+publisher:"Vanderbilt University" +contributor:("Martin J. Gallagher")

Vanderbilt University

1. Deel, Megan Elizabeth. Alterations in GABAA receptor expression and physiology in a mouse model of idiopathic generalized epilepsy.

Degree: MS, Neuroscience, 2012, Vanderbilt University

URL: http://hdl.handle.net/1803/14874

► The proper function of the nervous system is dependent upon a delicate balance between excitatory and inhibitory activity in the brain. GABAA receptors are extremely… (more)

Subjects/Keywords: childhood absence epilepsy; seizure; epilepsy; GABA; compensation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Deel, M. E. (2012). Alterations in GABAA receptor expression and physiology in a mouse model of idiopathic generalized epilepsy. (Thesis). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14874

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Deel, Megan Elizabeth. “Alterations in GABAA receptor expression and physiology in a mouse model of idiopathic generalized epilepsy.” 2012. Thesis, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/14874.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Deel, Megan Elizabeth. “Alterations in GABAA receptor expression and physiology in a mouse model of idiopathic generalized epilepsy.” 2012. Web. 16 Jan 2021.

Vancouver:

Deel ME. Alterations in GABAA receptor expression and physiology in a mouse model of idiopathic generalized epilepsy. [Internet] [Thesis]. Vanderbilt University; 2012. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/14874.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Deel ME. Alterations in GABAA receptor expression and physiology in a mouse model of idiopathic generalized epilepsy. [Thesis]. Vanderbilt University; 2012. Available from: http://hdl.handle.net/1803/14874

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University

2. Shen, Dingding. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.

Degree: PhD, Neuroscience, 2017, Vanderbilt University

URL: http://hdl.handle.net/1803/14271

► Epileptic encephalopathies (EEs) are a devastating group of severe childhood onset epilepsies with medication resistant seizures and poor developmental outcomes. Many EEs have a genetic… (more)

Subjects/Keywords: Epileptic encephalopathies; GABAA receptor

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Shen, D. (2017). Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14271

Chicago Manual of Style (16^th Edition):

Shen, Dingding. “Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.” 2017. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/14271.

MLA Handbook (7^th Edition):

Shen, Dingding. “Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.” 2017. Web. 16 Jan 2021.

Vancouver:

Shen D. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. [Internet] [Doctoral dissertation]. Vanderbilt University; 2017. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/14271.

Council of Science Editors:

Shen D. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. [Doctoral Dissertation]. Vanderbilt University; 2017. Available from: http://hdl.handle.net/1803/14271

Vanderbilt University

3. Arain, Fazal Manzoor. Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

URL: http://hdl.handle.net/1803/10463

► Epilepsy is a disease characterized by two or more unprovoked seizures. Two mutations, S326fs328X and A322D, in the α1 subunit of GABAA receptor (Gabra1), are… (more)

Subjects/Keywords: GABA; Epilepsy; Development

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Arain, F. M. (2014). Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10463

Chicago Manual of Style (16^th Edition):

Arain, Fazal Manzoor. “Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/10463.

MLA Handbook (7^th Edition):

Arain, Fazal Manzoor. “Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice.” 2014. Web. 16 Jan 2021.

Vancouver:

Arain FM. Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/10463.

Council of Science Editors:

Arain FM. Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/10463

Vanderbilt University

4. Gamble-George, Joyonna Carrie. Endocannabinoid Augmentation Through Substrate-Selective COX-2 Inhibition: Behavioral and Synaptic Effects In An Animal Model of Stress-Induced Anxiety.

Degree: PhD, Neuroscience, 2016, Vanderbilt University

URL: http://hdl.handle.net/1803/13270

► Cannabinoid receptors have been examined as potential targets to alleviate the negative consequences of anxiety, trauma-related, and stress-related disorders. However, in preclinical animal studies, synthetic… (more)

▼ Cannabinoid receptors have been examined as potential targets to alleviate the negative consequences of anxiety, trauma-related, and stress-related disorders. However, in preclinical animal studies, synthetic cannabinoids can produce adverse motoric and cognitive effects. Thus, pharmacological strategies that augment endocannabinoid levels in the brain, with the aim of enhancing signaling through cannabinoid receptors, are being investigated for their ability to modulate anxiety and stress responses. Previously, we have demonstrated that either genetic removal of prostaglandin-endoperoxide synthase 2 gene, which codes for the cyclooxygenase-2 (COX-2) enzyme that degrades the endocannabinoids, anandamide and 2-arachidonylglycerol, or pharmacologically inhibiting COX-2 activity with a substrate-selective COX-2 inhibitor (SSCI), LM-4131, can increase brain anandamide levels. These elevations in endocannabinoid levels in the rodent brain resulted in enhanced endocannabinoid signaling through the cannabinoid type 1 receptor and, subsequently, reduced anxiety-like behaviors in mice under basal conditions. Using the novelty-induced feeding suppression assay, elevated plus maze, and in vivo electrophysiology, we tested the hypothesis that endocannabinoid augmentation via SSCIs may have the potential to counteract stress-induced anxiety-like behaviors. We have found that the SSCIs, LM-4131 and lumiracoxib, and the selective COX-2 inhibitor, celecoxib, can reduce anxiety-like behaviors in mice subjected to footshock stress. In contrast, these inhibitors had little effect in non-stressed mice. The anxiolytic action of the SSCI, LM-4131, was mediated through the cannabinoid type 1 receptor under non-stressed (control) conditions, but mediated through the small conductance calcium-activated potassium (SK) channels when mice were subjected to footshock stress. Also, we have found that the anxiolytic effects of SSCIs in stressed mice may be due to a decrease in excitatory cell firing in the amygdala. Advisors/Committee Members: Andrew Holmes (committee member), Sachin Patel (committee member), Martin J. Gallagher (committee member), Christine Konradi (Committee Chair).

Subjects/Keywords: dopamine; depression; anandamide; stress; cannabinoid receptor; anxiety; PTSD; COX-2; endocannabinoid; SK channel

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Gamble-George, J. C. (2016). Endocannabinoid Augmentation Through Substrate-Selective COX-2 Inhibition: Behavioral and Synaptic Effects In An Animal Model of Stress-Induced Anxiety. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13270

Chicago Manual of Style (16^th Edition):

Gamble-George, Joyonna Carrie. “Endocannabinoid Augmentation Through Substrate-Selective COX-2 Inhibition: Behavioral and Synaptic Effects In An Animal Model of Stress-Induced Anxiety.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/13270.

MLA Handbook (7^th Edition):

Gamble-George, Joyonna Carrie. “Endocannabinoid Augmentation Through Substrate-Selective COX-2 Inhibition: Behavioral and Synaptic Effects In An Animal Model of Stress-Induced Anxiety.” 2016. Web. 16 Jan 2021.

Vancouver:

Gamble-George JC. Endocannabinoid Augmentation Through Substrate-Selective COX-2 Inhibition: Behavioral and Synaptic Effects In An Animal Model of Stress-Induced Anxiety. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/13270.

Council of Science Editors:

Gamble-George JC. Endocannabinoid Augmentation Through Substrate-Selective COX-2 Inhibition: Behavioral and Synaptic Effects In An Animal Model of Stress-Induced Anxiety. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/13270

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations