You searched for subject:(amygdala).
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Universidade de Coimbra
1.
Fernandes, Sara Beatriz Gomes.
Adenosine A2A recepto rs role in stress-induced neurobiological modifications
.
Degree: 2015, Universidade de Coimbra
URL: http://hdl.handle.net/10316/32943 
► Chronic caffeine consumption inversely correlates with the incidence of depression and anxiety, which are disabling disorders that increasingly affect millions of people around the world,…
(more)
▼ Chronic caffeine consumption inversely correlates with the incidence of depression and
anxiety, which are disabling disorders that increasingly affect millions of people around the world,
and prevents phenotypic changes caused by chronic stress in rodents through adenosine A2A
receptors (A2AR) antagonism, since they are significantly increased in these situations.
Notwithstanding, neither the neurobiology of depression nor the mechanisms by which the A2AR
can control mood dysfunction are well understood.
In this study we characterized an animal model of stress, namely restraint, by subjecting
rodents to different behavioural paradigms, namely reward-based, anxiety-based, memory
performance and social interaction test, pertinent for mood-related disorders, and studied the
impact of the A2AR located in
amygdala neurons thereupon.
Our results show that selective A2AR genetic deletion diminished the anxiogenic and loss
of memory performance induced by stress.These adaptations were accompanied by prevention
in synaptic alterations also stress-induced, such vGluT1 and vGAT levels in synaptic terminals.
These results are consistent with the hypothesis that A2A receptors play an essential role in
chronic stress deviations and is a potential target to backslide the consequences.
Advisors/Committee Members: Gonçalves, Nélio da Mota (advisor), Tomé, Ângelo José Ribeiro (advisor).
Subjects/Keywords: Stress, behaviour;
A2A Receptors;
Amygdala
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APA (6th Edition):
Fernandes, S. B. G. (2015). Adenosine A2A recepto rs role in stress-induced neurobiological modifications
. (Masters Thesis). Universidade de Coimbra. Retrieved from http://hdl.handle.net/10316/32943
Chicago Manual of Style (16th Edition):
Fernandes, Sara Beatriz Gomes. “Adenosine A2A recepto rs role in stress-induced neurobiological modifications
.” 2015. Masters Thesis, Universidade de Coimbra. Accessed September 23, 2018.
http://hdl.handle.net/10316/32943.
MLA Handbook (7th Edition):
Fernandes, Sara Beatriz Gomes. “Adenosine A2A recepto rs role in stress-induced neurobiological modifications
.” 2015. Web. 23 Sep 2018.
Vancouver:
Fernandes SBG. Adenosine A2A recepto rs role in stress-induced neurobiological modifications
. [Internet] [Masters thesis]. Universidade de Coimbra; 2015. [cited 2018 Sep 23].
Available from: http://hdl.handle.net/10316/32943.
Council of Science Editors:
Fernandes SBG. Adenosine A2A recepto rs role in stress-induced neurobiological modifications
. [Masters Thesis]. Universidade de Coimbra; 2015. Available from: http://hdl.handle.net/10316/32943
University of Texas – Austin
2.
Worthy, Emily Luther.
Affective priming following unilateral temporal lobectomy : the role of the amygdala.
Degree: 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 (6th Edition):
Worthy, E. L. (2012). Affective priming following unilateral temporal lobectomy : the role of the amygdala. (Thesis). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2012-08-5989
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):
Worthy, Emily Luther. “Affective priming following unilateral temporal lobectomy : the role of the amygdala.” 2012. Thesis, University of Texas – Austin. Accessed September 23, 2018.
http://hdl.handle.net/2152/ETD-UT-2012-08-5989.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Worthy, Emily Luther. “Affective priming following unilateral temporal lobectomy : the role of the amygdala.” 2012. Web. 23 Sep 2018.
Vancouver:
Worthy EL. Affective priming following unilateral temporal lobectomy : the role of the amygdala. [Internet] [Thesis]. University of Texas – Austin; 2012. [cited 2018 Sep 23].
Available from: http://hdl.handle.net/2152/ETD-UT-2012-08-5989.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Worthy EL. Affective priming following unilateral temporal lobectomy : the role of the amygdala. [Thesis]. University of Texas – Austin; 2012. Available from: http://hdl.handle.net/2152/ETD-UT-2012-08-5989
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
3.
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 (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 September 23, 2018.
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. 23 Sep 2018.
Vancouver:
Snow M. GABA Cells in the Central Nucleus of the Amygdala Control Cataplexy. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2018 Sep 23].
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 New South Wales
4.
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
► 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 (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
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 September 23, 2018.
http://handle.unsw.edu.au/1959.4/52286.
MLA Handbook (7th Edition):
Moul, Caroline. “The Development and assessment of a Differential Amygdala Activation Model in psychopathy.” 2012. Web. 23 Sep 2018.
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 2018 Sep 23].
Available from: http://handle.unsw.edu.au/1959.4/52286.
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
University of New South Wales
5.
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
► 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 ·
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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
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 September 23, 2018.
http://handle.unsw.edu.au/1959.4/53932.
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. 23 Sep 2018.
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 2018 Sep 23].
Available from: http://handle.unsw.edu.au/1959.4/53932.
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
Vanderbilt University
6.
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://etd.library.vanderbilt.edu/available/etd-11242014-223852/
;
► 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. (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://etd.library.vanderbilt.edu/available/etd-11242014-223852/ ;
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 September 23, 2018.
http://etd.library.vanderbilt.edu/available/etd-11242014-223852/ ;.
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. 23 Sep 2018.
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 2018 Sep 23].
Available from: http://etd.library.vanderbilt.edu/available/etd-11242014-223852/ ;.
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://etd.library.vanderbilt.edu/available/etd-11242014-223852/ ;
University of Texas Medical Branch – Galveston
7.
[No author].
Dopamine-induced synaptic plasticity in the amygdala in saline-and cocaine-treated animals undergoing conditioned place preference
.
Degree: 2008, University of Texas Medical Branch – Galveston
URL: http://hdl.handle.net/2152.3/295
► One of the biggest problems facing cocaine addicts is relapse and currently there are no treatments for relapse. These studies will provide insight into the…
(more)
▼ One of the biggest problems facing cocaine addicts is relapse and currently there are no treatments for relapse. These studies will provide insight into the underlying mechanisms of LTP mediating relapse to cocaine. A major mechanism of cocaine in addiction is to inhibit dopamine re-uptake and glutamate is an excitatory neurotransmitter involved in addiction. Previous studies have demonstrated a link between phospholipase D (PLD) and metabotropic glutamate receptors (mGluRs), while other studies show an interaction between dopamine receptors (DRs) and PLD. Therefore, we investigated the mechanisms of the dopamine agonist-induced synaptic plasticity that is enhanced in the
amygdala due to cocaine exposure in the Central-Basolateral
Amygdala (CeA-BLA) pathway. Electrophysiology recordings showed that the dopamine agonist-induced LTP is mediated via D1 receptors and is dependent upon mGluR1 and the mGluR linked to PLD and partially dependent upon mGluR5 and phospholipase C (PLC). Western blots and co-immunoprecipitations revealed increased expression of PLD after cocaine administration and possible physical interactions between group I mGluRs and PLD and DRs and PLD. PLD activity assays showed that PLD activity was decreased by antagonists of mGluR1 and the mGluR linked to PLD and was increased by the agonist for the mGluR linked to PLD. Basal PLD activity may also be mediated by D1 receptors and was not affected by mGluR5 antagonists.
Advisors/Committee Members: Patricia Shinnick-Gallagher, Ph.D (advisor), Joseph Holt, Ph.D. (committeeMember), Golda Anne Kevetter-Leonard, Ph.D. (committeeMember).
Subjects/Keywords: PLD;
dopamine;
cocaine addiction;
amygdala
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APA (6th Edition):
author], [. (2008). Dopamine-induced synaptic plasticity in the amygdala in saline-and cocaine-treated animals undergoing conditioned place preference
. (Thesis). University of Texas Medical Branch – Galveston. Retrieved from http://hdl.handle.net/2152.3/295
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):
author], [No. “Dopamine-induced synaptic plasticity in the amygdala in saline-and cocaine-treated animals undergoing conditioned place preference
.” 2008. Thesis, University of Texas Medical Branch – Galveston. Accessed September 23, 2018.
http://hdl.handle.net/2152.3/295.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
author], [No. “Dopamine-induced synaptic plasticity in the amygdala in saline-and cocaine-treated animals undergoing conditioned place preference
.” 2008. Web. 23 Sep 2018.
Vancouver:
author] [. Dopamine-induced synaptic plasticity in the amygdala in saline-and cocaine-treated animals undergoing conditioned place preference
. [Internet] [Thesis]. University of Texas Medical Branch – Galveston; 2008. [cited 2018 Sep 23].
Available from: http://hdl.handle.net/2152.3/295.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
author] [. Dopamine-induced synaptic plasticity in the amygdala in saline-and cocaine-treated animals undergoing conditioned place preference
. [Thesis]. University of Texas Medical Branch – Galveston; 2008. Available from: http://hdl.handle.net/2152.3/295
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Sydney
8.
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 ·
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Manager
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 September 23, 2018.
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. 23 Sep 2018.
Vancouver:
Kissiwaa SA. Pain induced synaptic plasticity in the amygdala
. [Internet] [Thesis]. University of Sydney; 2017. [cited 2018 Sep 23].
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 Waikato
9.
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 September 23, 2018.
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. 23 Sep 2018.
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 2018 Sep 23].
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
10.
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 ·
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MLA ·
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to Zotero / EndNote / Reference
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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 September 23, 2018.
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. 23 Sep 2018.
Vancouver:
Qin Z. The Role of LMO4 in the Regulation of Hippocampal and Amygdalar Synaptic Function
. [Internet] [Thesis]. University of Ottawa; 2013. [cited 2018 Sep 23].
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
Linnaeus University
11.
Karlsson, Liz.
Är förändringar i amygdala och närliggande regioner kopplat till upplevda symtom vid PTSD?.
Degree: Biology and Environmental Science, 2015, Linnaeus University
URL: http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-44666
► Posttraumatiskt stressyndrom (PTSD) är en sjukdom som är traumarelaterad och svår att få en övergripande bild av då statistiken för antalet drabbade är bristfällig…
(more)
▼ Posttraumatiskt stressyndrom (PTSD) är en sjukdom som är traumarelaterad och svår att få en övergripande bild av då statistiken för antalet drabbade är bristfällig framför allt av ett stort mörkertal. Symtombilden vid denna sjukdom är mycket individuell och de upplevda symtomen är många, vilket skapar en svårighet i att diagnostisera sjukdomen. Vem som helst kan drabbas när som helst under sin livstid och att få en behandling som fungerar är problematisk då ingen exakt bot finns. Under ett trauma påverkas vårt alarmsystem i kroppen för att varna om fara och då har hjärnstrukturen amygdala en övergripande roll. Eftersom amygdala har stor betydelse för vår uppfattning om faror har därför denna studie valt att se om dessa traumatiska händelser orsakar symtomen vid PTSD. Mer specifikt var syftet med denna litteraturstudie att se om förändringar i amygdala och närliggande regioner kan vara bidragande till symtomen som upplevs av individer med PTSD samt vilka neurologiska förändringar som skett/finns i dessa hjärnregioner som kan ha en bidragande faktor till uppkomsten av sjukdomen. Av sex utvalda orginalartiklar kunde det sammantaget konstateras att vissa neurologiska förändringar som amygdala aktivitet och kortikal volym möjligtvis kan ha en koppling till vissa upplevda symtom som bland annat förhöjd vaksamhet och känsloregleringsförmåga. Artikel 1 visade på minskad volym av grå substans i premotorcortex och i främre cingulate cortex (p<0.05)samt att de med PTSD hade svårare att hantera vardagliga utmaningar, var mindre positiva och mer negativa (p<0.0001).Artikel 2 visade på att volymen av grå substans hade korrelationer med svårighetsgraden av PTSD samt symtombilden. Artikel 3 visade att individer med PTSD hade en minskad aktivitet i högra och vänstra amygdala och ventrala striatum (p<0.005). Där emotionellt avtrubbande hade korrelationer med högra ventrala striatum(p<0.05).Artikel 4 såg att de med PTSD hade förändrad cortex, i högra hemisfären var det åttaregioner och i den vänstra sex regionersom antagligen hade samband med totala CAPS poäng. Artikel 5visade att PTSD gruppen hade en ökad respons i högra amygdala vid syn av skrämmande ansikten (p<0.05) samt att högra amygdala aktiviteten hade samband med symtomet förhöjd vaksamhet. Artikel 6 visade att förmågan att reglera känslor var förändrad hos individer med PTSD. Både vid intensifiering av en känsla (amygdala (p<0.04), bakre cingulate cortex (p<0.01), främre cingulate cortex (p<0.04), middle cingulate cortex (p<0.02), vänstra inferior frontal cortex (p<0.04), vänstra putamen (p<0.04), bilaterala inferior parietal loben (p<0.03)) samt vid minskning av känsla (inferior frontal cortex (p<0.01), vänstra putamen (p<0.02), bilaterala inferior parietal loben (p<0.01), insula (p<0.03)).Denna studie kunde alltså inte påvisa tydliga hjärnområden, kopplade till amygdala, vilka hade förändringar som kan ha orsakat uppkomsten av ångestrelaterade besvär vid PTSD. Eftersom hjärnan är mycket komplex och kan bearbeta intryck på…
Subjects/Keywords: Trauma; PTSD; the brain; amygdala; symptom; Trauma; PTSD; hjärnan; amygdala; symtom
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Karlsson, L. (2015). Är förändringar i amygdala och närliggande regioner kopplat till upplevda symtom vid PTSD?. (Thesis). Linnaeus University. Retrieved from http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-44666
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):
Karlsson, Liz. “Är förändringar i amygdala och närliggande regioner kopplat till upplevda symtom vid PTSD?.” 2015. Thesis, Linnaeus University. Accessed September 23, 2018.
