+publisher:"University of Texas – Austin" +contributor:("Golding, Nace")

1. Mathews, Paul James, 1978-. Voltage gated ion channels shape subthreshold synaptic integration in principal neurons of the medial superior olive.

Degree: PhD, Neuroscience, 2008, University of Texas – Austin

URL: http://hdl.handle.net/2152/18247

► Principal neurons of the medial superior olive (MSO) encode low-frequency sound localization cues by comparing the relative arrival time of sound to the two ears.… (more)

▼ Principal neurons of the medial superior olive (MSO) encode low-frequency sound localization cues by comparing the relative arrival time of sound to the two ears. In mammals, MSO neurons display biophysical specializations, such as voltage-gated sodium (Na[subscript v]) and potassium (K[subscript v]) channels that enable them to detect these cues with microsecond precision. In this dissertation electrophysiological techniques were used to examine the specific channel properties and functional role these channels play in MSO neurons following hearing onset. In addition, computational models that incorporated these physiological data were used to further study how the specific properties of these channels facilitate MSO function. Experiments in this dissertation showed that Na[subscript v] channels are heavily expressed in the persisomatic region of MSO neurons, but unlike those expressed in other neurons they minimally contribute to action potential generation. This is likely due to the low percentage of channels available for activation at the resting membrane potential. Current clamp recordings determined that Na[subscript v] channels counterbalance K[subscript v] channels voltage rectification by boosting near action potential threshold excitatory post-synaptic potentials (EPSPs). Further, computational modeling revealed that synaptic inputs are larger at the soma with Na[subscript v] channels restricted to the soma than when they are evenly distributed throughout the soma and dendrites. During the first few weeks after hearing onset current clamp experiments showed EPSP duration decreased while the temporal resolution for detecting the arrival time of synaptic inputs increased. These changes in EPSP duration are due in part to both the development of faster membrane response properties and increases in the expression of low voltage-activated K[subscript v] channels (K[subscript LVA]). Further investigation determined these channels display a somatically enriched distribution and act to counterbalance the distortions that result from dendritic cable filtering. This is accomplished by K[subscript LVA] actively decreasing the duration of EPSPs in a voltage dependent manner. Computational modeling confirmed these results as well as illustrating their effects on the integration of mono- versus bilateral excitation. Together these findings indicate that the expression of specialized Na[subscript v] and K[subscript v] channels facilitate the neuron’s computational task, detecting and comparing the relative timing of synaptic inputs used in low frequency sound localization. Advisors/Committee Members: Golding, Nace L. (advisor).

Subjects/Keywords: Ion channels; Directional hearing; Neurons – Physiology

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APA (6^th Edition):

Mathews, Paul James, 1. (2008). Voltage gated ion channels shape subthreshold synaptic integration in principal neurons of the medial superior olive. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/18247

Chicago Manual of Style (16^th Edition):

Mathews, Paul James, 1978-. “Voltage gated ion channels shape subthreshold synaptic integration in principal neurons of the medial superior olive.” 2008. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/18247.

MLA Handbook (7^th Edition):

Mathews, Paul James, 1978-. “Voltage gated ion channels shape subthreshold synaptic integration in principal neurons of the medial superior olive.” 2008. Web. 27 Feb 2021.

Vancouver:

Mathews, Paul James 1. Voltage gated ion channels shape subthreshold synaptic integration in principal neurons of the medial superior olive. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2008. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/18247.

Council of Science Editors:

Mathews, Paul James 1. Voltage gated ion channels shape subthreshold synaptic integration in principal neurons of the medial superior olive. [Doctoral Dissertation]. University of Texas – Austin; 2008. Available from: http://hdl.handle.net/2152/18247

University of Texas – Austin

2. Bieri, Kevin Wood. Slow and fast gamma rhythms represent distinct memory processing states in the hippocampus.

Degree: PhD, Neuroscience, 2015, University of Texas – Austin

URL: http://hdl.handle.net/2152/39202

► The hippocampus is central to learning and memory and participates in both the encoding of new memories and their retrieval. It is not known, however,… (more)

▼ The hippocampus is central to learning and memory and participates in both the encoding of new memories and their retrieval. It is not known, however, how these dual functions are processed within the same structure without causing interference between what is actively experienced and what is remembered. Different frequencies of gamma oscillations selectively route inputs to area CA1 of the hippocampus, suggesting that gamma subtypes play a role in differentiating between streams of incoming information. Slow gamma oscillations (~25–55 Hz) couple CA1 to area CA3, a region that is thought to store neuronal representations of past events and is thus important for memory retrieval. Fast gamma oscillations (~60–100 Hz) couple CA1 to MEC, a region that supplies the hippocampus with information about ongoing experiences. In this dissertation, I use hippocampal recordings in freely behaving rats to provide evidence that such slow and fast gamma coupling supports distinct memory retrieval and encoding modes in the hippocampus. This is first examined in the principal neurons of the hippocampus, called ‘place cells’, which are thought to provide the ‘where’ component of episodic memory. It was found that place cells alternated between distinct spatial coding modes, representing upcoming locations during slow gamma and recent locations during fast gamma. This concept was explored further in ‘place cell sequences’, which represent trajectories through space, and are thought to store sequential events of an experience. Sequences coded paths sweeping ahead of the animal during slow gamma, and coded ongoing, real-time locations during fast gamma. Also, it was found that different phases of the slow gamma cycle coded specific locations, suggesting a mechanism for how slow gamma promotes retrieval of multi-item memories. Lastly, slow and fast gamma were examined during novel and familiar experiences. Fast gamma was enhanced during encoding of novel object-place associations, while slow gamma coupling between CA3 and CA1 was associated with retrieval of familiar object-place associations. Taken together, these results support the hypothesis that distinct gamma subtypes provide a novel mechanism for separating the dual “reading” and “writing” functions of the hippocampus. Advisors/Committee Members: Colgin, Laura (advisor), Preston, Alison (committee member), Morikawa, Hitoshi (committee member), Drew, Michael (committee member), Golding, Nace (committee member).

Subjects/Keywords: Hippocampus; Gamma; Place cells

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APA (6^th Edition):

Bieri, K. W. (2015). Slow and fast gamma rhythms represent distinct memory processing states in the hippocampus. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/39202

Chicago Manual of Style (16^th Edition):

Bieri, Kevin Wood. “Slow and fast gamma rhythms represent distinct memory processing states in the hippocampus.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/39202.

MLA Handbook (7^th Edition):

Bieri, Kevin Wood. “Slow and fast gamma rhythms represent distinct memory processing states in the hippocampus.” 2015. Web. 27 Feb 2021.

Vancouver:

Bieri KW. Slow and fast gamma rhythms represent distinct memory processing states in the hippocampus. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/39202.

Council of Science Editors:

Bieri KW. Slow and fast gamma rhythms represent distinct memory processing states in the hippocampus. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/39202

University of Texas – Austin

3. Wolfe, Sarah Anne. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.

Degree: PhD, Cellular and Molecular Biology, 2017, University of Texas – Austin

URL: http://dx.doi.org/10.26153/tsw/2231

► Alcohol Use Disorder (AUD) and Major Depressive Disorder (MDD) are two widespread and debilitating disorders that share a high rate of comorbidity with the presence… (more)

▼ Alcohol Use Disorder (AUD) and Major Depressive Disorder (MDD) are two widespread and debilitating disorders that share a high rate of comorbidity with the presence of either disorder doubling the risk of developing the other. Despite their prevalence, few treatments are available to individuals with comorbid AUD and MDD. Both alcohol and antidepressants promote lasting neuroadaptive changes in synapses and dendrites. With alcohol these changes may provide relief from depressive symptoms, and the initial use of alcohol may be a form of self-medication for individuals with MDD, suggesting ethanol may have antidepressant properties underlying similarities in neurobiological abnormalities. However, the synaptic pathways that are shared by alcohol and antidepressants are unknown. This study aims to identify why acute exposure to ethanol produced lasting antidepressant and anxiolytic behaviors. To understand the functional basis of these behaviors, a molecular pathway activated by rapid antidepressants was investigated. Here ethanol, like rapid antidepressants, altered γ-aminobutyric acid type B receptor (GABA [subscript B] R) expression and signaling, to increase dendritic calcium. New GABA [subscript B] Rs were synthesized in response to ethanol treatment, requiring fragile-X mental retardation protein (FMRP). Ethanol-dependent changes in GABA [subscript B] R expression, dendritic signaling, and antidepressant efficacy were absent in Fmr1-knockout (KO) mice. These findings indicate that FMRP is an important regulator of protein synthesis following acute alcohol exposure, and provided a molecular basis for the antidepressant efficacy of acute ethanol exposure. We identify alterations on a global scale with acute alcohol and antidepressant by sequencing the synaptic transcriptome. We identified parallel alterations in exon usage with acute alcohol and antidepressant treatment. These shared differentially expressed exons may give rise to isoforms and proteins with altered function or localization in the synapse. Some of these differentially expressed exons were identified in genes known to have alternative isoforms with AUD and MDD. These data implicate alternative splicing and isoform expression in the acute antidepressant-like effects of ethanol and the development of comorbid alcohol and depression. Understanding the molecular basis for comorbidity may aid in development of treatment options for afflicted individuals with dual disorders, as well as explore the mechanism for the initiation of addiction with acute exposure to alcohol Advisors/Committee Members: Harris, R. Adron (advisor), Raab-Graham, Kimberly F. (advisor), Golding, Nace (committee member), Morrisett, Richard (committee member), Macdonald, Paul (committee member).

Subjects/Keywords: Alcohol use disorder; Major depressive disorder; Ethanol; Rapid antidepressants; FMRP; GABABR; Ro 25-6981; RNA-sequencing; Synaptoneurosomes; Exon usage

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APA (6^th Edition):

Wolfe, S. A. (2017). Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://dx.doi.org/10.26153/tsw/2231

Chicago Manual of Style (16^th Edition):

Wolfe, Sarah Anne. “Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.” 2017. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://dx.doi.org/10.26153/tsw/2231.

