cataplexy by activating GABA cells in the CeA.
M.Sc.
Advisors/Committee Members: Peever, John, Cell and Systems Biology.
Subjects/Keywords: Amygdala; Cataplexy; Chemogenetics; Narcolepsy; 0317
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APA ·
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APA (6th Edition):
Snow, M. (2016). GABA Cells in the Central Nucleus of the Amygdala Control Cataplexy. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/72794
Chicago Manual of Style (16th Edition):
Snow, Matthew. “GABA Cells in the Central Nucleus of the Amygdala Control Cataplexy.” 2016. Masters Thesis, University of Toronto. Accessed March 07, 2021.
http://hdl.handle.net/1807/72794.
MLA Handbook (7th Edition):
Snow, Matthew. “GABA Cells in the Central Nucleus of the Amygdala Control Cataplexy.” 2016. Web. 07 Mar 2021.
Vancouver:
Snow M. GABA Cells in the Central Nucleus of the Amygdala Control Cataplexy. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1807/72794.
Council of Science Editors:
Snow M. GABA Cells in the Central Nucleus of the Amygdala Control Cataplexy. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/72794
University of Florida
7.
Hernandez, Caesar M, III.
Neural Mechanisms of Age-Related Alterations to Decision Making.
Degree: PhD, Medical Sciences - Neuroscience (IDP), 2018, University of Florida
URL: https://ufdc.ufl.edu/UFE0052860
Subjects/Keywords: aging; amygdala
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APA (6th Edition):
Hernandez, Caesar M, I. (2018). Neural Mechanisms of Age-Related Alterations to Decision Making. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0052860
Chicago Manual of Style (16th Edition):
Hernandez, Caesar M, III. “Neural Mechanisms of Age-Related Alterations to Decision Making.” 2018. Doctoral Dissertation, University of Florida. Accessed March 07, 2021.
https://ufdc.ufl.edu/UFE0052860.
MLA Handbook (7th Edition):
Hernandez, Caesar M, III. “Neural Mechanisms of Age-Related Alterations to Decision Making.” 2018. Web. 07 Mar 2021.
Vancouver:
Hernandez, Caesar M I. Neural Mechanisms of Age-Related Alterations to Decision Making. [Internet] [Doctoral dissertation]. University of Florida; 2018. [cited 2021 Mar 07].
Available from: https://ufdc.ufl.edu/UFE0052860.
Council of Science Editors:
Hernandez, Caesar M I. Neural Mechanisms of Age-Related Alterations to Decision Making. [Doctoral Dissertation]. University of Florida; 2018. Available from: https://ufdc.ufl.edu/UFE0052860
8.
Putnam, Philip.
Neural Substrates of Social Behavior in the Primate Brain
.
Degree: 2019, University of Arizona
URL: http://hdl.handle.net/10150/631936
► Many brain structures are known for carrying out more than one function. Among these structures the amygdala emerged particularly versatile, as it has been implicated…
(more)
▼ Many brain structures are known for carrying out more than one function. Among these structures the
amygdala emerged particularly versatile, as it has been implicated in cognitive processes that range from sensory-perceptual, to decision-making, and to overt behaviors accompanied by autonomic responses. While no single functional definition can capture its role in the brain, the diversity of functions linked to the
amygdala is likely reflected in the response properties of its component neurons. The goal of this study was to determine the extent to which single neurons in the
amygdala can exhibit multiple types of stimulus-selectivity and/or task-related responses in the context of a complex task. The task involved learning and decision making based on stimulus-reward associations where the choices were presented as multiple simultaneously playing videos with social and non-social content. Here we report that
amygdala neurons are tuned to multiple stimulus and task dimensions. Furthermore a disproportionate number of neurons responded to all of the features examined. This demonstration of multi-dimensional selectivity in the
amygdala provides evidence that the
amygdala is not composed exclusively of discrete circuits, but rather of common overlapping populations that encode multiple types of information.
Advisors/Committee Members: Cowen, Stephen (advisor), Gothard, Katalin (committeemember), Bao, Shaowen (committeemember), Cai, Haijiang (committeemember).
Subjects/Keywords: amygdala;
Multi-dimensional selectivity;
rhesus
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APA ·
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APA (6th Edition):
Putnam, P. (2019). Neural Substrates of Social Behavior in the Primate Brain
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/631936
Chicago Manual of Style (16th Edition):
Putnam, Philip. “Neural Substrates of Social Behavior in the Primate Brain
.” 2019. Doctoral Dissertation, University of Arizona. Accessed March 07, 2021.
http://hdl.handle.net/10150/631936.
MLA Handbook (7th Edition):
Putnam, Philip. “Neural Substrates of Social Behavior in the Primate Brain
.” 2019. Web. 07 Mar 2021.
Vancouver:
Putnam P. Neural Substrates of Social Behavior in the Primate Brain
. [Internet] [Doctoral dissertation]. University of Arizona; 2019. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10150/631936.
Council of Science Editors:
Putnam P. Neural Substrates of Social Behavior in the Primate Brain
. [Doctoral Dissertation]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/631936
University of Sydney
9.
Kissiwaa, Sarah Abena.
Pain induced synaptic plasticity in the amygdala
.
Degree: 2017, University of Sydney
URL: http://hdl.handle.net/2123/17358
► Pain is an important defense against dangers in our environment, however some clinical conditions produce pain that outlasts this useful role and persist even after…
(more)
▼ Pain is an important defense against dangers in our environment, however some clinical conditions produce pain that outlasts this useful role and persist even after the injury has healed. The experience of pain consists of somatosensory elements of intensity and location, negative emotional/aversive feelings and subsequent restrictions on lifestyle due to learning to associate certain activities with pain. The amygdala contributes negative emotional value to nociceptive sensory information and forms the association between an aversive response and the environment in which it occurs. It can form this association because it receives nociceptive information via the spino-parabrachio-amygdaloid pathway and polymodal sensory information via its basolateral nucleus (BLA) and cortical and thalamic inputs. Within the spino-parabrachio-amygdaloid pathway, nociceptive information is sent from the external lateral nucleus of the parabrachial nucleus (PB) to the laterocapsular region of the central nucleus of the amygdala (CeLC). The PB-CeLC synapse and other brain regions undergo synaptic plasticity in chronic pain conditions with ongoing injury. However very little is known about how plasticity occurs in conditions where pain persists even after the injury has healed. In the first study of this thesis, I used immunohistochemistry, electrophysiology and behavioural assays, to show that a brief nociceptive stimulus with no ongoing injury can produce long-lasting synaptic plasticity at the rat parabrachial-amygdala synapse. I show that this plasticity is caused by an increase in number of postsynaptic AMPARs with a transient change in AMPAR subunit, similar to long-term potentiation. Furthermore, repeated stimuli lengthened this plasticity. The potentiation could be representative of the initial changes that occur in the transition from an acute to a chronic pain state. This could mean greater association of a painful experience with the environment and context and could ultimately facilitate the negative association of certain activities and situations with pain, leading to limiting or avoidance of these activities/situations. The next studies of this thesis focused on potential neuromodulators of activity at the PB-CeLC synapse and the polymodal BLA inputs to the CeLC. Opioids and Calcitonin gene-related peptide (CGRP) were chosen because of their presence at synapses in the amygdala and their role in pain particularly in the affective component of pain. Opioids reduce pain intensity and the emotional unpleasantness of pain. Opioids inhibit some synapses in the amygdala, however whether opioids specifically modulate the PB-CeLC and the BLA-CeLC is unknown. I used electrophysiology and optogenetics to show that opioids inhibit two synapses important for pain modulation in the amygdala. Given the evidence of the opioid’s role in reducing pain affect, modulation of these synapses could be, in part, the site of opioid action. CGRP is expressed at all levels of the spino-parabrachio-amygdala pathway and modulates pain, as CGRP…
Subjects/Keywords: amygdala;
pain;
synapse;
plasticity
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APA (6th Edition):
Kissiwaa, S. A. (2017). Pain induced synaptic plasticity in the amygdala
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/17358
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kissiwaa, Sarah Abena. “Pain induced synaptic plasticity in the amygdala
.” 2017. Thesis, University of Sydney. Accessed March 07, 2021.
http://hdl.handle.net/2123/17358.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kissiwaa, Sarah Abena. “Pain induced synaptic plasticity in the amygdala
.” 2017. Web. 07 Mar 2021.
Vancouver:
Kissiwaa SA. Pain induced synaptic plasticity in the amygdala
. [Internet] [Thesis]. University of Sydney; 2017. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2123/17358.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kissiwaa SA. Pain induced synaptic plasticity in the amygdala
. [Thesis]. University of Sydney; 2017. Available from: http://hdl.handle.net/2123/17358
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Sydney
10.
Falon, Jessica.
Cellular Characterisation of Endogenous Analgesic Systems
.
Degree: 2019, University of Sydney
URL: http://hdl.handle.net/2123/20801
► Pain places a great burden upon society, and a better understanding of pain circuitry will be critical to developing new therapies. Of interest is the…
(more)
▼ Pain places a great burden upon society, and a better understanding of pain circuitry will be critical to developing new therapies. Of interest is the connection between the medial nucleus of the central amygdala (CeM) and periaqueductal gray (PAG), due to its role in producing analgesia. Opioid and cannabinoid analgesics act upon this pathway, though their specific sites of action within amygdala pain circuitry has not been fully determined. Therefore, the present study aimed to address this using tract tracing and whole cell patch clamp electrophysiology. Retrograde tracer was injected into the rat PAG, and the effects of opioids and cannabinoids on inhibitory inputs to labelled and unidentified CeM neurons was recorded. Notably, while DAMGO reduced inhibitory input to the CeM in both unidentified and labelled projection neurons, deltorphin inhibited inputs to unidentified neurons alone, and U69593 to only projection neurons. DHPG also produced short-term inhibition of inhibitory inputs to CeM neurons, which was abolished by AM251 in unidentified but not labelled neurons. This inhibition was associated with an extended recovery time, which was reduced by AM251 in both populations. These findings suggest that pain processing amygdala circuitry is differentially modulated by opioid receptor agonists. DHPG also modulates this circuitry, however in projection neurons, short-term inhibition seemed to be cannabinoid-independent and longer-term inhibition to be cannabinoid-dependent, potentially indicative of cannabinoid-dependent long-term depression (LTD). Overall, this study is the first to electrophysiologically demonstrate a role for cannabinoids in modulating inputs to PAG-projecting CeM neurons, as well as for κ-receptor agonists in preferentially inhibiting these inputs. This broadens our understanding of how these analgesics interact with pain circuitry via the amygdala, and may lead to more successful manipulation of this pathway to effectively manage pain.