http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-44666.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Karlsson, Liz. “Är förändringar i amygdala och närliggande regioner kopplat till upplevda symtom vid PTSD?.” 2015. Web. 23 Sep 2018.
Vancouver:
Karlsson L. Är förändringar i amygdala och närliggande regioner kopplat till upplevda symtom vid PTSD?. [Internet] [Thesis]. Linnaeus University; 2015. [cited 2018 Sep 23].
Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-44666.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Karlsson L. Är förändringar i amygdala och närliggande regioner kopplat till upplevda symtom vid PTSD?. [Thesis]. Linnaeus University; 2015. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-44666
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
12.
Wonch, Kathleen Elizabeth.
Responsiveness to Infant Cues in Postpartum Depressed and Non-Depressed Mothers: Functional Neural Correlates and Their Relation to Behaviour.
Degree: PhD, 2017, University of Toronto
URL: http://hdl.handle.net/1807/79564
► Postpartum depression (PPD) is the most common maternal birth complication, affecting approximately 5-20% of women. PPD disrupts the normal repertoire of parenting abilities and is…
(more)
▼ Postpartum depression (PPD) is the most common maternal birth complication, affecting approximately 5-20% of women. PPD disrupts the normal repertoire of parenting abilities and is thought to have long-term consequences for the developing infant, even after the mothers’ depression remits. Despite its prevalence and potentially enduring effects, we understand very little about the neural correlates of PPD. Recent evidence suggests that postpartum depression (PPD) is associated with reduced
amygdala (AMY) response to negative stimuli. However, given the anhedonic features of PPD, it is also important to consider the brain response of depressed mothers specifically to positive infant stimuli and to other positively valenced stimuli. In the current work, mothers with clinically determined PPD (n=31) and without PPD (n=23) viewed smiling pictures of infants (both their own and other), and positive non-infant stimuli during an fMRI. Four studies were completed which examined: 1) multidimensional measures such as current parenting stress, early experiences (e.g., being parented themselves as well as experiences of trauma), current mood and anxiety levels, and relationship satisfaction to better characterize our sample of mothers with and without PPD, 2) PPD and Non-PPD mothers’ response to infants and other positive non-infant stimuli, using AMY region-of-interest as well as
amygdala connectivity analyses, 3) subregion-level differences in AMY response and connectivity during the viewing of infant and non-infant stimuli 4) whether and/or how behavioural measures of maternal sensitivity and responsiveness (quality of mother-infant interaction) relate to brain response in the AMY as a whole as well as at the subregion level. Knowing how a depressed mother’s brain responds to her own and other infants is critical as many of the symptoms of PPD focus on the mother-infant dyad and involve a subjective evaluation of one’s parenting abilities. This work adds to the existing literature that examines the brain response of mothers with PPD to various stimuli. Furthermore, it has the long-term potential to inform treatment and intervention programs designed for PPD.
Advisors/Committee Members: Fleming, Alison S, Psychology.
Subjects/Keywords: Amygdala; fMRI; Mothering; Postpartum Depression; 0621
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APA ·
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CSE |
Export
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Manager
APA (6th Edition):
Wonch, K. E. (2017). Responsiveness to Infant Cues in Postpartum Depressed and Non-Depressed Mothers: Functional Neural Correlates and Their Relation to Behaviour. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/79564
Chicago Manual of Style (16th Edition):
Wonch, Kathleen Elizabeth. “Responsiveness to Infant Cues in Postpartum Depressed and Non-Depressed Mothers: Functional Neural Correlates and Their Relation to Behaviour.” 2017. Doctoral Dissertation, University of Toronto. Accessed September 23, 2018.
http://hdl.handle.net/1807/79564.
MLA Handbook (7th Edition):
Wonch, Kathleen Elizabeth. “Responsiveness to Infant Cues in Postpartum Depressed and Non-Depressed Mothers: Functional Neural Correlates and Their Relation to Behaviour.” 2017. Web. 23 Sep 2018.
Vancouver:
Wonch KE. Responsiveness to Infant Cues in Postpartum Depressed and Non-Depressed Mothers: Functional Neural Correlates and Their Relation to Behaviour. [Internet] [Doctoral dissertation]. University of Toronto; 2017. [cited 2018 Sep 23].
Available from: http://hdl.handle.net/1807/79564.
Council of Science Editors:
Wonch KE. Responsiveness to Infant Cues in Postpartum Depressed and Non-Depressed Mothers: Functional Neural Correlates and Their Relation to Behaviour. [Doctoral Dissertation]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/79564
13.
Pagliaccio, David.
The Effects of HPA Axis Genetic Variation and Early Life Stress on Cortisol Levels in Preschool Age Children and on Amygdala and Hippocampus Volumes, Reactivity, and Connectivity at School Age.
Degree: PhD, Biology & Biomedical Sciences (Neurosciences), 2015, Washington University in St. Louis
URL: https://openscholarship.wustl.edu/art_sci_etds/473
► Internalizing psychopathology has been linked to increased cortisol reactivity and alterations in limbic brain structure and function, yet the mechanisms underlying these alterations are…
(more)
▼ Internalizing psychopathology has been linked to increased cortisol reactivity and alterations in limbic brain structure and function, yet the mechanisms underlying these alterations are unclear. One key hypothesis is that stress plays a major causal role in these mechanisms. Animal studies find that chronic stress or glucocorticoid administration lead to alterations in hippocampal and
amygdala structure and function. Relatedly, life stress is a major risk factors for depression while candidate gene studies have related variation in hypothalamic-pituitary-adrenal (HPA) axis genes to increased prevalence and severity of depression. The present work tested the hypothesis that genetic profile scores combining variance across 10 single nucleotide polymorphisms from four HPA axis genes (CRHR1, NR3C2, NR3C1, FKBP5) and early life stress would predict increases in stress cortisol levels in preschool-age children as well as alterations in hippocampal and
amygdala volumes, reactivity, and resting state functional connectivity in these same children at school age. The current results indicate that (1) childhood stress exposure and genetic profile scores both predict stress cortisol, (2) these factors interact to predict volumetric alterations, partially mediated by cortisol, (3) life stress predicts left
amygdala reactivity while genetic profile scores interact with sex and pubertal status to predict
amygdala and hippocampus reactivity to negative emotional stimuli, and (4) these factors and their interaction predict weakened
amygdala functional connectivity with subcortical and prefrontal regions. Overall, these findings suggest a key role for stress exposure, genetic risk, and cortisol in contributing to individual differences in
amygdala and hippocampus structure and function typically associated with internalizing pathology.
Advisors/Committee Members: Deanna M Barch, Joan L Luby, Ryan Bogdan, Arpana Agrawal, Tamara Hershey.
Subjects/Keywords: amygdala, childhood, depression, genetics, hippocampus, stress; Biology
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APA (6th Edition):
Pagliaccio, D. (2015). The Effects of HPA Axis Genetic Variation and Early Life Stress on Cortisol Levels in Preschool Age Children and on Amygdala and Hippocampus Volumes, Reactivity, and Connectivity at School Age. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/473
Chicago Manual of Style (16th Edition):
Pagliaccio, David. “The Effects of HPA Axis Genetic Variation and Early Life Stress on Cortisol Levels in Preschool Age Children and on Amygdala and Hippocampus Volumes, Reactivity, and Connectivity at School Age.” 2015. Doctoral Dissertation, Washington University in St. Louis. Accessed September 23, 2018.
https://openscholarship.wustl.edu/art_sci_etds/473.
MLA Handbook (7th Edition):
Pagliaccio, David. “The Effects of HPA Axis Genetic Variation and Early Life Stress on Cortisol Levels in Preschool Age Children and on Amygdala and Hippocampus Volumes, Reactivity, and Connectivity at School Age.” 2015. Web. 23 Sep 2018.
Vancouver:
Pagliaccio D. The Effects of HPA Axis Genetic Variation and Early Life Stress on Cortisol Levels in Preschool Age Children and on Amygdala and Hippocampus Volumes, Reactivity, and Connectivity at School Age. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2015. [cited 2018 Sep 23].
Available from: https://openscholarship.wustl.edu/art_sci_etds/473.
Council of Science Editors:
Pagliaccio D. The Effects of HPA Axis Genetic Variation and Early Life Stress on Cortisol Levels in Preschool Age Children and on Amygdala and Hippocampus Volumes, Reactivity, and Connectivity at School Age. [Doctoral Dissertation]. Washington University in St. Louis; 2015. Available from: https://openscholarship.wustl.edu/art_sci_etds/473
University of Oxford
14.
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
;
http://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 ·
Chicago ·
MLA ·
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Export
to Zotero / EndNote / Reference
Manager
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 ; http://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 September 23, 2018.
http://ora.ox.ac.uk/objects/uuid:91017ce3-7c42-4310-94fb-be659ec2e52e ; http://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. 23 Sep 2018.
Vancouver:
Lapray M. Role of intercalated and NPY-expressing cells in neuronal circuit of the amygdala. [Internet] [Doctoral dissertation]. University of Oxford; 2014. [cited 2018 Sep 23].
Available from: http://ora.ox.ac.uk/objects/uuid:91017ce3-7c42-4310-94fb-be659ec2e52e ; http://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 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595998
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 (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 September 23, 2018.
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. 23 Sep 2018.
Vancouver:
Chia-chi J. Mevinphos Induces Seizure-like EEG Activity and Decreases Blood Pressure by an Action on Amygdala. [Internet] [Thesis]. NSYSU; 2011. [cited 2018 Sep 23].
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
University of Saskatchewan
16.
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. (advisor), Cayabyab, Francisco S. (committee member), Elias, Lorin J. (committee member), Caruncho, Hector J. (committee member), Menard, Janet L. (committee member), Kalynchuk, Lisa (committee member).
Subjects/Keywords: corticosterone; depression; fear conditioning; amygdala; fluoxetine
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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 September 23, 2018.
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. 23 Sep 2018.
Vancouver:
Marks W. Fear Learning as a Component of a Depressive Phenotype in Rodents. [Internet] [Thesis]. University of Saskatchewan; 2014. [cited 2018 Sep 23].
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
Georgia State University
17.
Sargent, Kayla.
The Role of Comorbid Anxiety Symptoms in Children and Adolescents with Autism Spectrum Disorders (ASD) on an Emotional Perception Task.
Degree: MA, Psychology, 2015, Georgia State University
URL: https://scholarworks.gsu.edu/psych_theses/138
► The focus of the present study is to investigate the relationship between anxiety symptoms and neural outcomes of emotion processing in children and adolescents…
(more)
▼ The focus of the present study is to investigate the relationship between anxiety symptoms and neural outcomes of emotion processing in children and adolescents with autism spectrum disorders (ASD) and neurotypical controls. Eighteen child and adolescent participants (9 ASD, 3 female) completed questionnaires, behavioral testing, and an fMRI scan. Participants with ASD demonstrated significantly higher scores on parent-reported anxiety measures than typically developing (TD) participants; however, observed
amygdala activations were not related to parent-reported anxiety scores and OFC activation was not observed during emotional stimuli for either group. ASD and TD participants demonstrated significant bilateral responses in the superior temporal sulcus during emotional stimuli. The current study was unable to demonstrate potential functional neuropathology in the
amygdala as a mechanism for apparent differential diagnostic patterns in ASDs.
Advisors/Committee Members: Diana Robins, PhD, Tricia King, PhD, Robin Morris, PhD.
Subjects/Keywords: autism; anxiety; autism spectrum disorders; amygdala; fMRI
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APA (6th Edition):
Sargent, K. (2015). The Role of Comorbid Anxiety Symptoms in Children and Adolescents with Autism Spectrum Disorders (ASD) on an Emotional Perception Task. (Thesis). Georgia State University. Retrieved from https://scholarworks.gsu.edu/psych_theses/138
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):
Sargent, Kayla. “The Role of Comorbid Anxiety Symptoms in Children and Adolescents with Autism Spectrum Disorders (ASD) on an Emotional Perception Task.” 2015. Thesis, Georgia State University. Accessed September 23, 2018.
https://scholarworks.gsu.edu/psych_theses/138.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Sargent, Kayla. “The Role of Comorbid Anxiety Symptoms in Children and Adolescents with Autism Spectrum Disorders (ASD) on an Emotional Perception Task.” 2015. Web. 23 Sep 2018.
Vancouver:
Sargent K. The Role of Comorbid Anxiety Symptoms in Children and Adolescents with Autism Spectrum Disorders (ASD) on an Emotional Perception Task. [Internet] [Thesis]. Georgia State University; 2015. [cited 2018 Sep 23].
Available from: https://scholarworks.gsu.edu/psych_theses/138.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Sargent K. The Role of Comorbid Anxiety Symptoms in Children and Adolescents with Autism Spectrum Disorders (ASD) on an Emotional Perception Task. [Thesis]. Georgia State University; 2015. Available from: https://scholarworks.gsu.edu/psych_theses/138
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Baylor University
18.
Tran, Lee.
Molecular mechanisms in low-serotonin induced mood and anxiety disorders.
Degree: Biomedical Studies., 2010, Baylor University
URL: http://hdl.handle.net/2104/8060
► The amygdala has been shown to be involved in both epilepsy and emotional disturbances such as in mood and anxiety disorders. It is suggested that…
(more)
▼ The
amygdala has been shown to be involved in both epilepsy and emotional disturbances such as in mood and anxiety disorders. It is suggested that anxiety and mood disorders may be the result of sub-seizure hyperexcitability in limbic areas such as the
amygdala. Epilepsy-like mechanisms involve increased glutamatergic activity, whereas low serotonin (5-hydroxytryptamine, 5-HT) is associated with abnormal emotion. Although much evidence suggests low 5-HT increases excitability, the molecular mechanisms underlying this process are not known. Here we explored the ability of low serotonin to increase glutamate receptor (GluR) expression resulting in increased anxiety-like behavior. Using qRT-PCR, we found that individually-housed rats treated with p-chlorophenylalanine (300 mg/kg i.p.), an inhibitor of tyrosine hydroxylase, resulted in 21.8 fold higher GluR1 mRNA expression in
amygdala neurons. Similar results were found in rats treated with bilateral infusions of 5’7-dihydroxytryptamine (DHT, 8 μg/side) into the lateral nucleus of the
amygdala (LA) resulting in a 10³ fold increase in GluR1 mRNA. Further, Western blot analysis confirmed an overall 50.0% increase in GluR1 protein expression without any significant increase in other GluR subunits. These results suggested that low serotonin induces hyperexcitability of LA neurons by increasing GluR1 mRNA, and led to increased expression of GluR1. Additionally, we showed that these molecular changes resulted in behavioral differences in the open field maze, but not the plus maze. Rats treated with 5,7-DHT had a higher degree of center avoidance. The signaling pathway involved was also of interest. We found that the increase in GluRs may be mediated by CaMKII as shown by a ~60% increase in CaMKII phosphorylation. In order to further investigate, RNAi delivered by an AAV vector was used to knock down CaMKII expression and the effects on GluR expression was assessed. We showed that knockdown of CaMKII resulted in up to 37% decrease in GluR1 mRNA. CaMKII knockdown was also able to reverse the anxiogenic effects of decreased 5-HT, increasing center entries up to 30% and center duration up to 40% compared to controls. These results suggested that low serotonin induced hyperexcitability in LA neurons by increasing GluR1 possibly through a CaMKII mediated pathway, and led to increased open-field anxiety. This mechanism could be important in the pathophysiology of mood and anxiety disorders.
Advisors/Committee Members: Keele, N. Bradley (advisor).
Subjects/Keywords: Amygdala.;
Hyperexcitability.;
Serotonin.;
Glutamate Receptors.;
Anxiety.
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APA (6th Edition):
Tran, L. (2010). Molecular mechanisms in low-serotonin induced mood and anxiety disorders.
(Thesis). Baylor University. Retrieved from http://hdl.handle.net/2104/8060
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):
Tran, Lee. “Molecular mechanisms in low-serotonin induced mood and anxiety disorders.
” 2010. Thesis, Baylor University. Accessed September 23, 2018.
http://hdl.handle.net/2104/8060.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Tran, Lee. “Molecular mechanisms in low-serotonin induced mood and anxiety disorders.
” 2010. Web. 23 Sep 2018.
Vancouver:
Tran L. Molecular mechanisms in low-serotonin induced mood and anxiety disorders.
[Internet] [Thesis]. Baylor University; 2010. [cited 2018 Sep 23].
Available from: http://hdl.handle.net/2104/8060.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Tran L. Molecular mechanisms in low-serotonin induced mood and anxiety disorders.
[Thesis]. Baylor University; 2010. Available from: http://hdl.handle.net/2104/8060
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Baylor University
19.
Blakeley, Hillary Joy.
Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.
Degree: 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 ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Blakeley, H. J. (2011). Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.
(Thesis). Baylor University. Retrieved from http://hdl.handle.net/2104/8182
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):
Blakeley, Hillary Joy. “Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.
” 2011. Thesis, Baylor University. Accessed September 23, 2018.
http://hdl.handle.net/2104/8182.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Blakeley, Hillary Joy. “Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.
” 2011. Web. 23 Sep 2018.
Vancouver:
Blakeley HJ. Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.
[Internet] [Thesis]. Baylor University; 2011. [cited 2018 Sep 23].
Available from: http://hdl.handle.net/2104/8182.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Blakeley HJ. Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.
[Thesis]. Baylor University; 2011. Available from: http://hdl.handle.net/2104/8182
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – San Diego
20.
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 September 23, 2018.
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. 23 Sep 2018.
Vancouver:
Groeniger KM. Decreased Density of Serotonin Transporting Fibers in the Infant Williams Syndrome Amygdala. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2018 Sep 23].
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
Baylor University
21.
[No author].
Sex differences in ethanol-induced inhibition of hyperpolarization-activated current and excitability of amygdala neurons after traumatic stress.
Degree: 2018, Baylor University
URL: http://hdl.handle.net/2104/10343
► The basolateral amygdala (BLA) plays a vital role in integrating sensory information and establishing emotional salience of the environment. Ethanol potentiates GABAergic inhibition in BLA…
(more)
▼ The basolateral
amygdala (BLA) plays a vital role in integrating sensory information and establishing emotional salience of the environment. Ethanol potentiates GABAergic inhibition in BLA neurons, regulating excitatory transmission and playing an integral role in controlling anxiety-like behaviors. While the effect of ethanol on the
amygdala and anxiety-like behaviors is well-established, sex differences in the effects of ethanol on BLA neurophysiology and the effect of ethanol on traumatic stress-induced changes to BLA activity are currently unknown. Understanding the sex-related factors that contribute to BLA neuron membrane properties in stressed animals may point to potential neural mechanisms associated with gender differences in resilience or susceptibility to stress and improve individualized treatment. Ethanol-mediated inhibition is stronger in BLA neurons from males than females and ethanol-mediated inhibition of hyperpolarization-activated, cyclic nucleotide gated current (Ih) is stronger in males, owing in part to the low amplitude of Ih in females in the absence of ethanol. In response to SPS, action potential firing in the BLA did not change between males and females. However, ethanol significantly decreased action potential firing in BLA neurons exposed to SPS in females only, suggesting that the inhibitory effect of alcohol is greater in females than in males exposed to stress. Ethanol decreased Ih amplitude only in BLA neurons from males exposed to SPS, in part because Ih amplitude is larger in BLA neurons from males than it is in females. Since ethanol reduced BLA excitability only in males, these data suggest that ethanol may be more anxiolytic in males than in females. This difference may contribute to the sex differences in comorbid PTSD and alcohol abuse.
Advisors/Committee Members: Keele, N. Bradley (advisor).
Subjects/Keywords: Sex differences. Basolateral amygdala. Alcohol. Neurophysiology.
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APA ·
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CSE |
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Manager
APA (6th Edition):
author], [. (2018). Sex differences in ethanol-induced inhibition of hyperpolarization-activated current and excitability of amygdala neurons after traumatic stress.
(Thesis). Baylor University. Retrieved from http://hdl.handle.net/2104/10343
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):
author], [No. “Sex differences in ethanol-induced inhibition of hyperpolarization-activated current and excitability of amygdala neurons after traumatic stress.
” 2018. Thesis, Baylor University. Accessed September 23, 2018.
http://hdl.handle.net/2104/10343.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
author], [No. “Sex differences in ethanol-induced inhibition of hyperpolarization-activated current and excitability of amygdala neurons after traumatic stress.
” 2018. Web. 23 Sep 2018.
Vancouver:
author] [. Sex differences in ethanol-induced inhibition of hyperpolarization-activated current and excitability of amygdala neurons after traumatic stress.
[Internet] [Thesis]. Baylor University; 2018. [cited 2018 Sep 23].
Available from: http://hdl.handle.net/2104/10343.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
author] [. Sex differences in ethanol-induced inhibition of hyperpolarization-activated current and excitability of amygdala neurons after traumatic stress.
[Thesis]. Baylor University; 2018. Available from: http://hdl.handle.net/2104/10343
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
22.
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 (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 September 23, 2018.
http://hdl.handle.net/1807/75824.
MLA Handbook (7th Edition):
Morrison, Daniel. “The Sparse Engram of the Lateral Amygdala.” 2016. Web. 23 Sep 2018.
Vancouver:
Morrison D. The Sparse Engram of the Lateral Amygdala. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2018 Sep 23].
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
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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Chicago ·
MLA ·
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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 September 23, 2018.
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. 23 Sep 2018.
Vancouver:
Jacob AD. Coallocation of Appetitive and Aversive Memories in the Lateral Amygdala. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2018 Sep 23].
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
UCLA
24.
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 September 23, 2018.
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. 23 Sep 2018.
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 2018 Sep 23].
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 Notre Dame
25.
Ashley Nicole Ferreira.
Dissecting brain circuitry of fear and anxiety: The medial
prefrontal cortex (mPFC)- Amygdala- periaqueductal grey (PAG)
circuit.
Degree: MS, Biological Sciences, 2015, University of Notre Dame
URL: https://curate.nd.edu/show/x059c53702z
► Anxiety, a debilitating sense of fear, involves an interconnected brain network that includes the medial prefrontal cortex (mPFC), amygdala, and periaqueductal grey (PAG). However,…
(more)
▼ Anxiety, a debilitating sense of fear,
involves an interconnected brain network that includes the medial
prefrontal cortex (mPFC),
amygdala, and periaqueductal grey (PAG).
However, the specific organization and cellular physiology of
distinct pathways within this network are undefined but critical
for understanding anxiety disorders. This thesis elucidated the
circuitry, pharmacology, and intrinsic physiology of defined
pathways within the mPFC-
amygdala-PAG circuit. Comparison of mPFC
neurons projecting to the PAG versus
amygdala revealed significant
differences in intrinsic properties, local circuitry, and
neuromodulation by stress peptides. In the central
amygdala (CeA),
neurons projecting to the PAG (CeA-PAG neurons) expressed different
levels of hyperpolarization-activated current. CeA-PAG neurons were
altered by anxiogenic peptide corticotropin-releasing factor (CRF)
but not anxiolytic neuropeptide-Y (NPY). Optogenetic activation of
axons originating in the PAG or IL drove both excitation and
inhibition in CeA-PAG neurons. Together, this thesis has uncovered
critical characteristics of a neural network implicated in
anxiety.
Advisors/Committee Members: Patrick L. Sheets, Committee Chair, Zainulabeuddin Syed, Committee Member, Sunny Boyd, Committee Member.