MLA Handbook (7^th Edition):

Wolfe, Sarah Anne. “Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.” 2017. Web. 27 Feb 2021.

Vancouver:

Wolfe SA. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2017. [cited 2021 Feb 27]. Available from: http://dx.doi.org/10.26153/tsw/2231.

Council of Science Editors:

Wolfe SA. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. [Doctoral Dissertation]. University of Texas – Austin; 2017. Available from: http://dx.doi.org/10.26153/tsw/2231

University of Texas – Austin

4. Renteria, Rafael III. Synaptic encoding of in vivo ethanol experience in the nucleus accumbens.

Degree: PhD, Neuroscience, 2015, University of Texas – Austin

URL: http://hdl.handle.net/2152/31598

► The nucleus accumbens (NAc) is a critical component of the brain reward system and neuroadaptations in the NAc are thought to underlie the development and… (more)

▼ The nucleus accumbens (NAc) is a critical component of the brain reward system and neuroadaptations in the NAc are thought to underlie the development and persistence of addiction. The NAc is composed of two subregions, the core and shell, in which medium spiny neurons (MSNs) are the primary cell type. There are two distinct subtypes of MSNs in the NAc depending on the dopamine receptor expression: D1 dopamine receptor expressing (D1+) MSNs and D2 dopamine receptor expressing MSNs (D1-). We conducted whole-cell patch clamp recordings using transgenic mice to selectively record from D1+ and D1- MSNs in the NAc and found that chronic intermittent ethanol (CIE) vapor exposure resulted in cell type specific alterations in the intrinsic properties and expression of plasticity. To detect changes in plasticity of AMPA receptor (AMPAR) mediated currents we used a well described form of NMDAR-dependent long-term depression (LTD) that is induced by pairing low frequency stimulation with postsynaptic depolarization. Similar to previous findings from our lab we found that LTD was expressed exclusively in D1+ MSNs of ethanol naïve mice. In slices prepared from CIE treated mice, the induction protocol instead resulted in long-term potentiation (LTP) in D1+ MSNs. The expression of LTP in D1+ MSNs was accompanied by an increase in excitability as well as an increase in the frequency of spontaneous EPSCs. Interestingly, CIE exposure uncovered the expression of LTD in D1- MSNs. To further our understanding as to how these neuroadaptations contribute to maladaptive ethanol drinking behaviors we used CIE vapor exposure to induce an increase in voluntary ethanol consumption. Electrophysiological experiments were conducted in the core and shell to determine if excitatory signaling and plasticity is differentially modulated between the two subregions. CIE induced an increase in ethanol drinking and resulted in the long-lasting disruption of LTD in D1+ MSNs of the NAc shell with no changes in the core. In addition we found that AMPAR conductance was significantly reduced at positive holding potentials suggesting the presence of GluA2-lacking AMPARs. These findings may constitute important neuroadaptations that underlie alcohol dependence and excessive alcohol consumption. Advisors/Committee Members: Morrisett, Richard A. (advisor), Gonzales, Rueben A (committee member), Harris, Robert A (committee member), Golding, Nace L (committee member), Morikawa, Hitoshi (committee member).

Subjects/Keywords: Plasticity; Ethanol

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APA (6^th Edition):

Renteria, R. I. (2015). Synaptic encoding of in vivo ethanol experience in the nucleus accumbens. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/31598

Chicago Manual of Style (16^th Edition):

Renteria, Rafael III. “Synaptic encoding of in vivo ethanol experience in the nucleus accumbens.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/31598.

MLA Handbook (7^th Edition):

Renteria, Rafael III. “Synaptic encoding of in vivo ethanol experience in the nucleus accumbens.” 2015. Web. 27 Feb 2021.

Vancouver:

Renteria RI. Synaptic encoding of in vivo ethanol experience in the nucleus accumbens. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/31598.

Council of Science Editors:

Renteria RI. Synaptic encoding of in vivo ethanol experience in the nucleus accumbens. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/31598

5. Sosanya, Natasha Marie. mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p.

Degree: PhD, Cell and Molecular Biology, 2014, University of Texas – Austin

URL: http://hdl.handle.net/2152/46489

► Little is known about how a neuron undergoes site-specific changes in intrinsic excitability in normal and diseased conditions. We provide evidence for a novel mechanism… (more)

▼ Little is known about how a neuron undergoes site-specific changes in intrinsic excitability in normal and diseased conditions. We provide evidence for a novel mechanism for the mammalian Target of Rapamycin Complex 1 (mTORC1) kinase dependent translational regulation of the voltage-gated potassium channel Kv1.1 mRNA (Chapter 2). First, we identified a microRNA, miR-129-5p, that represses Kv1.1 mRNA translation when mTORC1 is active. When mTORC1 is inactive, we found that the RNA-binding protein, HuD, binds to Kv1.1 mRNA and promotes its translation. Surprisingly, mTORC1 activity does not alter levels of miR-129 and HuD to favor binding to Kv1.1 mRNA but affects the degradation of high-affinity HuD target mRNAs, freeing HuD to bind Kv1.1 mRNA. Thus, high affinity HuD target mRNAs can serve two purposes under normal physiological conditions: 1) to provide functional proteins, such as CaMKIIα, that change the architecture of the synapse and 2) serve as a sponge sequestering HuD from translating mRNAs like Kv1.1. To determine if this mechanism for repression of Kv1.1 expression is conserved in a disease model where mTORC1 activity is overactive, we assessed the expression levels of active mTORC1, Kv1.1, and miR-129-5p in a rat model of temporal lobe epilepsy (TLE; Chapter 3). We found that when mTOR activity is low in TLE, Kv1.1 expression is high and behavioral seizure number is low. In contrast, when behavioral seizure activity starts to rise there is a corresponding increase in mTOR activity and Kv1.1 protein levels dramatically drop. In addition, we found that miR-129-5p, the negative regulator of Kv1.1 mRNA translation increases by 21 days post status epilepticus (SE) to sustain Kv1.1 mRNA translational repression. Thus, long-term changes in Kv1.1 protein levels result in a hyperpolarized threshold for action potential firing. Our results suggest that increased mTOR activity following SE results in two phases of Kv1.1 repression (1) in an initial repression of Kv1.1 mRNA translation by mTOR activity that is followed by (2) an onset of elevated miR-129-5p expression that sustains Kv1.1 repression. These studies suggest that dynamic changes in miR- 129-5p provide potential novel targets for epilepsy interventions. mTOR is a protein kinase that promotes CaMKIIα mRNA translation (Sosanya et al., 2013; Chapter 2); however, the mechanism and site of dendritic expression are unknown. Herein (Chapter 4), we show that mTOR activity mediates the dendritic branch specific expression of CaMKIIα, favoring one secondary, daughter branch over the other in a single neuron. Notably, reduction in mTOR activity decreases the overall dendritic expression of CaMKIIα protein and RNA through the shortening of its poly(A) tail. Overexpression of HuD both increases total CaMKIIα levels and rescues the selective expression of CaMKIIα in one daughter branch over the other. These results suggest that differential branch targeting of HuD may mediate the branch specific expression of CaMKIIα in neuronal dendrites during mTOR activity.… Advisors/Committee Members: Raab-Graham, Kimberly F. (advisor), Atkinson, Nigel (committee member), Golding, Nace (committee member), Haris, Adron (committee member), Iyer, Vishwanath (committee member).

Subjects/Keywords: mTOR; Kv1.1; miR-129; HuD; mRNA degradation; Temporal lobe epilepsy

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APA (6^th Edition):

Sosanya, N. M. (2014). mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/46489

Chicago Manual of Style (16^th Edition):

Sosanya, Natasha Marie. “mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p.” 2014. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/46489.

MLA Handbook (7^th Edition):

Sosanya, Natasha Marie. “mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p.” 2014. Web. 27 Feb 2021.

Vancouver:

Sosanya NM. mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2014. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/46489.

Council of Science Editors:

Sosanya NM. mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p. [Doctoral Dissertation]. University of Texas – Austin; 2014. Available from: http://hdl.handle.net/2152/46489

University of Texas – Austin

6. Kreeger, Lauren Josephine. Genetically identified cholecystokinin neurons of the inferior colliculus provide direct excitation and inhibition to the medial geniculate body of the gerbil.

Degree: PhD, Neuroscience, 2018, University of Texas – Austin

URL: http://hdl.handle.net/2152/68460

► Neurons in the central nucleus of the inferior colliculus (ICC) exhibit diverse morphologies, electrophysiological properties, and projection targets. Despite thorough characterization of these features, individual… (more)

▼ Neurons in the central nucleus of the inferior colliculus (ICC) exhibit diverse morphologies, electrophysiological properties, and projection targets. Despite thorough characterization of these features, individual parameters cannot define functional classes. Neurochemical markers could be the answer to connecting form and function. By combining anatomy, physiology, and neurochemical markers, the experiments presented in this dissertation genetically identify cholecystokinin (CCK) neurons in the ICC of the Mongolian gerbil. CCK neurons comprise two classes, one excitatory and one inhibitory, that can be distinguished by both endogenous neurochemical markers and electrophysiological properties. Interdependent adeno-associated viruses were used to express fluorophores and opsins in CCK neurons in the ICC. The specificity of viral expression was confirmed using multiplexed in situ hybridization. To characterize the relationship between endogenous neurochemical markers and electrophysiological properties, we targeted genetically identified CCK neurons in the ICC for in vitro whole-cell current clamp recordings. Both excitatory and inhibitory CCK neurons have an adapting firing pattern. The two groups have distinct action potential signatures, which can be an electrophysiological marker to distinguish the groups. To find synaptic connections between CCK neurons and other neurons in the intrinsic ICC circuit, recordings were made from ICC neurons while CCK inputs were activated with channelrhodopsin. Excitatory and inhibitory post-synaptic potentials from CCK neurons are small and widespread, making connections with more than half of ICC neurons. CCK neurons in the ICC exclusively target the ventral division of the medial geniculate body (MGB), suggesting a functional role in the ascending lemniscal auditory pathway. Axons are highly branched with both fine axons with small boutons and en passant swellings, and medium to large axons with large terminal boutons. To characterize CCK inputs to the MGB, neurons in the vMGB were targeted for whole-cell recordings and CCK inputs were activated with channelrhodopsin. EPSPs and IPSPs are large, with EPSPs large enough to reliably induce action potentials in the post-synaptic vMGB neuron. EPSPs have both ionotropic and metabotropic components and exhibit short-term depression. Advisors/Committee Members: Golding, Nace L. (advisor), Chandrasekaran, Bharath (committee member), Johnston, Daniel (committee member), Priebe, Nicholas (committee member), Zemelman, Boris (committee member).