Subjects/Keywords: pain;
amygdala;
opoid;
cannabinoid
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Chicago ·
MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
Falon, J. (2019). Cellular Characterisation of Endogenous Analgesic Systems
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/20801
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Falon, Jessica. “Cellular Characterisation of Endogenous Analgesic Systems
.” 2019. Thesis, University of Sydney. Accessed March 07, 2021.
http://hdl.handle.net/2123/20801.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Falon, Jessica. “Cellular Characterisation of Endogenous Analgesic Systems
.” 2019. Web. 07 Mar 2021.
Vancouver:
Falon J. Cellular Characterisation of Endogenous Analgesic Systems
. [Internet] [Thesis]. University of Sydney; 2019. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2123/20801.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Falon J. Cellular Characterisation of Endogenous Analgesic Systems
. [Thesis]. University of Sydney; 2019. Available from: http://hdl.handle.net/2123/20801
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of New South Wales
11.
Moul, Caroline.
The Development and assessment of a Differential Amygdala Activation Model in psychopathy.
Degree: Psychology, 2012, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/52286
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10958/SOURCE01?view=true
► This thesis introduces a novel hypothesis regarding amygdala function in psychopathy. The first chapter of the thesis will introduce a model of differential amygdala activation…
(more)
▼ This thesis introduces a novel hypothesis regarding
amygdala function in psychopathy. The first chapter of the thesis will introduce a model of differential
amygdala activation (DAAM) in which the basolateral
amygdala (BLA) is underactive while the activity of the central
amygdala (CeA) is of average to above average levels. This model is proposed to provide a more accurate and up-to-date account for the specific cognitive and emotional deficits found in psychopathy and integrates current knowledge regarding the function of neurochemical systems implicated in the disorder. The remainder of the thesis then tests some of the hypotheses that are generated by the model.The main sample used in this thesis comprised children aged between 4 and 12 years old referred to clinical services for antisocial behaviour problems. The functions of the serotonin and oxytocin systems were indexed via both peripheral blood measures and genetic data. An emotion-recognition task was used to assess fear-recognition deficits and a novel learning task was developed in order to enable the assessment of learning-style.It was hypothesised that high levels of callous-unemotional (CU) traits would be associated with diminished function of both the serotonin and oxytocin systems. Evidence was found from both peripheral measures and from genetic analyses to support these hypotheses. With regards to cognitive deficits, it was predicted that people with high levels of psychopathic traits would demonstrate a bias in learning-style. Pilot data from the novel learning task supported this hypothesis and the relationship between findings from this task and serotonin-system function was concordant with the hypotheses made by the DAAM. Finally, it was predicted that fear-recognition ability would be associated with callous-unemotional traits and that this would be uniquely related to serotonin-system function. Results from the analysis of both peripheral serotonin levels and genetic data supported this hypothesis.In all, the results presented in this thesis provide initial support for the hypotheses made by the DAAM regarding the role of the serotonin and oxytocin systems in psychopathy and the influence of these on basic cognitive functions. The limitations and implications of these findings are discussed.
Advisors/Committee Members: Dadds, Mark, Psychology, Faculty of Science, UNSW, Killcross, Simon, Psychology, Faculty of Science, UNSW.
Subjects/Keywords: Callous-unemotional; Psychopathy; Amygdala; Genetic
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APA ·
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MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Moul, C. (2012). The Development and assessment of a Differential Amygdala Activation Model in psychopathy. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52286 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10958/SOURCE01?view=true
Chicago Manual of Style (16th Edition):
Moul, Caroline. “The Development and assessment of a Differential Amygdala Activation Model in psychopathy.” 2012. Doctoral Dissertation, University of New South Wales. Accessed March 07, 2021.
http://handle.unsw.edu.au/1959.4/52286 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10958/SOURCE01?view=true.
MLA Handbook (7th Edition):
Moul, Caroline. “The Development and assessment of a Differential Amygdala Activation Model in psychopathy.” 2012. Web. 07 Mar 2021.
Vancouver:
Moul C. The Development and assessment of a Differential Amygdala Activation Model in psychopathy. [Internet] [Doctoral dissertation]. University of New South Wales; 2012. [cited 2021 Mar 07].
Available from: http://handle.unsw.edu.au/1959.4/52286 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10958/SOURCE01?view=true.
Council of Science Editors:
Moul C. The Development and assessment of a Differential Amygdala Activation Model in psychopathy. [Doctoral Dissertation]. University of New South Wales; 2012. Available from: http://handle.unsw.edu.au/1959.4/52286 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10958/SOURCE01?view=true
University of New South Wales
12.
Campbell-Smith, Emma.
Infusion of oxytocin into the basolateral amygdala facilitates, whereas infusion into the central nucleus impairs extinction of context conditioned fear responses in rats.
Degree: Psychology, 2013, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/53932
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12642/SOURCE02?view=true
► Increasing oxytocin (OT) in the central amygdala (CeA) via infusion of a selective OT agonist (Viviani et al., 2011) or optogenetic stimulation of hypothalamic neurons…
(more)
▼ Increasing oxytocin (OT) in the central
amygdala (CeA) via infusion of a selective OT agonist (Viviani et al., 2011) or optogenetic stimulation of hypothalamic neurons (Knobloch et al., 2012) reduced conditioned freezing responses. In contrast, intracerebroventricular (i.c.v.) administration of OT increased conditioned freezing responses (Toth, Neumann, & Slattery, 2012). The route of administration may account for these differences in fear responses. Specifically, i.c.v. OT may target other
amygdala areas such as the basolateral
amygdala (BLA), thereby increasing freezing responses. This thesis investigated CeA and BLA infusions of OT on the acquisition and extinction of context conditioned fear responses. In two experiments investigating the effects of OT on fear acquisition, rats were trained to fear a context under a drug infusion and their retention of fear assessed when drug-free. Intra-CeA and intra-BLA infusions of OT had no effect on freezing responses across the conditioning session. However, fear responses were reduced at test indicating that OT impaired the acquisition of context conditioned fear. In 8 experiments investigating the effects of OT on fear extinction, rats were trained to fear a context, their fear extinguished under a drug infusion or the drug was infused immediately after extinction and their retention of extinguished fear assessed when drug-free. Infusion of OT into the CeA impaired, whereas infusion into the BLA facilitated the extinction of fear responses. This was blocked by co-infusion of a selective OT antagonist (OTA; desGly-NH2-d(CH2)5[D-Tyr2,Thr4]OVT) suggesting OT receptor specificity. OT infused into the BLA after extinction training had no effect on fear responses at test suggesting that OT does not affect the consolidation of extinction learning in the BLA. In contrast, OT infused into the CeA after extinction training reduced fear responses at test suggesting that OT had impaired the consolidation of extinction learning in this nucleus. OTA infused into the CeA reduced freezing responses across the extinction session whereas BLA-OTA had no effect. This suggests that endogenous CeA-OT maintains freezing responses across the extinction session whereas endogenous BLA-OT may not influence fear responding or the depression of fear responses that occur across extinction training. Lastly, an infusion of muscimol into the BLA and CeA had effects similar to OT on long-term depression of fear responses suggesting that OT may influence fear extinction via an increase in GABA activity.
Advisors/Committee Members: Westbrook, Fred, Psychology, Faculty of Science, UNSW, McNally, Gavan, Psychology, Faculty of Science, UNSW.
Subjects/Keywords: Extinction; Oxytocin; Fear; Amygdala
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Campbell-Smith, E. (2013). Infusion of oxytocin into the basolateral amygdala facilitates, whereas infusion into the central nucleus impairs extinction of context conditioned fear responses in rats. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/53932 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12642/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Campbell-Smith, Emma. “Infusion of oxytocin into the basolateral amygdala facilitates, whereas infusion into the central nucleus impairs extinction of context conditioned fear responses in rats.” 2013. Doctoral Dissertation, University of New South Wales. Accessed March 07, 2021.
http://handle.unsw.edu.au/1959.4/53932 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12642/SOURCE02?view=true.
MLA Handbook (7th Edition):
Campbell-Smith, Emma. “Infusion of oxytocin into the basolateral amygdala facilitates, whereas infusion into the central nucleus impairs extinction of context conditioned fear responses in rats.” 2013. Web. 07 Mar 2021.
Vancouver:
Campbell-Smith E. Infusion of oxytocin into the basolateral amygdala facilitates, whereas infusion into the central nucleus impairs extinction of context conditioned fear responses in rats. [Internet] [Doctoral dissertation]. University of New South Wales; 2013. [cited 2021 Mar 07].
Available from: http://handle.unsw.edu.au/1959.4/53932 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12642/SOURCE02?view=true.
Council of Science Editors:
Campbell-Smith E. Infusion of oxytocin into the basolateral amygdala facilitates, whereas infusion into the central nucleus impairs extinction of context conditioned fear responses in rats. [Doctoral Dissertation]. University of New South Wales; 2013. Available from: http://handle.unsw.edu.au/1959.4/53932 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12642/SOURCE02?view=true
University of Texas – Austin
13.
Worthy, Emily Luther.
Affective priming following unilateral temporal lobectomy : the role of the amygdala.
Degree: PhD, Clinical Psychology, 2012, University of Texas – Austin
URL: http://hdl.handle.net/2152/ETD-UT-2012-08-5989
► The way that emotions are processed in the brain has been widely debated. The two leading hypotheses are the cognitive appraisal viewpoint (Lazarus, 1982) and…
(more)
▼ The way that emotions are processed in the brain has been widely debated. The two leading hypotheses are the cognitive appraisal viewpoint (Lazarus, 1982) and the affective primacy hypothesis (Zajonc, 1980). The former argues that higher cortical structures are needed to evaluate affective stimuli whereas the latter asserts that humans can use information only processed at the subcortical level to influence behavior. The current study tested the presence of this subcortical pathway by using an affective priming task developed by Murphy and Zajonc (1993). Happy and angry faces were presented for 4 ms before the presentation of a neutral stimulus (Chinese Ideograph) that participants were asked to rate based on how much they liked each one. Individuals do not report conscious awareness of primes presented at this suboptimal speed. In a young adult sample, participants rated ideographs preceded by happy primes significantly higher than those preceded by angry primes. Also, the priming effect was only observed in participants who reported a high positive mood. Next, when primes were presented in the left or right hemifield priming was only found in the right hemifield, and was driven by increased ratings for ideographs preceded by happy primes. Patients with epilepsy who have undergone a temporal lobectomy provide a unique opportunity to study emotional processing. In this procedure, not only is the seizure focus (typically the hippocampus) removed, but the
amygdala and surrounding areas of the mesial temporal lobe are removed as well. Nine patients post right temporal lobectomy and three patients post left temporal lobectomy completed the study and did not show an effect of priming. However, 21 pre-surgical epilepsy patients were found to give higher liking ratings to ideographs preceded by angry primes as compared to those preceded by happy primes. Overall, these results support the affective primacy hypothesis however they also suggest that patients with temporal lobe dysfunction may process emotional stimuli differentially from controls. In this population, ideographs preceded by angry primes were rated as more liked than those preceded by happy primes. Directions for future studies to clarify the role of the
amygdala in emotional processing are discussed.