Subjects/Keywords: electrophysiology; periaqueductal grey; amygdala; medial prefrontal cortex
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Manager
APA (6th Edition):
Ferreira, A. N. (2015). Dissecting brain circuitry of fear and anxiety: The medial
prefrontal cortex (mPFC)- Amygdala- periaqueductal grey (PAG)
circuit. (Masters Thesis). University of Notre Dame. Retrieved from https://curate.nd.edu/show/x059c53702z
Chicago Manual of Style (16th Edition):
Ferreira, Ashley Nicole. “Dissecting brain circuitry of fear and anxiety: The medial
prefrontal cortex (mPFC)- Amygdala- periaqueductal grey (PAG)
circuit.” 2015. Masters Thesis, University of Notre Dame. Accessed September 23, 2018.
https://curate.nd.edu/show/x059c53702z.
MLA Handbook (7th Edition):
Ferreira, Ashley Nicole. “Dissecting brain circuitry of fear and anxiety: The medial
prefrontal cortex (mPFC)- Amygdala- periaqueductal grey (PAG)
circuit.” 2015. Web. 23 Sep 2018.
Vancouver:
Ferreira AN. Dissecting brain circuitry of fear and anxiety: The medial
prefrontal cortex (mPFC)- Amygdala- periaqueductal grey (PAG)
circuit. [Internet] [Masters thesis]. University of Notre Dame; 2015. [cited 2018 Sep 23].
Available from: https://curate.nd.edu/show/x059c53702z.
Council of Science Editors:
Ferreira AN. Dissecting brain circuitry of fear and anxiety: The medial
prefrontal cortex (mPFC)- Amygdala- periaqueductal grey (PAG)
circuit. [Masters Thesis]. University of Notre Dame; 2015. Available from: https://curate.nd.edu/show/x059c53702z
University of Southern California
26.
Sobhani, Mona.
Psychopathic traits and the fronto-amygdala circuit in a
community sample: the role of trait anxiety.
Degree: PhD, Neuroscience, 2013, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/324192/rec/5301
► Psychopathy is a personality disorder comprised of a constellation of traits, such as lack of remorse, lack of empathy, impulsivity, and irresponsibility. Although much research…
(more)
▼ Psychopathy is a personality disorder comprised of a
constellation of traits, such as lack of remorse, lack of empathy,
impulsivity, and irresponsibility. Although much research has been
conducted on this personality disorder, the neural correlates
remain poorly understood. Progress in this realm has been hindered
by two factors. First, given the large body of work supporting
delineation of psychopathy into subtypes (based on trait anxiety),
the exploration of dissociable neural correlates between subtypes
has been insufficiently studied. Second, many studies utilize a
single neuroimaging modality to explore a given neural property,
and thus, cannot answer comprehensive questions about neural
network dynamics. The current work addresses both limitations in
the literature by examining, in a community sample, the
relationships between psychopathic traits, trait anxiety, and
neural properties (function, functional connectivity,
microstructural integrity) using multiple neuroimaging methods. The
two overarching aims of this dissertation are to determine whether
the relationship between psychopathic traits and neural properties
is dependent upon trait anxiety, and whether these relationships
are evident across several different neuroimaging
modalities.
Advisors/Committee Members: Aziz-Zadeh, LisaBaker, Laura A. (Committee Chair), Damasio, Hanna (Committee Member), Saks, Elyn (Committee Member).
Subjects/Keywords: psychopathy; prefrontal; amygdala; community; fMRI; DTI
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APA ·
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MLA ·
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Export
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Manager
APA (6th Edition):
Sobhani, M. (2013). Psychopathic traits and the fronto-amygdala circuit in a
community sample: the role of trait anxiety. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/324192/rec/5301
Chicago Manual of Style (16th Edition):
Sobhani, Mona. “Psychopathic traits and the fronto-amygdala circuit in a
community sample: the role of trait anxiety.” 2013. Doctoral Dissertation, University of Southern California. Accessed September 23, 2018.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/324192/rec/5301.
MLA Handbook (7th Edition):
Sobhani, Mona. “Psychopathic traits and the fronto-amygdala circuit in a
community sample: the role of trait anxiety.” 2013. Web. 23 Sep 2018.
Vancouver:
Sobhani M. Psychopathic traits and the fronto-amygdala circuit in a
community sample: the role of trait anxiety. [Internet] [Doctoral dissertation]. University of Southern California; 2013. [cited 2018 Sep 23].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/324192/rec/5301.
Council of Science Editors:
Sobhani M. Psychopathic traits and the fronto-amygdala circuit in a
community sample: the role of trait anxiety. [Doctoral Dissertation]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/324192/rec/5301
University of Southern California
27.
Pang, Raina D.
Genotype and sex effects on anxiety behavior and functional
activation in corticolimbic circuits in serotonin transporter
knockout mice (5-HITT KO).
Degree: PhD, Neuroscience, 2012, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43601/rec/3020
► In humans, the serotonin transporter linked polymorphic region (5-HTTLPR) results in altered transcriptional efficiency of the transporter gene, as well as uptake of serotonin (5-HT)…
(more)
▼ In humans, the serotonin transporter linked
polymorphic region (5-HTTLPR) results in altered transcriptional
efficiency of the transporter gene, as well as uptake of serotonin
(5-HT) by neurons. The low expressing `s' allele of this
polymorphism has been linked to increased susceptibility to stress
and altered connectivity of corticolimbic neural circuits, the
disruption of which is widely invoked to explain emotional
dysregulation in anxiety and mood disorders. ❧ Serotonin
transporter (5-HTT) knockout (KO) mice offer a promising model for
psychiatric research as close parallels exist between the human
polymorphism and the mouse model at the level of serotonergic
profile, behavior, physiological function, and stress hormone
response. Although much work has gone into characterizing 5-HTT KO
mice, little work to date has examined functional activation
patterns and connectivity of circuits involved in emotional
regulation in these mice. The experiments outlined in this
dissertation address this gap in knowledge by examining sex and
genotypic differences in the underlying functional activation of
corticolimbic circuits. The inclusion of females in this study
provides important information about how sex differences in
serotonergic function alter brain function. Functional connectivity
analysis is also undertaken in a combined male/female groups to
determine genotypic effects on a network level. ❧ Overall, the
experiments contained in this dissertation contribute novel
information about the role of sex and 5-HTT genotype in anxiety
like behavior and function of corticolimbic circuits. Specifically,
this is the first study using whole brain functional perfusion
mapping in the 5-HTT KO mouse model. Furthermore, these studies
support sex differences in functional regulation of the
prefrontal-
amygdala network in a fear-conditioned paradigm. These
studies establish the translational value of functional brain
mapping endpoints and suggest greater specificity than the
behavioral endpoints. Future studies could address the underlying
molecular and structural changes accompanying functional changes
seen in 5-HTT KO mice.