Subjects/Keywords: Neuroscience; Auditory; Physiology

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APA (6^th Edition):

Kreeger, L. J. (2018). Genetically identified cholecystokinin neurons of the inferior colliculus provide direct excitation and inhibition to the medial geniculate body of the gerbil. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/68460

Chicago Manual of Style (16^th Edition):

Kreeger, Lauren Josephine. “Genetically identified cholecystokinin neurons of the inferior colliculus provide direct excitation and inhibition to the medial geniculate body of the gerbil.” 2018. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/68460.

MLA Handbook (7^th Edition):

Kreeger, Lauren Josephine. “Genetically identified cholecystokinin neurons of the inferior colliculus provide direct excitation and inhibition to the medial geniculate body of the gerbil.” 2018. Web. 27 Feb 2021.

Vancouver:

Kreeger LJ. Genetically identified cholecystokinin neurons of the inferior colliculus provide direct excitation and inhibition to the medial geniculate body of the gerbil. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2018. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/68460.

Council of Science Editors:

Kreeger LJ. Genetically identified cholecystokinin neurons of the inferior colliculus provide direct excitation and inhibition to the medial geniculate body of the gerbil. [Doctoral Dissertation]. University of Texas – Austin; 2018. Available from: http://hdl.handle.net/2152/68460

University of Texas – Austin

7. -0411-6559. Variation of ion channel expression in hippocampal CA1 neurons in temporal lobe epilepsy.

Degree: PhD, Neuroscience, 2018, University of Texas – Austin

URL: http://dx.doi.org/10.26153/tsw/2831

► The CDC estimates one percent of adults in the United States have epilepsy. Temporal Lobe Epilepsy (TLE), which affects the hippocampus and surrounding cortices, is… (more)

▼ The CDC estimates one percent of adults in the United States have epilepsy. Temporal Lobe Epilepsy (TLE), which affects the hippocampus and surrounding cortices, is the most common form of focal epilepsy. Hypersynchronous seizure activity increases the likelihood of future seizures and causes progressive brain damage. In animal models of TLE, CA1 neurons have been shown to be susceptible to selective changes in ion channel expression, called acquired channelopathies, which increase the excitability of a neuron. In addition, several recent studies in normal rodents find differences in ion channel expression along the dorsoventral axis of CA1. It is unknown if the presence of acquired channelopathies depends on the dorsoventral region of CA1. Here, we show the excitability of dorsal and ventral CA1 neurons becomes uniform in a status epilepticus (SE) model of Temporal Lobe Epilepsy. Dorsal CA1 neurons post-SE have an increased firing rate, reduced interspike interval and increased input resistance, while the properties of ventral CA1 neurons remain stable post-SE. Potential mechanisms for these changes include a dysregulation in M, GIRK or HCN channels, which all have dorsoventral expression gradients and an existing link to epilepsy. Current clamp recordings with pharmacology and immunohistochemistry demonstrate the expression of M and GIRK channels do not change across the dorsoventral axis of CA1 post-SE. The expression of HCN channels, however, is downregulated in dorsal CA1 neurons post-SE contributing to the increased excitability of these neurons. This acquired channelopathy is not present in ventral CA1 neurons post-SE. These results suggest the excitability of dorsal CA1 neurons post-SE become more like ventral CA1 neurons, which likely makes the hippocampal circuit more permissible to seizures, and contributes to the cognitive impairments associated with chronic epilepsy. Advisors/Committee Members: Johnston, Daniel, 1947- (advisor), Aldrich, Richard W (committee member), Golding, Nace L (committee member), Colgin, Laura L (committee member), Raab-Graham, Kimberly (committee member).