Advisors/Committee Members: Beevers, Chris G. (advisor), Tucker, David M., 1953- (advisor), Schnyer, David (committee member), Shen, Jason (committee member), Maddox, Todd (committee member).
Subjects/Keywords: Amygdala; Emotional processing; Priming; Epilepsy
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Worthy, E. L. (2012). Affective priming following unilateral temporal lobectomy : the role of the amygdala. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2012-08-5989
Chicago Manual of Style (16th Edition):
Worthy, Emily Luther. “Affective priming following unilateral temporal lobectomy : the role of the amygdala.” 2012. Doctoral Dissertation, University of Texas – Austin. Accessed March 07, 2021.
http://hdl.handle.net/2152/ETD-UT-2012-08-5989.
MLA Handbook (7th Edition):
Worthy, Emily Luther. “Affective priming following unilateral temporal lobectomy : the role of the amygdala.” 2012. Web. 07 Mar 2021.
Vancouver:
Worthy EL. Affective priming following unilateral temporal lobectomy : the role of the amygdala. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152/ETD-UT-2012-08-5989.
Council of Science Editors:
Worthy EL. Affective priming following unilateral temporal lobectomy : the role of the amygdala. [Doctoral Dissertation]. University of Texas – Austin; 2012. Available from: http://hdl.handle.net/2152/ETD-UT-2012-08-5989
University of Sydney
14.
Gregoriou, Gabrielle.
Opioid withdrawal induced neuroadaptations in the amygdala
.
Degree: 2020, University of Sydney
URL: http://hdl.handle.net/2123/23168
► Opioid withdrawal induces long-lasting effects on neuronal function and synaptic transmission in opioid-sensitive neurons throughout the brain. These persistent changes are thought to drive drug-seeking…
(more)
▼ Opioid withdrawal induces long-lasting effects on neuronal function and synaptic transmission in opioid-sensitive neurons throughout the brain. These persistent changes are thought to drive drug-seeking and relapse behaviours during the withdrawal state and beyond into abstinence. Despite this, the mechanisms and circuits underlying the altered behaviours following opioid withdrawal are only partially understood, limiting the development of addiction treatments. Neural circuits within the amygdala mediate drug-seeking and relapse behaviours, thus, the current thesis hypothesised that neuroadaptations would manifest in opioid-sensitive amygdala cells during opioid withdrawal. Using patch-clamp electrophysiology in rat brain slices, the effects of opioid withdrawal on the highly opioid-sensitive intercalated amygdala neurons and their connections were investigated. The broad aims of this thesis were firstly, to define the activity and connections of the intercalated neurons and also their regulation by various neuromodulators under normal physiological conditions. Then, to determine whether opioid withdrawal induced any neuroadaptive changes to normal functioning. To this end, Chapter 3 defined that the activity of an enkephalin-degrading peptidase, neprilysin, was a key regulator of synaptic transmission in the main intercalated cell nucleus. Chapter 4 highlighted that the activity of neprilysin was increased in the intercalated cells during withdrawal, a change that reduced peptide control of synaptic transmission between amygdala nuclei. Finally, Chapter 5 revealed that the increased peptidase activity changed synaptic transmission onto a population of amygdala neurons that mediate the learning and memory processes that become maladaptive during withdrawal, potentially triggering drug-seeking behaviours during the withdrawal state and abstinence. As amygdala neural circuits are involved in the development of addiction behaviours, the current thesis has identified that peptide systems in the amygdala are viable targets for the development of novel pharmacotherapies for drug relapse, a feature of addiction that severely limits the efficacy of current treatment options. Restoring endogenous peptide activity within the amygdala during withdrawal may return synaptic transmission to normal, mitigate the withdrawal-induced neuroadaptations and rescue the addiction behaviours exhibited during opioid withdrawal and abstinence.
Subjects/Keywords: Opioid withdrawal;
neuroadaptations;
amygdala
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APA ·
Chicago ·
MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Gregoriou, G. (2020). Opioid withdrawal induced neuroadaptations in the amygdala
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/23168
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Gregoriou, Gabrielle. “Opioid withdrawal induced neuroadaptations in the amygdala
.” 2020. Thesis, University of Sydney. Accessed March 07, 2021.
http://hdl.handle.net/2123/23168.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Gregoriou, Gabrielle. “Opioid withdrawal induced neuroadaptations in the amygdala
.” 2020. Web. 07 Mar 2021.
Vancouver:
Gregoriou G. Opioid withdrawal induced neuroadaptations in the amygdala
. [Internet] [Thesis]. University of Sydney; 2020. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2123/23168.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Gregoriou G. Opioid withdrawal induced neuroadaptations in the amygdala
. [Thesis]. University of Sydney; 2020. Available from: http://hdl.handle.net/2123/23168
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
15.
Chia-chi, Jacqueline.
Mevinphos Induces Seizure-like EEG Activity and Decreases Blood Pressure by an Action on Amygdala.
Degree: Master, Biological Sciences, 2011, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730111-113324
► Mevinphos (Mev) is an orgnophosphate insectide used for suicidal purposes in Taiwan; seizure and cardiovascular depression are commom syptoms observed in organophosphate-poisoned patients. The amygdala…
(more)
▼ Mevinphos (Mev) is an orgnophosphate insectide used for suicidal purposes in Taiwan; seizure and cardiovascular depression are commom syptoms observed in organophosphate-poisoned patients. The
amygdala (AMG) is part of the limbic system and the basolateral nucleus of AMG (BLA) is one of the most seizure-prone brain structures. The central neucleus of AMG (CeA) is thought to play a central role in behavioral, physiological response and cardiovascular regulation. However, detailed mechanisms in Mev-induced seizure and cardiovascular depression by an action on AMG are lacking. Based on electroencephalographic (EEG) activity to indicate neuronal electrical activity and arterial blood pressure (AP) and heart rate (HR) to indicate cardiovascular responses, the present study investigated whether Mev acts on AMG to elicit seizure or cardiovascular depression.
Microinjection of Mev into BLA of adult male Sprague-Dawley (SD) rats maintained under propofol anesthesia increased EEG activity in AMG, cortex and CA3 of hippocampus leading to seizure initiation; however AP, HR, respiration rate (RR) and the power density of low-frequency (LF) component of AP was not significantly changed. Microinjection of Mev into BLA also time-dependently increased protein level and mRNA of cytokines interleukin (IL)-12, IL-13, tumor suppressor factor alpha (TNFα) and interferon gamma (IFNγ) and cyclooxygenase (COX) activity in AMG. Microinjection of Mev into CA3 induced less seizure activity in cortex and CA3 than that induced by microinjection of Mev into BLA. In addition, microinjection Mev into CA3 did not induce seizure in AMG. These results suggest that Mev acted on BLA to initiate limbic seizures. Intraperitoneal injection of muscarinic receptor antagonist atropine (ATR), which can pass the blood-brain barrier (BBB), activator of GABAergic neurotransmission midazolam (MDZ) or antiinflaamatory agent pentoxifylline (PTX) and Lisofylline (LSF), but not muscarinic receptor antagonist atropine methyl nitrate (AMN), which can not pass BBB, inhibited Mev-induced seizure and increase of cytokines in AMG by an action on BLA. Microinjection of ATR, COX-1 inhibitor naproxen (NPX) or COX-2 inhibitor NS-398, antiserum against receptor of IL-12, IL-13, TNFα or IFNγ, but not nicotinic receptor antagonist mecamylamine (MEL), into BLA inhibited Mev-induced seizure and increase of cytokines and COX activity in AMG by an action on BLA. However, caspase 3 activity and DNA fragmentation at AMG were not changed by microinjection of Mev into BLA.
Microinjection of Mev into CeA induced a decrease in AP and RR leading to cardiovascular depression and an increase of power desity of LF, accompanied with insignificant HR and EEG activity change. Microinjection of Mev into CeA induced the time-dependently increase of caspase 3 activity and DNA fragmentation leading to apoptosis in AMG. Microinjection of ATR or caspase 3-dependent apoptosome inhibitor NS-3694, but not MEL, into CeA inhibited cardiovascular depression and the increase of caspase 3 activity and DNA…
Advisors/Committee Members: Yen, Jiin-Cherng (chair), Chang, Alice Y.W. (committee member), Chan, Samuel H.H. (chair), Gean, Po-Wu (chair).
Subjects/Keywords: Apoptosis; Amygdala; Mevinphos; Inflammation; Cardiovascular Response; Seizure
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APA ·
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APA (6th Edition):
Chia-chi, J. (2011). Mevinphos Induces Seizure-like EEG Activity and Decreases Blood Pressure by an Action on Amygdala. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730111-113324
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chia-chi, Jacqueline. “Mevinphos Induces Seizure-like EEG Activity and Decreases Blood Pressure by an Action on Amygdala.” 2011. Thesis, NSYSU. Accessed March 07, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730111-113324.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chia-chi, Jacqueline. “Mevinphos Induces Seizure-like EEG Activity and Decreases Blood Pressure by an Action on Amygdala.” 2011. Web. 07 Mar 2021.
Vancouver:
Chia-chi J. Mevinphos Induces Seizure-like EEG Activity and Decreases Blood Pressure by an Action on Amygdala. [Internet] [Thesis]. NSYSU; 2011. [cited 2021 Mar 07].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730111-113324.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chia-chi J. Mevinphos Induces Seizure-like EEG Activity and Decreases Blood Pressure by an Action on Amygdala. [Thesis]. NSYSU; 2011. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730111-113324
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
UCLA
16.