Advisors/Committee Members: Holschneider, Daniel P. (Committee Chair), Jakowec, Michael (Committee Member), Celikel, Tansu (Committee Member), Watts, Alan G. (Committee Member).
Subjects/Keywords: serotonin transporter knockout mice; amygdala; functional neuroimaging
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APA ·
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MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Pang, R. D. (2012). Genotype and sex effects on anxiety behavior and functional
activation in corticolimbic circuits in serotonin transporter
knockout mice (5-HITT KO). (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43601/rec/3020
Chicago Manual of Style (16th Edition):
Pang, Raina D. “Genotype and sex effects on anxiety behavior and functional
activation in corticolimbic circuits in serotonin transporter
knockout mice (5-HITT KO).” 2012. Doctoral Dissertation, University of Southern California. Accessed September 23, 2018.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43601/rec/3020.
MLA Handbook (7th Edition):
Pang, Raina D. “Genotype and sex effects on anxiety behavior and functional
activation in corticolimbic circuits in serotonin transporter
knockout mice (5-HITT KO).” 2012. Web. 23 Sep 2018.
Vancouver:
Pang RD. Genotype and sex effects on anxiety behavior and functional
activation in corticolimbic circuits in serotonin transporter
knockout mice (5-HITT KO). [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2018 Sep 23].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43601/rec/3020.
Council of Science Editors:
Pang RD. Genotype and sex effects on anxiety behavior and functional
activation in corticolimbic circuits in serotonin transporter
knockout mice (5-HITT KO). [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43601/rec/3020
28.
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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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
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 September 23, 2018.
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. 23 Sep 2018.
Vancouver:
Isaacs S. The Roles of the Amygdala and the Hippocampus in Fear Conditioning. [Internet] [Thesis]. University of Skövde; 2015. [cited 2018 Sep 23].
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
University of Toronto
29.
Hsiang, Hwa-Lin.
Manipulating a "cocaine-cue engram" in mice.
Degree: PhD, 2017, University of Toronto
URL: http://hdl.handle.net/1807/79005
► Experience with drugs of abuse (such as cocaine) produces powerful, long-lasting memories that may be key in the development and persistence of drug addiction. The…
(more)
▼ Experience with drugs of abuse (such as cocaine) produces powerful, long-lasting memories that may be key in the development and persistence of drug addiction. The neural mechanisms that mediate how and where these cocaine-cue memories are encoded, consolidated, and stored in the brain are unknown. Here we used cocaine-induced conditioned place preference to examine the precise neural circuits that support a cocaine-cue memory (cocaine-cue “memory trace” or “engram”) in mice. We found that a small population of neurons (~10%) in the lateral nucleus of the
amygdala (LA) was recruited at the time of cocaine-conditioning to become part of the cocaine-cue engram supporting that memory. Moreover, neurons with increased levels of the transcription factor CREB (cAMP response element-binding protein) were preferentially recruited or allocated to the cocaine-cue engram. Pre-test ablation or silencing of neurons overexpressing CREB (but not a similar number of LA neurons not allocated to the cocaine-cue memory engram) disrupted the expression of a previously acquired cocaine-cue memory, suggesting that neurons overexpressing CREB become critical nodes in the LA of what is likely a larger (perhaps brain-wide) cocaine-cue engram. Previous research has suggested that coordinated post-encoding reactivation of neurons within an engram or cell assembly is crucial for memory consolidation (Marr, 1971; Buzsáki, 1989; Wilson McNaughton, 1994; McClelland et al., 1995; Girardeau et al., 2009; Dupret et al., 2010; Carr et al., 2011). Consistent with this, we also found that post-training suppression or non-discriminate activation of CREB overexpressing neurons impaired consolidation of the cocaine-cue memory. We also showed that these neurons were important for the reinstatement of a cocaine-cue memory. Following extinction of a cocaine-cue memory, re-exposure to cocaine may reinstate the original memory (Brown et al., 2010; Bilbao et al., 2008; Mueller Stewart, 2000). These results suggest that those neurons that are initially important in a cocaine-cue memory continue to be important to that memory, even following extinction. Finally, we found that in the LA, neurons that have relatively higher levels of neuronal excitability are more likely to be recruited to an engram supporting a cocaine-cue memory. Together, these findings reveal mechanisms underlying how and where drug memories are encoded and stored in the brain.
Advisors/Committee Members: Josselyn, Sheena, Medical Science.
Subjects/Keywords: Amygdala; Cocaine; Conditioned place preference; Memory; 0317
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APA ·
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MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hsiang, H. (2017). Manipulating a "cocaine-cue engram" in mice. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/79005
Chicago Manual of Style (16th Edition):
Hsiang, Hwa-Lin. “Manipulating a "cocaine-cue engram" in mice.” 2017. Doctoral Dissertation, University of Toronto. Accessed September 23, 2018.
http://hdl.handle.net/1807/79005.
MLA Handbook (7th Edition):
Hsiang, Hwa-Lin. “Manipulating a "cocaine-cue engram" in mice.” 2017. Web. 23 Sep 2018.
Vancouver:
Hsiang H. Manipulating a "cocaine-cue engram" in mice. [Internet] [Doctoral dissertation]. University of Toronto; 2017. [cited 2018 Sep 23].
Available from: http://hdl.handle.net/1807/79005.
Council of Science Editors:
Hsiang H. Manipulating a "cocaine-cue engram" in mice. [Doctoral Dissertation]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/79005
University of Washington
30.
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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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 September 23, 2018.
http://hdl.handle.net/1773/35628.
MLA Handbook (7th Edition):
Akers, Christina Akiko. “Threshold dependence of central amygdala CRF in fear behaviors.” 2016. Web. 23 Sep 2018.
Vancouver:
Akers CA. Threshold dependence of central amygdala CRF in fear behaviors. [Internet] [Doctoral dissertation]. University of Washington; 2016. [cited 2018 Sep 23].
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
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