Subjects/Keywords: Hippocampus; CA1 pyramidal neuron; Dorsoventral axis; Septotemporal axis; Epilepsy; Kainic acid; Intrinsic properties; Dendrites; Channel; Whole cell electrophysiology; Immunohistochemistry

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APA (6^th Edition):

-0411-6559. (2018). Variation of ion channel expression in hippocampal CA1 neurons in temporal lobe epilepsy. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://dx.doi.org/10.26153/tsw/2831

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Chicago Manual of Style (16^th Edition):

-0411-6559. “Variation of ion channel expression in hippocampal CA1 neurons in temporal lobe epilepsy.” 2018. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://dx.doi.org/10.26153/tsw/2831.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7^th Edition):

-0411-6559. “Variation of ion channel expression in hippocampal CA1 neurons in temporal lobe epilepsy.” 2018. Web. 27 Feb 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-0411-6559. Variation of ion channel expression in hippocampal CA1 neurons in temporal lobe epilepsy. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2018. [cited 2021 Feb 27]. Available from: http://dx.doi.org/10.26153/tsw/2831.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

-0411-6559. Variation of ion channel expression in hippocampal CA1 neurons in temporal lobe epilepsy. [Doctoral Dissertation]. University of Texas – Austin; 2018. Available from: http://dx.doi.org/10.26153/tsw/2831

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

University of Texas – Austin

8. Chirillo, Michael August. Coordinated structural plasticity across synapses in the adult hippocampus.

Degree: PhD, Neuroscience, 2015, University of Texas – Austin

URL: http://hdl.handle.net/2152/31594

► Neural circuitry is determined primarily by trillions of synaptic junctions that link cells in the nervous system. Understanding how the structure of the synapse influences… (more)

▼ Neural circuitry is determined primarily by trillions of synaptic junctions that link cells in the nervous system. Understanding how the structure of the synapse influences its function has been a central goal of cellular neuroscience since synapses were first recognized more than a century ago. Long-term potentiation (LTP), a long lasting enhancement of synaptic efficacy, is a well-characterized cellular correlate of learning and memory that results in dramatic structural remodeling of the synapse. Research has focused heavily on the postsynaptic structural remodeling that occurs to support LTP, but concomitant presynaptic and subcellular remodeling during LTP has been left largely unexplored. To address these questions, three-dimensional reconstructions from serial section electron microscopy of presynaptic boutons, vesicle pools, and dendritic smooth endoplasmic reticulum (SER) in hippocampal area CA1 were created and quantified. The data presented in this dissertation demonstrate that coordinated structural plasticity occurs at both pre- and postsynaptic sides of adult hippocampal synapses by 2 hours during LTP induced with theta burst stimulation. Presynaptically, the number of presynaptic boutons correlated perfectly with fewer dendritic spines during LTP that were previously reported, suggesting that synaptic units act as cohesive structures. Vesicle pools were mobilized and vesicle transport packets were moved into boutons or were released in transit. Dendritic SER is a ubiquitous intracellular membranous network involved in calcium signaling and protein modification. The complexity of SER influences the movement of diffusible membrane cargo. SER was dramatically remodeled during LTP, redistributing from the shaft of the dendrite into spines and becoming highly complex near synapses that were largest during LTP. As a preliminary investigation into how normal mechanisms of structural plasticity described in this dissertation might go awry under conditions of synaptic pathology, three-dimensional reconstructions of CA1 synaptic ultrastructure in a mouse model of Fragile X, which is known to express exaggerated mGluR-dependent long-term depression (LTD), were created and quantified. Synaptic ultrastructure was similar with that of the wild-type mouse, suggesting that structural malformation in FX might be confined to development or to other brain regions. Advisors/Committee Members: Harris, Kristen M. (advisor), Bear, Mark F (committee member), Colgin, Laura L (committee member), Golding, Nace L (committee member), Raab-Graham, Kimberly F (committee member).

Subjects/Keywords: Synaptic plasticity; Electron microscopy; Cell biology; Endoplasmic reticulum; Hippocampus; Structural plasticity; Neuroscience; Long-term potentiation

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APA (6^th Edition):

Chirillo, M. A. (2015). Coordinated structural plasticity across synapses in the adult hippocampus. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/31594

Chicago Manual of Style (16^th Edition):

Chirillo, Michael August. “Coordinated structural plasticity across synapses in the adult hippocampus.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/31594.

MLA Handbook (7^th Edition):

Chirillo, Michael August. “Coordinated structural plasticity across synapses in the adult hippocampus.” 2015. Web. 27 Feb 2021.

Vancouver:

Chirillo MA. Coordinated structural plasticity across synapses in the adult hippocampus. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/31594.

Council of Science Editors:

Chirillo MA. Coordinated structural plasticity across synapses in the adult hippocampus. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/31594

9. -7451-5937. Reconstructing the connectome from an ensemble of measurements.

Degree: MSin Neuroscience, Neuroscience, 2016, University of Texas – Austin

URL: http://hdl.handle.net/2152/38169

► While connectomics paradigms have been undergoing rapid development in the experimental community, the problem of analyzing the resulting data has remained largely unaddressed. Recently, the… (more)

Subjects/Keywords: Connectome; Matrix completion

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APA (6^th Edition):

-7451-5937. (2016). Reconstructing the connectome from an ensemble of measurements. (Masters Thesis). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/38169

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Chicago Manual of Style (16^th Edition):

-7451-5937. “Reconstructing the connectome from an ensemble of measurements.” 2016. Masters Thesis, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/38169.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7^th Edition):

-7451-5937. “Reconstructing the connectome from an ensemble of measurements.” 2016. Web. 27 Feb 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-7451-5937. Reconstructing the connectome from an ensemble of measurements. [Internet] [Masters thesis]. University of Texas – Austin; 2016. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/38169.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

-7451-5937. Reconstructing the connectome from an ensemble of measurements. [Masters Thesis]. University of Texas – Austin; 2016. Available from: http://hdl.handle.net/2152/38169

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

10. Li, Na, 1980 Oct. 2-. Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus.

Degree: PhD, Neuroscience, 2010, University of Texas – Austin

URL: http://hdl.handle.net/2152/ETD-UT-2010-12-2065

► Many cells in the inferior colliculus (IC) are excited by contralateral and inhibited by ipsilateral stimulation and are thought to be important for sound localization.… (more)

▼ Many cells in the inferior colliculus (IC) are excited by contralateral and inhibited by ipsilateral stimulation and are thought to be important for sound localization. These excitatory-inhibitory (EI) cells comprise a diverse group, even though they exhibit a common binaural response property. Previous extracellular studies proposed specific excitatory and/or inhibitory events that should be evoked by each ear and thereby generate each of the EI discharge properties. The proposals were inferences based on the well established response features of neurons in lower nuclei, the projections of those nuclei, their excitatory or inhibitory neurochemistry, and the changes in response features that occurred when inhibition was blocked. Here we recorded the inputs, the postsynaptic potentials, discharges evoked by monaural and binaural signals in EI cells with in vivo whole cell recordings from the inferior colliculus (IC) of awake bats. We also computed the excitatory and inhibitory synaptic conductances from the recorded sound evoked responses. First, we showed that a minority of EI cells either inherited their binaural property from a lower binaural nucleus or the EI property was created in the IC via inhibitory projections from the ipsilateral ear, features consistent with those observed in extracellular studies. Second, we showed that in a majority of EI cells ipsilateral signals evoked subthreshold EPSPs that behaved paradoxically in that EPSP amplitudes increased with intensity, even though binaural signals with the same ipsilateral intensities generated progressively greater spike suppressions. These ipsilateral EPSPs were unexpected since they could not have been detected with extracellular recordings. These additional responses suggested that the circuitry underlying EI cells was more complex than previously suggested. We also proposed the functional significance of ipsilaterally evoked EPSPs in responding to moving sound sources or multiple sounds. Third, by computing synaptic conductances, we showed the circuitry of the EI cells was even more complicated than those suggested by PSPs, and we also evaluated how the binaural property was produced by the contralateral and ipsilateral synaptic events. Advisors/Committee Members: Pollak, G. D. (George D.), 1942- (advisor), Huk, Alex (committee member), Priebe, Nicholas (committee member), Golding, Nace (committee member), Zakon, Harold (committee member), Morrisett, Richard (committee member).

Subjects/Keywords: Patch clamp recording; Inferior colliculus; Excitatory-inhibitory; Precedence effect; Sound localization; EI cells; Ipsilateral response; Binaural property

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APA (6^th Edition):

Li, Na, 1. O. 2. (2010). Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2010-12-2065

Chicago Manual of Style (16^th Edition):

Li, Na, 1980 Oct 2-. “Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus.” 2010. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2010-12-2065.

MLA Handbook (7^th Edition):

Li, Na, 1980 Oct 2-. “Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus.” 2010. Web. 27 Feb 2021.

Vancouver:

Li, Na 1O2. Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2010-12-2065.

Council of Science Editors:

Li, Na 1O2. Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus. [Doctoral Dissertation]. University of Texas – Austin; 2010. Available from: http://hdl.handle.net/2152/ETD-UT-2010-12-2065

11. Khurana, Sukant. Roles of voltage-gated ion channels in regulating the responses of principal neurons of the medial superior olive.

Degree: PhD, Neuroscience, 2009, University of Texas – Austin

URL: http://hdl.handle.net/2152/ETD-UT-2009-12-534

► The principal neurons of the medial superior olive (MSO) are considered to be responsible for transforming the temporal information present in the binaural acoustic stimulus… (more)

Subjects/Keywords: Medial superior olive; Hyperpolarization activated cationic current; Low voltage activated potassium current; Temporal processing

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APA (6^th Edition):

Khurana, S. (2009). Roles of voltage-gated ion channels in regulating the responses of principal neurons of the medial superior olive. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2009-12-534

Chicago Manual of Style (16^th Edition):

Khurana, Sukant. “Roles of voltage-gated ion channels in regulating the responses of principal neurons of the medial superior olive.” 2009. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2009-12-534.

MLA Handbook (7^th Edition):

Khurana, Sukant. “Roles of voltage-gated ion channels in regulating the responses of principal neurons of the medial superior olive.” 2009. Web. 27 Feb 2021.