Perusini, Jennifer Nicole.
The Mechanisms of Fear Sensitization Caused by Acute Traumatic Stress: from Induction to Expression to Long-Lasting Reversal.
Degree: Psychology, 2014, UCLA
URL: http://www.escholarship.org/uc/item/3578829d
► Fear is an adaptive response that is normally proportional to the level of imposed threat, which allows for a balance between defensive behavior and other…
(more)
▼ Fear is an adaptive response that is normally proportional to the level of imposed threat, which allows for a balance between defensive behavior and other behaviors necessary for survival. However, fear becomes maladaptive when the level is inappropriate to the level of imposed threat. Exposure to a severe stressor can alter future fear learning to become disproportionate to the actual level of threat, potentially leading to generalized fear to less threatening circumstances (Rau, DeCola, and Fanselow, 2005). Inappropriate fear regulation after severe stress is a hallmark of post-traumatic stress disorder (PTSD). The primary goal of the experiments in this dissertation is to investigate the biological mechanisms that underlie both induction and expression of stress-enhanced fear learning (SEFL), a model developed and tested in rats to demonstrate that an acute footshock stressor nonassociatively and permanently enhances conditional fear learning.In the SEFL procedure, rats are given 15 unsignaled footshocks in a certain context, and some time later, are given a single footshock in a novel context. When rats are tested for changes in freezing levels in the novel context in absence of a shock, they show exaggerated levels of freezing behavior, which is called SEFL. Many features of SEFL are similar to the symptoms of PTSD. Experiments in Chapter 1 of this dissertation show that corticosterone (CORT) is necessary to induce SEFL. This effect is demonstrated using intraperitoneal injections of metyrapone, a CORT synthesis blocker. Metyrapone before, but not after the 15 shocks dose-dependently attenuated SEFL and plasma CORT levels during the 15-shock stressor. Moreover, it is shown that the basolateral amygdala (BLA) must be functional during, but not after the 15-shock stressor. A glucocorticoid receptor (GR) antagonist infused into the BLA also attenuated SEFL; so, CORT acting on GRs in the BLA is necessary to induce SEFL.Further work in Chapter 2 explored the mechanisms underlying expression of SEFL. CORT drove long-term alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) subunit glutamate receptor 1 (GluA1), expression in the BLA, but not GluA2, or the glutamate N-methyl-D aspartate receptor (NMDAR) subunit GluN1. Infusing an AMPAR antagonist into the BLA after the severe stressor temporarily prevented sensitized fear expression. Experiments in Chapter 3 targeted GluA1 synthesis in the BLA using antisense oligonucleotide (ASO) treatments post-stress, which surprisingly reversed SEFL long-term. The most interesting finding in this set of experiments was that reversal of SEFL by ASO treatment did not prevent fear learning or amygdala function, nor did it affect associative fear to the stressor context. Moreover, in Chapter 3 we examined the functional importance of increased GluA1 in the BLA after SEFL. This was accomplished with post-stressor intra-BLA infusions of a GluA2-lacking AMPAR blocker, IEM-1460, which reduced SEFL. In conclusion, these results elucidate novel neurobiological…
Subjects/Keywords: Neurosciences; amygdala; antisense oligonucleotides; corticosterone; fear; PTSD
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APA (6th Edition):
Perusini, J. N. (2014). The Mechanisms of Fear Sensitization Caused by Acute Traumatic Stress: from Induction to Expression to Long-Lasting Reversal. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/3578829d
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Perusini, Jennifer Nicole. “The Mechanisms of Fear Sensitization Caused by Acute Traumatic Stress: from Induction to Expression to Long-Lasting Reversal.” 2014. Thesis, UCLA. Accessed March 07, 2021.
http://www.escholarship.org/uc/item/3578829d.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Perusini, Jennifer Nicole. “The Mechanisms of Fear Sensitization Caused by Acute Traumatic Stress: from Induction to Expression to Long-Lasting Reversal.” 2014. Web. 07 Mar 2021.
Vancouver:
Perusini JN. The Mechanisms of Fear Sensitization Caused by Acute Traumatic Stress: from Induction to Expression to Long-Lasting Reversal. [Internet] [Thesis]. UCLA; 2014. [cited 2021 Mar 07].
Available from: http://www.escholarship.org/uc/item/3578829d.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Perusini JN. The Mechanisms of Fear Sensitization Caused by Acute Traumatic Stress: from Induction to Expression to Long-Lasting Reversal. [Thesis]. UCLA; 2014. Available from: http://www.escholarship.org/uc/item/3578829d
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – San Diego
17.
Groeniger, Kimberly Mieko.
Decreased Density of Serotonin Transporting Fibers in the Infant Williams Syndrome Amygdala.
Degree: Biology, 2018, University of California – San Diego
URL: http://www.escholarship.org/uc/item/5t38t9bs
► Williams Syndrome (WS) is a rare neurodevelopmental disorder characterized by a known genetic profile, hypersociability, and increased attention. This unique embodiment of social atypicalities allows…
(more)
▼ Williams Syndrome (WS) is a rare neurodevelopmental disorder characterized by a known genetic profile, hypersociability, and increased attention. This unique embodiment of social atypicalities allows for distinctions to be drawn between WS and other neurodevelopmental disorders, such as Autism Spectrum Disorder (ASD), as well as emotional disorders such as Major Depressive Disorder (MDD), Bipolar Disorder (BD), and Schizophrenia (SZ). While these disorders are not the focus of this study, the breadth of research performed with regards to these disorders involving neuroanatomy and its relation to social and behavioral profiles has provided a solid foundation for this study. Aspects of the WS social and behavioral phenotype have been extensively studied, however there has been less examination of the neuroanatomical characteristics which correlate with observed behaviors. The amygdala has been associated with the processing of socially salient information and coordination of responses to social stimuli, and within this structure serotonin is an active neurotransmitter responsible for modulating mood and emotional responses. To ascertain the role which serotonin plays within the infant WS amygdala, I examined the density of immunoreactive serotonin transporting (SERT-ir) fibers in the primary amygdaloid nuclei (lateral, basal, accessory basal, and central) of infants with WS compared to those of typically developing (TD) controls. Density in all four nuclei was decreased in WS as compared to TD, and in both WS and TD the central nucleus contained the highest density of SERT- ir fibers. This study contributes preliminary findings for future examinations of the serotonergic system in the WS amygdala.
Subjects/Keywords: Neurosciences; amygdala; serotonin; serotonin transporter; Williams Syndrome
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APA ·
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APA (6th Edition):
Groeniger, K. M. (2018). Decreased Density of Serotonin Transporting Fibers in the Infant Williams Syndrome Amygdala. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/5t38t9bs
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Groeniger, Kimberly Mieko. “Decreased Density of Serotonin Transporting Fibers in the Infant Williams Syndrome Amygdala.” 2018. Thesis, University of California – San Diego. Accessed March 07, 2021.
http://www.escholarship.org/uc/item/5t38t9bs.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Groeniger, Kimberly Mieko. “Decreased Density of Serotonin Transporting Fibers in the Infant Williams Syndrome Amygdala.” 2018. Web. 07 Mar 2021.
Vancouver:
Groeniger KM. Decreased Density of Serotonin Transporting Fibers in the Infant Williams Syndrome Amygdala. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2021 Mar 07].
Available from: http://www.escholarship.org/uc/item/5t38t9bs.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Groeniger KM. Decreased Density of Serotonin Transporting Fibers in the Infant Williams Syndrome Amygdala. [Thesis]. University of California – San Diego; 2018. Available from: http://www.escholarship.org/uc/item/5t38t9bs
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Saskatchewan
18.
Marks, Wendie.
Fear Learning as a Component of a Depressive Phenotype in Rodents.
Degree: 2014, University of Saskatchewan
URL: http://hdl.handle.net/10388/ETD-2014-06-1553
► Depression is a complex psychiatric illness that affects a large proportion of the population. Many researchers make use of preclinical animal models to study the…
(more)
▼ Depression is a complex psychiatric illness that affects a large proportion of the population. Many researchers make use of preclinical animal models to study the behavioural and neurobiological characteristics of this disease. However, although a bias towards maladaptive thinking patterns and emotional responses is a cardinal symptom of depression, these symptoms have been rarely considered in preclinical models. One way to investigate maladaptive thinking is through the use of fear conditioning paradigms. Fear conditioning evaluates emotional memory by assessing a rodent’s ability to associate neutral cues with an aversive experience. It requires the activation of brain structures critically involved in emotion-related learning and memory processes, most notably the hippocampus and
amygdala, to successfully learn the task. The primary goal of this dissertation was to gain a better understanding of the consequences of repeated corticosterone injections—a validated preclinical model of depression – on emotionally driven behaviour, the involvement of the hippocampus and
amygdala in mediating these behaviours, and whether the antidepressant, fluoxetine, can prevent the effects of corticosterone on these behaviours. To begin, in Chapter 2 I confirmed that the depressogenic effects of corticosterone in the forced swim test, which is a traditional behavioural assay for depression in rodents, are not due to procedural differences or non-specific motor effects. I then investigated the impact of repeated corticosterone injections on the learning and memory of delay and contextual fear conditioning. I examined whether altering the order in which rats recall context versus tone cued fear associations determines the magnitude of corticosterone’s effect on conditioned fear. I found that corticosterone dose-dependently increased freezing to contextual cues whereas freezing to tone cues was increased regardless of dose. Furthermore, the order of the presentation of context versus tone cues during recall determined whether corticosterone produced significant enhancements in freezing. In Chapter 4, I investigated whether neuronal activity in the hippocampus and
amygdala after recall of contextual or tone cued fear was associated with the effects of corticosterone found in Chapter 3. Recall of contextual cues was associated with neuronal activity in specific sub regions of the
amygdala without any observed changes in the hippocampus. In Chapter 5, I investigated whether repeated corticosterone injections would also enhance the learning and memory of trace fear conditioning, a task that is heavily reliant on the hippocampus. I found that corticosterone increased freezing during recall of trace cues and enhanced the acquisition of trace cues. The results from this chapter, taken together with the results from chapters 3 and 4, suggest that repeated corticosterone exposure readily enhances learning and memory processes that evoke emotional arousal. In Chapter 6, I asked whether repeated treatment with the antidepressant, fluoxetine,…
Advisors/Committee Members: Kalynchuk, Lisa E., Cayabyab, Francisco S., Elias, Lorin J., Caruncho, Hector J., Menard, Janet L., Kalynchuk, Lisa.
Subjects/Keywords: corticosterone; depression; fear conditioning; amygdala; fluoxetine
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APA ·
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APA (6th Edition):
Marks, W. (2014). Fear Learning as a Component of a Depressive Phenotype in Rodents. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/ETD-2014-06-1553
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Marks, Wendie. “Fear Learning as a Component of a Depressive Phenotype in Rodents.” 2014. Thesis, University of Saskatchewan. Accessed March 07, 2021.
http://hdl.handle.net/10388/ETD-2014-06-1553.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Marks, Wendie. “Fear Learning as a Component of a Depressive Phenotype in Rodents.” 2014. Web. 07 Mar 2021.
Vancouver:
Marks W. Fear Learning as a Component of a Depressive Phenotype in Rodents. [Internet] [Thesis]. University of Saskatchewan; 2014. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10388/ETD-2014-06-1553.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Marks W. Fear Learning as a Component of a Depressive Phenotype in Rodents. [Thesis]. University of Saskatchewan; 2014. Available from: http://hdl.handle.net/10388/ETD-2014-06-1553
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Newcastle
19.
Adams, Cameron Darcy.
Channelrhodopsin-assisted circuit mapping of medial amygdaloid connectivity to the paraventricular nucleus of the hypothalamus.
Degree: PhD, 2018, University of Newcastle
URL: http://hdl.handle.net/1959.13/1387401
► Research Doctorate - Doctor of Philosophy (PhD)
Understanding how the brain is connected is an important first step if we are to successfully treat its…
(more)
▼ Research Doctorate - Doctor of Philosophy (PhD)
Understanding how the brain is connected is an important first step if we are to successfully treat its conditions. Currently, much of what we know about the brain connectome has been discovered through neuroanatomical tracing studies. This approach however, lacks functionality in that we cannot determine the physiological consequences of manipulating a given pathway or its overall necessity to a specific behavioural outcome. Dysregulated social and emotional functioning, including hypothalamic-pituitary-adrenal (HPA) axis responses, are cardinal features of depressive disorders. Not surprisingly, HPA axis activity is tightly regulated by limbic structures including the medial (MeA) and central amygdala (CeA) which act to increase hypothalamic neuroendocrine output. The lack of direct connectivity between these amygdaloid structures and the neuroendocrine hypothalamus has led to suggestions the MeA and CeA mediate HPA axis responses to stress via indirect relays. While historically, the CeA has received considerable attention in regards to HPA axis regulation, both traditional and modern tracing techniques provide anatomical evidence of direct MeA to hypothalamic neuroendocrine connectivity. At this time however, functional evidence supporting this connection is lacking. Fortunately, recent advances in technology now allows for a functional assessment of individual pathways within the brain connectome. Through the application of optogenetics, the primary goal of this thesis is to investigate the functional characteristics of a direct MeA to neuroendocrine hypothalamus projection. In this regard, I demonstrate the capacity of the MeA to drive stress neuroendocrine responses through direct, functional projections to the hypothalamus. Moreover, that a group of MeA neurons, which may be derived from a neuroendocrine lineage, provide direct glutamatergic input to corticotropin-releasing factor (CRF) neurons, which sit at the apex of the HPA axis. Together, these results suggest therapeutically targeting the MeA, as opposed to the CeA, may prove to be more successful in the treatment of mood related disorders.
Advisors/Committee Members: University of Newcastle. Faculty of Health & Medicine, School of Biomedical Sciences and Pharmacy.
Subjects/Keywords: amygdala; CRF; HPA Axis; optogenetics; PVN; stress
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Adams, C. D. (2018). Channelrhodopsin-assisted circuit mapping of medial amygdaloid connectivity to the paraventricular nucleus of the hypothalamus. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1387401
Chicago Manual of Style (16th Edition):
Adams, Cameron Darcy. “Channelrhodopsin-assisted circuit mapping of medial amygdaloid connectivity to the paraventricular nucleus of the hypothalamus.” 2018. Doctoral Dissertation, University of Newcastle. Accessed March 07, 2021.
http://hdl.handle.net/1959.13/1387401.
MLA Handbook (7th Edition):
Adams, Cameron Darcy. “Channelrhodopsin-assisted circuit mapping of medial amygdaloid connectivity to the paraventricular nucleus of the hypothalamus.” 2018. Web. 07 Mar 2021.
Vancouver:
Adams CD. Channelrhodopsin-assisted circuit mapping of medial amygdaloid connectivity to the paraventricular nucleus of the hypothalamus. [Internet] [Doctoral dissertation]. University of Newcastle; 2018. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1959.13/1387401.
Council of Science Editors:
Adams CD. Channelrhodopsin-assisted circuit mapping of medial amygdaloid connectivity to the paraventricular nucleus of the hypothalamus. [Doctoral Dissertation]. University of Newcastle; 2018. Available from: http://hdl.handle.net/1959.13/1387401
University of Toronto
20.
Morrison, Daniel.
The Sparse Engram of the Lateral Amygdala.
Degree: 2016, University of Toronto
URL: http://hdl.handle.net/1807/75824
► Memories are stored by discrete changes in the brain, collectively referred to as an engram, that allow activity related to an experience to be reactivated…
(more)
▼ Memories are stored by discrete changes in the brain, collectively referred to as an engram, that allow activity related to an experience to be reactivated in the future. Associative memories related to threatening stimuli are stored in the lateral amygdala (LA), where the engram is composed of a sparse proportion of neurons. The work in this thesis tests the prediction that this proportion is consistent between memories and investigates mechanisms that may contribute to this consistency. First, it is shown that the proportion of LA engram neurons remains constant between memories of different strengths. Then, it is shown that this proportion increases when inhibitory, parvalbumin-positive interneurons are suppressed during learning. Together, these results provide additional support for the idea memories are stored in sparse assemblies of neurons and suggest a novel role for parvalbumin-positive interneurons in memory formation.
M.Sc.
Advisors/Committee Members: Josselyn, Sheena A, Physiology.
Subjects/Keywords: Amygdala; Engram; Interneurons; Memory; Parvalbumin; 0317
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APA ·
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APA (6th Edition):
Morrison, D. (2016). The Sparse Engram of the Lateral Amygdala. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/75824
Chicago Manual of Style (16th Edition):
Morrison, Daniel. “The Sparse Engram of the Lateral Amygdala.” 2016. Masters Thesis, University of Toronto. Accessed March 07, 2021.
http://hdl.handle.net/1807/75824.
MLA Handbook (7th Edition):
Morrison, Daniel. “The Sparse Engram of the Lateral Amygdala.” 2016. Web. 07 Mar 2021.
Vancouver:
Morrison D. The Sparse Engram of the Lateral Amygdala. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1807/75824.
Council of Science Editors:
Morrison D. The Sparse Engram of the Lateral Amygdala. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/75824
21.
Christian, Daniel T.
A STUDY ON THE EFFECTS OF CHRONIC ALCOHOL AND WITHDRAWAL IN THE BASOLATERAL AMYGDALA OF SPRAGUE DAWLEY RATS: AFFERENT SPECIFIC MODIFICATION OF GLUTAMATERGIC NEUROTRANSMISSION.
Degree: 2012, Wake Forest University
URL: http://hdl.handle.net/10339/37667
► The lateral and basolateral amygdala (BLA) are major amygdala subdivisions that process environmental stimuli in an associative process that ultimately results in anxiety-like or fearful…
(more)
▼ The lateral and basolateral amygdala (BLA) are major amygdala subdivisions that process environmental stimuli in an associative process that ultimately results in anxiety-like or fearful behavioral responses. These nuclei receive glutamatergic input via two major pathways differentiated by their anatomical arrangement and the upstream brain areas giving rise to the pathways. The external capsule (EC) brings primarily cortical information while the stria terminalis/internal capsule (IC) brings information from more mid-line structures like medial prefrontal cortex and thalamus. Recent work suggests that long-term anxiogenic effects of alcohol withdrawal may be related to adaptations in BLA glutamatergic neurotransmission. The current studies serve to characterize glutamatergic signaling at multiple glutamatergic afferents into the BLA following chronic intermittent ethanol exposure (CIE) and withdrawal (WD). The current studies indicated that EC-BLA and IC-BLA inputs into the BLA can be electrically isolated in an electrophysiological slice recording setup, and remain isolated in the face of CIE and WD. These data allowed the characterization of input specific alterations in glutamate function following both CIE and WD. In chapter II, we conducted electrophysiological recordings to explore pre- and postsynaptic functional alterations to glutamatergic signaling at EC-BLA afferents. These studies indicate that EC-BLA afferents demonstrate increased AMPA mediated post-synaptic signaling in response to WD treatment, while demonstrating no alterations in putative pre-synaptic functional measures. Additionally, investigations of biochemical alterations in response to CIE and WD were measured using Western Blot techniques. Our findings detail dynamic increases in AMPA receptor surface expression and phosphorylation following both CIE and WD. Changes in protein expression and phosphorylation levels of kinases associated with AMPA receptors (CAMKII/PKC) are also dynamically regulated by CIE and WD. Chapter III presents data indicating IC-BLA afferents undergo functional alterations in presynaptic glutamate synaptic transmission following WD, but not CIE, with no measureable alterations to postsynaptic functional. These functional increases in presynaptic glutamate function are paralleled by an upregulation in the expression of vesicle associated proteins. Taken together, our data parrallel synaptic plasticity literature suggesting CIE and WD are inducing plastic-like alterations to glutamatergic signaling systems at both EC- and IC-BLA afferents.
Subjects/Keywords: Basolateral Amygdala
…EFFECTS OF CHRONIC ALCOHOL AND WITHDRAWAL IN
THE BASOLATERAL AMYGDALA OF SPRAGUE DAWLEY RATS… …lateral and basolateral amygdala (BLA) nuclei are major amygdala subdivisions that… …have not been well
characterized.
10
THE AMYGDALA
The amygdala is a brain region that… …x29;. The amygdala is comprised of multiple
nuclei, including the lateral and basolateral… …nuclei. For our purposes, these nuclei are
grouped as the basolateral amygdala (BLA)…
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APA ·
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Export
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APA (6th Edition):
Christian, D. T. (2012). A STUDY ON THE EFFECTS OF CHRONIC ALCOHOL AND WITHDRAWAL IN THE BASOLATERAL AMYGDALA OF SPRAGUE DAWLEY RATS: AFFERENT SPECIFIC MODIFICATION OF GLUTAMATERGIC NEUROTRANSMISSION. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/37667
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Christian, Daniel T. “A STUDY ON THE EFFECTS OF CHRONIC ALCOHOL AND WITHDRAWAL IN THE BASOLATERAL AMYGDALA OF SPRAGUE DAWLEY RATS: AFFERENT SPECIFIC MODIFICATION OF GLUTAMATERGIC NEUROTRANSMISSION.” 2012. Thesis, Wake Forest University. Accessed March 07, 2021.
http://hdl.handle.net/10339/37667.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Christian, Daniel T. “A STUDY ON THE EFFECTS OF CHRONIC ALCOHOL AND WITHDRAWAL IN THE BASOLATERAL AMYGDALA OF SPRAGUE DAWLEY RATS: AFFERENT SPECIFIC MODIFICATION OF GLUTAMATERGIC NEUROTRANSMISSION.” 2012. Web. 07 Mar 2021.
Vancouver:
Christian DT. A STUDY ON THE EFFECTS OF CHRONIC ALCOHOL AND WITHDRAWAL IN THE BASOLATERAL AMYGDALA OF SPRAGUE DAWLEY RATS: AFFERENT SPECIFIC MODIFICATION OF GLUTAMATERGIC NEUROTRANSMISSION. [Internet] [Thesis]. Wake Forest University; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10339/37667.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Christian DT. A STUDY ON THE EFFECTS OF CHRONIC ALCOHOL AND WITHDRAWAL IN THE BASOLATERAL AMYGDALA OF SPRAGUE DAWLEY RATS: AFFERENT SPECIFIC MODIFICATION OF GLUTAMATERGIC NEUROTRANSMISSION. [Thesis]. Wake Forest University; 2012. Available from: http://hdl.handle.net/10339/37667
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
22.
Wu, Yinhao.
The Anticonvulsant Effects of 5a-dihydroprogesterone in the Rat Amygdala-Kindled Model.
Degree: 2017, University of Toronto
URL: http://hdl.handle.net/1807/97188
► The present study investigated the anti-seizure effects of 5-dihydroprogesterone (5-DHP) in an animal model of human drug-resistant complex partial seizures - the rat amygdala-kindling model…
(more)
▼ The present study investigated the anti-seizure effects of 5-dihydroprogesterone (5-DHP) in an animal model of human drug-resistant complex partial seizures - the rat amygdala-kindling model - using different routes of administration and solvents.
5-DHP in -cyclodextrin administered via the subcutaneous (SQ) route was weakly effective (Rmax=30%). 5-DHP via the intraperitoneal (IP) route in the "benzyl" vehicle, however, suppressed both generalized and focal seizures with ataxia shortly after injection; and generalized seizures around 130 minutes post-injection. The "benzyl" vehicle itself, however, was active at the earlier time, and benzyl alcohol was found to be anticonvulsant. 5-DHP in -cyclodextrin via the intravenous (IV) route suppressed both generalized seizures and focal seizures, with ataxia. A time-response IV study at 5mg/kg showed immediate onset of anticonvulsant action that lasted for about 60 minutes post-injection.
In conclusion, 5-DHP demonstrated efficacy in the present study, and 5-DHP analogs might be developed as a new anti-seizure therapy.
M.Sc.
2019-11-06 00:00:00
Advisors/Committee Members: Burnham, Willets M, Pharmacology.
Subjects/Keywords: 5a-dihydroprogesterone; amygdala-kindling; DHP; epilepsy; 0419
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APA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Wu, Y. (2017). The Anticonvulsant Effects of 5a-dihydroprogesterone in the Rat Amygdala-Kindled Model. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/97188
Chicago Manual of Style (16th Edition):
Wu, Yinhao. “The Anticonvulsant Effects of 5a-dihydroprogesterone in the Rat Amygdala-Kindled Model.” 2017. Masters Thesis, University of Toronto. Accessed March 07, 2021.
http://hdl.handle.net/1807/97188.
MLA Handbook (7th Edition):
Wu, Yinhao. “The Anticonvulsant Effects of 5a-dihydroprogesterone in the Rat Amygdala-Kindled Model.” 2017. Web. 07 Mar 2021.
Vancouver:
Wu Y. The Anticonvulsant Effects of 5a-dihydroprogesterone in the Rat Amygdala-Kindled Model. [Internet] [Masters thesis]. University of Toronto; 2017. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1807/97188.
Council of Science Editors:
Wu Y. The Anticonvulsant Effects of 5a-dihydroprogesterone in the Rat Amygdala-Kindled Model. [Masters Thesis]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/97188
University of Toronto
23.
Jacob, Alexander Douglas.
Coallocation of Appetitive and Aversive Memories in the Lateral Amygdala.
Degree: 2016, University of Toronto
URL: http://hdl.handle.net/1807/79743
► The amygdala plays a key role in representing memories for both fear and reward. However, it is currently not understood how neurons in this structure…
(more)
▼ The amygdala plays a key role in representing memories for both fear and reward. However, it is currently not understood how neurons in this structure differentially code memory traces for such strikingly different emotions. Amygdala neurons might be valence-specific, able to encode only fear or reward. Alternatively, these neurons may be equipotent â able to encode memories of any valence. We examined these two alternatives by allocating a fearful and rewarding memory to a single population of neurons in the lateral amygdala (LA). Here we show that co-allocation of these memories leads to overwriting: the fear memory formed first is erased and replaced by the reward memory formed second. These results provide evidence that LA neurons are equipotent and capable of switching the valence they encode. Together, these findings establish support for a dynamic, activity-dependent view of valence allocation in the lateral amygdala.
M.A.
Advisors/Committee Members: Josselyn, Sheena, Psychology.
Subjects/Keywords: Amygdala; Memory; Memory allocation; Valence; 0621
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APA (6th Edition):
Jacob, A. D. (2016). Coallocation of Appetitive and Aversive Memories in the Lateral Amygdala. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/79743
Chicago Manual of Style (16th Edition):
Jacob, Alexander Douglas. “Coallocation of Appetitive and Aversive Memories in the Lateral Amygdala.” 2016. Masters Thesis, University of Toronto. Accessed March 07, 2021.
http://hdl.handle.net/1807/79743.
MLA Handbook (7th Edition):
Jacob, Alexander Douglas. “Coallocation of Appetitive and Aversive Memories in the Lateral Amygdala.” 2016. Web. 07 Mar 2021.
Vancouver:
Jacob AD. Coallocation of Appetitive and Aversive Memories in the Lateral Amygdala. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1807/79743.
Council of Science Editors:
Jacob AD. Coallocation of Appetitive and Aversive Memories in the Lateral Amygdala. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/79743
Baylor University
24.
Blakeley, Hillary Joy.
Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.
Degree: PhD, Psychology and Neuroscience., 2011, Baylor University
URL: http://hdl.handle.net/2104/8182
► The amygdala is a critical part of the limbic system with important roles in social behavior. Abnormal activity in the lateral amygdala nucleus (LA) has…
(more)
▼ The
amygdala is a critical part of the limbic system with important roles in social behavior. Abnormal activity in the lateral
amygdala nucleus (LA) has been implicated in several disorders, including autism spectrum disorder (ASD) in which abnormal social functioning is a primary symptom. The peptide hormones arginine-vasopressin (AVP) and oxytocin (OT) are strongly implicated in social behavior, and may also be involved in the pathophysiology of ASD. Here, we show that AVP causes an increase in excitability, through eliciting a decrease in action potential accommodation and hyperpolarization-activated current (Ih) amplitude in LA pyramidal cells. OT exerts complementary effects, causing an increase in action potential accommodation and Ih amplitude, resulting in decreased excitability. These results suggest AVP and OT may modulate social behavior by controlling excitability in the
amygdala.
Advisors/Committee Members: Keele, N. Bradley. (advisor).
Subjects/Keywords: Amygdala.; Excitability.; Vasopressin.; Oxytocin.; H-current.
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APA (6th Edition):
Blakeley, H. J. (2011). Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current. (Doctoral Dissertation). Baylor University. Retrieved from http://hdl.handle.net/2104/8182
Chicago Manual of Style (16th Edition):
Blakeley, Hillary Joy. “Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.” 2011. Doctoral Dissertation, Baylor University. Accessed March 07, 2021.
http://hdl.handle.net/2104/8182.
MLA Handbook (7th Edition):
Blakeley, Hillary Joy. “Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.” 2011. Web. 07 Mar 2021.
Vancouver:
Blakeley HJ. Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current. [Internet] [Doctoral dissertation]. Baylor University; 2011. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2104/8182.
Council of Science Editors:
Blakeley HJ. Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current. [Doctoral Dissertation]. Baylor University; 2011. Available from: http://hdl.handle.net/2104/8182
25.
Hart, Evan.
Basic mechanisms and translational approaches to understanding effort-based choice.
Degree: Psychology, 2019, UCLA
URL: http://www.escholarship.org/uc/item/679005kr
► Effort is a cost that must be overcome to procure rewards, and organisms frequently make cost benefit decisions based on effort in choosing which options…
(more)
▼ Effort is a cost that must be overcome to procure rewards, and organisms frequently make cost benefit decisions based on effort in choosing which options to pursue. The majority of previous work probing the neural mechanisms of effort-based choice has focused on the striatum and dopaminergic signaling therein, and less work has investigated behavioral or environmental factors that contribute. In all of the following experiments, an effort-based choice task was adopted from previous findings where rats could freely choose between a high effort, preferred option and a low effort, less preferred option. The high effort option was lever progressing on a progressive ratio schedule for sucrose pellets in which each successive reward became more difficult to earn. The low effort option was freely available lab chow concurrently available that had no work requirement, but was less palatable. Thus, rats could freely choose between these options and self- titrate the amount of effort they were willing to exert. A number of control tasks were used to control for changes in motoric ability, appetite, or food preference. By omitting the freely available lab chow and testing subjects for progressive ratio performance, any impairment in motoric ability, memory, and general willingness to exert effort, rather than cost-benefit valuation per se, could be ruled out. To test whether manipulations had effects on appetite or food preference, rats were tested with both food options freely concurrently available where they did not have to work for either. In the case of manipulations that took place prior to behavioral testing, we recorded the number of sessions it took to reach stable performance to rule out impairments in learning.In the second chapter of this dissertation, the basolateral amygdala (BLA) was tested for its effects in effort-based choice. In a series of experiments, we found that BLA pharmacological inactivations reduced high effort lever pressing specifically in the context of choice, without impairing progressive ration responding when it was the only option. These effects were also not due to changes in appetite or food preference. Chapter three details effects of anterior cingulate cortex (ACC) lesions. Much like BLA inactivations, lesions of ACC decreased choice lever pressing without affecting lever pressing ability, appetite, or food preference. In chapter four, we tested whether a behavioral manipulation, withdrawal from methamphetamine self-administration, had effects on effort based choice. Methamphetamine withdrawn animals exhibited decreased choice lever pressing, which was not due to general work aversion, learning impairments, changes in appetite, or changes in food preference. This decreased effort was accompanied by decreased activation of anterior cingulate, ventral striatum, and amygdala. In the last set of experiments, we replicated results from the ACC lesion experiments using a modern chemogenetic approach. Finally, all of the above findings are discussed with their relevance to future studies and…
Subjects/Keywords: Psychology; amygdala; chemogenetic; cingulate; depression; effort
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APA (6th Edition):
Hart, E. (2019). Basic mechanisms and translational approaches to understanding effort-based choice. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/679005kr
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Hart, Evan. “Basic mechanisms and translational approaches to understanding effort-based choice.” 2019. Thesis, UCLA. Accessed March 07, 2021.
http://www.escholarship.org/uc/item/679005kr.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hart, Evan. “Basic mechanisms and translational approaches to understanding effort-based choice.” 2019. Web. 07 Mar 2021.