Vancouver:

Khurana S. Roles of voltage-gated ion channels in regulating the responses of principal neurons of the medial superior olive. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2009. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2009-12-534.

Council of Science Editors:

Khurana S. Roles of voltage-gated ion channels in regulating the responses of principal neurons of the medial superior olive. [Doctoral Dissertation]. University of Texas – Austin; 2009. Available from: http://hdl.handle.net/2152/ETD-UT-2009-12-534

12. Ko, Kwang Woo. Control and modulation of action potential initiation in principal neurons of the medial superior olive.

Degree: PhD, Cell and Molecular Biology, 2015, University of Texas – Austin

URL: http://hdl.handle.net/2152/46769

► The axon initial segment (AIS) serves as the site of action potential initiation in most neurons, but the technical difficulty in isolating the effects of… (more)

Subjects/Keywords: Axon Initial Segment (AIS); Action potential (AP); Medial Superior Olive (MSO); HCN channels; Serotonin; Threshold; Photoswitches; AAQ; DENAQ

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ko, K. W. (2015). Control and modulation of action potential initiation in principal neurons of the medial superior olive. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/46769

Chicago Manual of Style (16^th Edition):

Ko, Kwang Woo. “Control and modulation of action potential initiation in principal neurons of the medial superior olive.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/46769.

MLA Handbook (7^th Edition):

Ko, Kwang Woo. “Control and modulation of action potential initiation in principal neurons of the medial superior olive.” 2015. Web. 27 Feb 2021.

Vancouver:

Ko KW. Control and modulation of action potential initiation in principal neurons of the medial superior olive. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/46769.

Council of Science Editors:

Ko KW. Control and modulation of action potential initiation in principal neurons of the medial superior olive. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/46769

University of Texas – Austin

13. George, Andrew Anthony. Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity.

Degree: PhD, Neuroscience, 2009, University of Texas – Austin

URL: http://hdl.handle.net/2152/ETD-UT-2009-12-407

► Although the processes used for temporarily storing and manipulating neural information have been extensively studied at the synaptic level far less attention has been given… (more)

▼ Although the processes used for temporarily storing and manipulating neural information have been extensively studied at the synaptic level far less attention has been given to the underlying cellular and molecular mechanisms that contribute to change in the intrinsic excitability of neurons. More importantly, how do these mechanisms of plasticity integrate with ongoing mechanisms of regulation of neural intrinsic excitability and, in turn, homeostasis of entire neural circuits? In this dissertation I describe the underlying mechanisms that contribute to persistent neural activity and, more globally, sensorimotor adaptation using weakly electric fish as my model system. Weakly electric fish have evolved a behavior adaptation known as the jamming avoidance response (JAR), and it is this adaptation that allows the organism to elevate its own electrical discharge in response to intraspecific interactions and subsequent distortions of the animal’s electric field. The elevation operates over a wide range and in vivo can last tens of hours upon cessation of a jamming stimulus. I demonstrate that the underlying mechanisms of the adaptation are mediated by calcium-dependent signaling in the pacemaker nucleus and that calcium-mediated phosphorylation plays an important role in the regulation of the long-term frequency elevation (LTFE). I demonstrate using an in vitro brain slice preparation from the weakly electric fish, Apteronotus leptorhynchus that the engram of memory formation depends on the cooperativity of calcium-dependent protein kinases and protein phosphatases. In addition, I show that the memory formation (in the form of LTFE) does not depend on the continued flux of calcium, but rather the phosphorylation events downstream of NMDA receptor activation. Moreover, I describe the differences in the expression of protein phosphatases and protein kinases as they relate to species-specific differences in sensorimotor adaptation. It is important to note that this is the first time that the cooperativity between different isoforms of protein kinase C (PKC) have been shown to play a role in graded long-term change in neuronal activity and, in turn, providing the neural basis of species-specific behavior. The neural adaptation of the electromotor system in weakly electric fish provides an excellent model system to study the underlying cellular and molecular events of vertebrate memory formation. Advisors/Committee Members: Zakon, H. H. (advisor), Aldrich, Richard W. (committee member), Atkinson, Nigel S. (committee member), Mihic, S. John (committee member), Golding, Nace L. (committee member), Dalby, Kevin N. (committee member).

Subjects/Keywords: Electric Fish; Neuronal Intrinsic Excitability; Calcium; Homeostasis; Neuronal Plasticity; PKC; Calcineurin

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APA (6^th Edition):

George, A. A. (2009). Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2009-12-407

Chicago Manual of Style (16^th Edition):

George, Andrew Anthony. “Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity.” 2009. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2009-12-407.

MLA Handbook (7^th Edition):

George, Andrew Anthony. “Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity.” 2009. Web. 27 Feb 2021.

Vancouver:

George AA. Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2009. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2009-12-407.

Council of Science Editors:

George AA. Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity. [Doctoral Dissertation]. University of Texas – Austin; 2009. Available from: http://hdl.handle.net/2152/ETD-UT-2009-12-407

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