Vancouver:
Hart E. Basic mechanisms and translational approaches to understanding effort-based choice. [Internet] [Thesis]. UCLA; 2019. [cited 2021 Mar 07].
Available from: http://www.escholarship.org/uc/item/679005kr.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hart E. Basic mechanisms and translational approaches to understanding effort-based choice. [Thesis]. UCLA; 2019. Available from: http://www.escholarship.org/uc/item/679005kr
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Oxford
26.
Lapray, Miroslawa.
Role of intercalated and NPY-expressing cells in neuronal circuit of the amygdala.
Degree: PhD, 2014, University of Oxford
URL: http://ora.ox.ac.uk/objects/uuid:91017ce3-7c42-4310-94fb-be659ec2e52e
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595998
► Local inhibitory microcircuit of amygdala is an active component in processing emotional information. Despite prominent evidence of its importance, our understanding of GABAergic cell types,…
(more)
▼ Local inhibitory microcircuit of amygdala is an active component in processing emotional information. Despite prominent evidence of its importance, our understanding of GABAergic cell types, their connectivity and role in amygdala network is limited. The aim of this thesis is to understand connectivity and physiology of two specific components of GABAergic microcircuit of amygdala: so-called intercalated cells and neuropeptide Y (NPY) expressing interneurons. Intercalated cells (ITCs) of the amygdala are clusters of GABAergic neurons that surround the basolateral complex of amygdala (BLA). There is growing evidence suggesting that ITCs are required for the expression of fear extinction. The main intercalated nucleus (Im) is the largest of the ITC clusters and could be also important for emotional processing. Using patch-clamp whole-cell recordings paired with subsequent anatomical analysis I described basic physiology and anatomy of neurons within the Im. I found that these neurons share common characteristics to earlier described neurons within the medial ITC cluster, yet they can be divided into three distinct groups. Next, I provided anatomical and functional evidence that Im neurons project to central and basal nucleus of amygdala and that they are reciprocally connected with medial and lateral ITCs clusters. I found that Im neurons receive excitatory inputs from BLA as well as cortex; next I verified that heterogeneous inputs do not interact with each other. I have shown that the Im neurons express both AMPA and NMDA receptors, suggesting that they may undergo NMDA-dependent plasticity. I have reported that dopamine hyperpolarizes Im neurons via dopamine receptor 1, therefore providing a cellular substrate for disinhibition of the amygdala at the systemic level. Thus, the Im is likely to be an additional site of integration of the distributed network underlying acquisition, expression and extinction of conditioned fear. In another project, I report novel interneuron type of the BLA and call it neurogliaform cell (NGFC) of amygdala. I used a mouse line expressing green fluorescent protein (GFP) under NPY promoter and patch clamp technique combined with pharmacology and electron microscope analysis. I performed paired recordings between presynaptic NPY-GFP positive (+) cells and postsynaptic principal neurons (PNs). Presynaptic NPY-GFP+ neurons display small soma and short dendrites embedded in a cloud of highly arborized axon. I showed that NPY-GFP+ cells are source of GABAA receptor-mediated slow inhibitory postsynaptic currents (IPSCs, decay time constant > 30 ms) evoked in PNs and in themselves (autapses). These slow IPSCs are known in literature as GABAA,slow. My results indicate that the slow kinetics of these IPSCs was likely caused by the low concentration and spillover of extracellular GABA. Physiologically-relevant in vivo firing re-played in NPY+-NGFCs in vitro evoked a transient depression of the IPSCs. Presynaptic GABAB receptors controlled the strength of this short-term plasticity. Interestingly,…
Subjects/Keywords: 612.8; Pharmacology; Neuroscience; Amygdala; Interneurons; Intercalated Cells
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APA ·
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Export
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APA (6th Edition):
Lapray, M. (2014). Role of intercalated and NPY-expressing cells in neuronal circuit of the amygdala. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:91017ce3-7c42-4310-94fb-be659ec2e52e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595998
Chicago Manual of Style (16th Edition):
Lapray, Miroslawa. “Role of intercalated and NPY-expressing cells in neuronal circuit of the amygdala.” 2014. Doctoral Dissertation, University of Oxford. Accessed March 07, 2021.
http://ora.ox.ac.uk/objects/uuid:91017ce3-7c42-4310-94fb-be659ec2e52e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595998.
MLA Handbook (7th Edition):
Lapray, Miroslawa. “Role of intercalated and NPY-expressing cells in neuronal circuit of the amygdala.” 2014. Web. 07 Mar 2021.
Vancouver:
Lapray M. Role of intercalated and NPY-expressing cells in neuronal circuit of the amygdala. [Internet] [Doctoral dissertation]. University of Oxford; 2014. [cited 2021 Mar 07].
Available from: http://ora.ox.ac.uk/objects/uuid:91017ce3-7c42-4310-94fb-be659ec2e52e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595998.
Council of Science Editors:
Lapray M. Role of intercalated and NPY-expressing cells in neuronal circuit of the amygdala. [Doctoral Dissertation]. University of Oxford; 2014. Available from: http://ora.ox.ac.uk/objects/uuid:91017ce3-7c42-4310-94fb-be659ec2e52e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595998
27.
Isaacs, Sofie.
The Roles of the Amygdala and the Hippocampus in Fear Conditioning.
Degree: Bioscience, 2015, University of Skövde
URL: http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-11284
► The amygdala, a small structure located deep bilaterally in the medial temporal lobe, is the key structure for the emotional processing and storage of…
(more)
▼ The amygdala, a small structure located deep bilaterally in the medial temporal lobe, is the key structure for the emotional processing and storage of memories associated with emotional events, especially fear. The structure has also been shown to enable humans and animals to detect and respond to environmental threats. Fear conditioning became the main model to examine the neural substrates of emotional learning in mammals and specifically in rats’. With the fear conditioning method, researchers can tests rats’, responses to aversive stimuli during the delivery of a cue and then measure how the responses change after learning of the association between the stimuli and the cue. After learning of the two stimuli, the delivery of a cue alone will prompt a fear response in the rats. The fear response can also be elicited by placing the rats in the same chamber in which the aversive stimuli has previously been experienced, which depends on both the amygdala and the hippocampus. Where the amygdala stores the memories of stimulus related to fear, the hippocampus seems to hold all the fear memories in relation to contextual information about the stimulus. The aim of this paper will be to make a comprehensive overview of internal neural processes of both the amygdala and hippocampus and the interaction between the two structures during fear conditioning, to see how the structures separately work to overlap emotion and memory processes.
Subjects/Keywords: context; fear; memory; conditioning; amygdala; hippocampus
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Export
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Manager
APA (6th Edition):
Isaacs, S. (2015). The Roles of the Amygdala and the Hippocampus in Fear Conditioning. (Thesis). University of Skövde. Retrieved from http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-11284
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Isaacs, Sofie. “The Roles of the Amygdala and the Hippocampus in Fear Conditioning.” 2015. Thesis, University of Skövde. Accessed March 07, 2021.
http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-11284.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Isaacs, Sofie. “The Roles of the Amygdala and the Hippocampus in Fear Conditioning.” 2015. Web. 07 Mar 2021.
Vancouver:
Isaacs S. The Roles of the Amygdala and the Hippocampus in Fear Conditioning. [Internet] [Thesis]. University of Skövde; 2015. [cited 2021 Mar 07].
Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-11284.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Isaacs S. The Roles of the Amygdala and the Hippocampus in Fear Conditioning. [Thesis]. University of Skövde; 2015. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-11284
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
IUPUI
28.
Smoker, Michael P.
Effect of GABRA2 expression in the central nucleus of the amygdala on anxiety and alcohol's anxiolytic capacity in C57BL/6J mice.
Degree: 2016, IUPUI
URL: http://hdl.handle.net/1805/10874
► Indiana University-Purdue University Indianapolis (IUPUI)
The GABRA2 gene, which encodes the α2 subunit of GABAA receptors, is one of the genes most frequently associated with…
(more)
▼ Indiana University-Purdue University Indianapolis (IUPUI)
The GABRA2 gene, which encodes the α2 subunit of GABAA receptors, is one of the genes most frequently associated with alcohol-related behavior in human studies (Demers, Bogdan, & Agrawal, 2014). Polymorphisms in GABRA2 have been found to be associated with alcohol dependence, changes in drinking frequency, and alcohol’s stimulating and euphoric effects (Arias et al., 2014; Dick et al., 2014; Edenberg et al., 2004). However, the GABRA2-alcohol relationship may not be direct, as anxiety and impulsiveness have been found to be mediating factors (Enoch, Schwartz, Albaugh, Virkkunen, & Goldman, 2006; Villafuerte, Strumba, Stoltenberg, Zucker, & Burmeister, 2013).
Comorbidity of anxiety and alcohol use disorders is both prevalent and clinically relevant (J. P. Smith & Randall, 2012), and GABAA receptors play a significant role in each. Benzodiazepines, primary pharmacologic treatments for anxiety disorders and alcohol withdrawal, facilitate signaling at GABAA receptors, and their anxiolytic effects appear to depend on the presence of α2 subunits in these receptors (Low et al., 2000). The amygdala is widely implicated in both anxiety disorders as well as addiction (Janak & Tye, 2015), and its central nucleus is an important mediator of responses to both alcohol- and stress-related stimuli (Roberto, Gilpin, & Siggins, 2012), some of which may be related to GABRA2 expression within this region (Jin et al., 2014).
The aim of the current study was to explore the role of Gabra2 (mouse ortholog of GABRA2) expression within the central nucleus of the amygdala (CeA) in anxiety-related behavior and alcohol’s anxiolytic effects in mice. C57BL/6J (B6) mice underwent surgery for bilateral infusion of GFP-tagged lentivirus targeting Gabra2 or a scramble control lentivirus into the CeA. Following 12-13 days of recovery, mice were assessed for anxiety-like behavior in the elevated plus maze (EPM) naïve or following IP injection of 0, 0.75, or 1.5 g/kg ethanol. After assessment, brains were extracted and sectioned through the CeA. Finally, GFP was quantified, the CeA was collected via laser microdissection, and α2 protein was quantified via ELISA.
In mice expressing GFP in the CeA, α2 protein concentrations were lower for Virus mice relative to Control mice. The EPM was anxiogenic, and alcohol was found to be anxiolytic. In naïve mice, while there was no difference between Control mice and Virus mice on any behavioral measure, there were significant correlations between CeA α2 protein concentration and time spent in closed arms as well as both total and average time spent in open arms. In mice receiving injection of 0, 0.75, or 1.5 g/kg ethanol, there was a main effect of dose on several behavioral measures, but no interaction between viral condition and dose, and only a main effect of viral condition on average time spent in closed arms. There were no significant correlations between CeA α2 protein concentration and behavioral measures within any injected dose.…
Advisors/Committee Members: Boehm, Stephen L., Lapish, Christopher C., Czachowski, Cristine Lynn, Grahame, Nicholas J..
Subjects/Keywords: GABRA2; Anxiety; Alcohol; Amygdala; C57BL/6J
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Manager
APA (6th Edition):
Smoker, M. P. (2016). Effect of GABRA2 expression in the central nucleus of the amygdala on anxiety and alcohol's anxiolytic capacity in C57BL/6J mice. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/10874
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Smoker, Michael P. “Effect of GABRA2 expression in the central nucleus of the amygdala on anxiety and alcohol's anxiolytic capacity in C57BL/6J mice.” 2016. Thesis, IUPUI. Accessed March 07, 2021.
http://hdl.handle.net/1805/10874.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Smoker, Michael P. “Effect of GABRA2 expression in the central nucleus of the amygdala on anxiety and alcohol's anxiolytic capacity in C57BL/6J mice.” 2016. Web. 07 Mar 2021.
Vancouver:
Smoker MP. Effect of GABRA2 expression in the central nucleus of the amygdala on anxiety and alcohol's anxiolytic capacity in C57BL/6J mice. [Internet] [Thesis]. IUPUI; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1805/10874.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Smoker MP. Effect of GABRA2 expression in the central nucleus of the amygdala on anxiety and alcohol's anxiolytic capacity in C57BL/6J mice. [Thesis]. IUPUI; 2016. Available from: http://hdl.handle.net/1805/10874
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Washington
29.
Akers, Christina Akiko.
Threshold dependence of central amygdala CRF in fear behaviors.
Degree: PhD, 2016, University of Washington
URL: http://hdl.handle.net/1773/35628
► The central nucleus of the amygdala (CeA) is critical for threat association and defensive behavior. Distinct populations of neurons in the CeA are known to…
(more)
▼ The central nucleus of the
amygdala (CeA) is critical for threat association and defensive behavior. Distinct populations of neurons in the CeA are known to express an array of neuropeptides, but the role of these different neurons and their cognate neuropeptides in the modulation of fear is only beginning to be discerned. The neuropeptide corticotropin-releasing factor (CRF) is robustly produced in the CeA, yet whether CRF neurons represent a subset of neurons that modulate threat association is unknown. In the present study, we used a combination of molecular, physiological, and behavioral strategies to determine how CRF neurons contribute to adaptive fear processes. Using immunohistochemistry and gene expression analyses, we found that CRF neurons represent a population of neurons distinct from other previously characterized cell types. Electrophysiological experiments demonstrate CRF neurons, like other defined populations in the CeA, undergo synaptic plasticity in a fear-dependent manner. In vivo fiber optic imaging of calcium activity revealed stimulus-specific responses of CRF neurons following cued fear conditioning. We further showed, using a number of behavioral assays coupled with cell-selective silencing and conditional gene inactivation, that CRF neuronal activity is required for the acquisition of cued fear to sub-generalization threat levels and that the CRF peptide produced by the CeA is the principal mediator during this process. CRF neurons in the CeA engage in complex local and long range circuitry, and may thus regulate different aspects of fear through distinct pathways. Determining the function of downstream neurons is critical for understanding how CRF-dependent fear learning is processed. We therefore generated a novel mouse line expressing Cre-recombinase under the endogenous promoter of the gene expressing the primary receptor for CRF, CRFR1 (Crhr1IRES-Cre). This targeted knock-in mutation allows for cell-selective manipulation and labeling of neurons directly downstream of CRF neurons. We found that a significant portion of Sst neurons express Crhr1, likely representing the primary target of locally projecting CRF neurons. The results describing CRF neuronal function in cued fear behaviors, together with the Crhr1IRES-Cre mouse line, have provided a detailed report of the intricate circuitry underlying specific fear behaviors. Furthermore, the work presented here highlights how complex emotional states can be regulated at multiple levels, with distinct biochemical signaling and anatomical arrangements.
Advisors/Committee Members: Zweifel, Larry S (advisor).
Subjects/Keywords: amygdala; CRF; fear; Pharmacology; Neurosciences; pharmacology
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to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Akers, C. A. (2016). Threshold dependence of central amygdala CRF in fear behaviors. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/35628
Chicago Manual of Style (16th Edition):
Akers, Christina Akiko. “Threshold dependence of central amygdala CRF in fear behaviors.” 2016. Doctoral Dissertation, University of Washington. Accessed March 07, 2021.
http://hdl.handle.net/1773/35628.
MLA Handbook (7th Edition):
Akers, Christina Akiko. “Threshold dependence of central amygdala CRF in fear behaviors.” 2016. Web. 07 Mar 2021.
Vancouver:
Akers CA. Threshold dependence of central amygdala CRF in fear behaviors. [Internet] [Doctoral dissertation]. University of Washington; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1773/35628.
Council of Science Editors:
Akers CA. Threshold dependence of central amygdala CRF in fear behaviors. [Doctoral Dissertation]. University of Washington; 2016. Available from: http://hdl.handle.net/1773/35628
30.
RODDY, DARREN WILLIAM.
The hippocampus, amygdala and their principal output tracts in major depressive disorder.
Degree: School of Medicine. Discipline of Psychiatry, 2019, Trinity College Dublin
URL: http://hdl.handle.net/2262/87263
► Major depressive disorder is a common, debilitating illness. Despite its high prevalence rate and global disease burden, the biological mechanisms underlying this disorder remain largely…
(more)
▼ Major depressive disorder is a common, debilitating illness. Despite its high prevalence rate and global disease burden, the biological mechanisms underlying this disorder remain largely unknown. Evidence points towards the involvement of the limbic system deep within the brain. This system processes memory, emotion and arousal, all of which are affected by depression symptoms. Two key regions in the limbic system are the hippocampus and the
amygdala.
The hippocampus is important for memory formation, with the left hippocampus particularly important for episodic memory. The previously well-documented changes in this structure in depression may account for the common global memory and cognition impairments found in this condition. The
amygdala has been shown to be fundamental to the generation and recognition of emotional responses, with the right side demonstrating more involvement in negative emotional responses compared to the left side, which processes more positive emotions. Although evidence exists for a role of this structure in depression, this evidence is less extensive than that of the hippocampus. Both of these structures have widespread connections across the entire brain and each has a clearly defined major white matter bundle, or output tract, that connects each structure to its principal downstream effectors. These tracts are the fornix, which conveys processed memory information from the hippocampus, and the stria terminalis, which conducts emotionally-laden output from the
amygdala. Both these tracts terminate in the basal forebrain and hypothalamus, regions important for pleasure and stress responses, respectively. There is limited evidence for the involvement of both of these tracts in depression.
Using advanced volumetric and diffusion neuroimaging methods, combined with novel bespoke analyses of these images, this study has found noteworthy differences in all four structures in a well-characterised group of eighty-three patients with depression compared to eighty controls. Hippocampal differences were found to be confined to the core processing areas, more so on the left. There was evidence of an
extension of pathology in patients with recurrent depression when compared to first presentation patients who exhibited more restrictive structural changes. The
amygdala showed an exaggeration in the normal right-left volume imbalance, driven by enlargement of right stress-associated centromedial output areas. Through measurement of the cortisol awakening response in a subset of participants, the right
amygdala revealed an association with abnormal stress responses in depression. Both the fornix and the stria terminalis showed localised differences along distinct sections of their tracts suggestive of abnormal axonal connectivity in depression. The aforementioned centromedial areas of the
amygdala were found to be predictors of a depression diagnosis. These
amygdala areas and a specific substructure within the hippocampus, the CA1 region, were also found to be predictors of disease duration in…
Advisors/Committee Members: O'Keane, Veronica.
Subjects/Keywords: hippocampus; depression; amygdala; stria terminalis; fornix
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APA (6th Edition):
RODDY, D. W. (2019). The hippocampus, amygdala and their principal output tracts in major depressive disorder. (Thesis). Trinity College Dublin. Retrieved from http://hdl.handle.net/2262/87263
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
RODDY, DARREN WILLIAM. “The hippocampus, amygdala and their principal output tracts in major depressive disorder.” 2019. Thesis, Trinity College Dublin. Accessed March 07, 2021.
http://hdl.handle.net/2262/87263.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
RODDY, DARREN WILLIAM. “The hippocampus, amygdala and their principal output tracts in major depressive disorder.” 2019. Web. 07 Mar 2021.
Vancouver:
RODDY DW. The hippocampus, amygdala and their principal output tracts in major depressive disorder. [Internet] [Thesis]. Trinity College Dublin; 2019. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2262/87263.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
RODDY DW. The hippocampus, amygdala and their principal output tracts in major depressive disorder. [Thesis]. Trinity College Dublin; 2019. Available from: http://hdl.handle.net/2262/87263
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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