Postdoctoral Fellows

George “Gef” Farmer, Ph.D.

gef.farmer@unthsc.edu

farmerI am a neuroscientist in the Institute for Cardiovascular and Metabolic Diseases where I investigate neural influences on blood pressure and hydromineral balance. I have over 12 years of experience using both in vivo and in vitro neurophysiology techniques.

I earned my Ph.D. in Cognition and Neuroscience in 2012 from the University of Texas at Dallas where my research focused on learning dependent plasticity in the hippocampus and amygdala following an emotionally arousing task. It was here that I described the time course for changes in post burst afterhyperpolarizations (AHPs) in the hippocampus and amygdala following the acquisition of an emotionally arousing task as well as demonstrating that plasticity in hippocampal AHPs following such a task is dependent on an intact amygdala. My first post doc appointment (2012-2014) was a joint appointment with the University of South Florida and the James A Haley VA Hospital where my research focused on stress and memory in an animal model of post-traumatic stress disorder. Additionally, I was involved in developing an in vitro model of the stress responses and its time dependent effects on hippocampal plasticity. My current research interests involve the role of Angiotensin and chloride transport in intermittent hypoxia-induced hypertension and the role of BDNF in the homeostatic regulation of supraoptic neurons.

Selected Publications:

Farmer, G. E., Park, C. R., Bullard, L. A., Diamond D. M. (2014). Evolutionary, Historical and Mechanistic Perspectives on How Stress Affects Memory and Hippocampal Synaptic Plasticity. in M. Popoli et al. (eds.), Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders, Springer Science+Business Media, New York, 2014

Farmer, G. E. and L. T. Thompson (2012). Learning-dependent plasticity of hippocampal CA1 pyramidal neuron postburst afterhyperpolarizations and increased excitability after inhibitory avoidance learning depend upon basolateral amygdala inputs.Hippocampus 22(8): 1703-1719.

Garcia-Oscos, F., Salgado, H., Hall, S., Thomas, F., Farmer, G. E., Bermeo, J., Galindo, L. C., Ramirez, R. D., D’Mello, S., Rose-John, S., Atzori, M. (2012). The Stress-Induced Cytokine Interleukin-6 Decreases the Inhibition/Excitation Ratio in the Rat Temporal Cortex via Trans-Signaling. Biol Psychiatry 71(7): 574-582.

 

Lei Wang, Ph.D.

lei.wang@unthsc.edu

photo-lei-wangI am a research associate in the Institute for Cardiovascular and Metabolic Disease.  My current research focuses on the neural control of cardiovascular function.

I received my Ph.D. degree in pharmacodynamics at the University of Florida in August 2016.  During my PhD training, I studied how the brain renin-angiotensin system regulate behavioral, endocrine, and cardiovascular responses to psychological stress.  My research has revealed that deletion of angiotensin type 1 a receptor (AT1a) from the PVN attenuated anxiety-like behavior and diminished sympathetic excitation and pressor response to restraint stress (Wang L et al Physiological Genomics 2016).  These altered behavioral and sympatho-cardiovacular responses may be the results of attenuated CRH transcription in the PVN caused by loss of AT1a signaling pathway.  Consistent with these results, I also found that optogenetic activation of AT1a neurons within the PVN significantly increased the blood pressure.  Another study during my Ph.D. focused on the stress-relieving effect of brain angiotensin converting enzyme 2 (ACE2), the enzyme that convers angiotensin-II (Ang-II) to angiotensin-(1-7), which can activate mas receptor (MasR).  This study demonstrated that overexpression of ACE2 in the brain decreased anxiety-like behavior by promoting MasR-mediated GABAergic inhibitory neurotransmission within the basolateral amygdala (Wang L et al Neuropharmacology 2016).  The third study of my Ph.D. dissertation showed that selective overexpression of ACE2 in CRH-producing neurons inhibited the activation of the hypothalamic-adrenal-pituitary (HPA) axis and reduced anxiety-like behavior.  Combined, these three studies suggest that brain renin-angiotensin system is heavily involved in the regulation of behavioral, endocrine, and sympatho-cardiovacular responses to stress.

Selected Publications

Wang L, Hiller H, Smith JA, de Kloet AD, Krause EG. Angiotensin type 1a receptors in the paraventricular nucleus of the hypothalamus control cardiovascular reactivity and anxiety-like behavior in male mice. Physiological Genomics. 2016.

Wang L, de kloet AD, Pati D, Hiller H, Smith JA, Pioquinto DJ, Ludin JA, Oh SP, Katovich MJ, Raizada MK, Frazier CJ, Krause EG. Angiotensin converting enzyme 2 decreases anxiety-like behavior by acting on mas receptor in the brain. Neuropharmacology. 2016.

Smith JA, Wang L, Hiller H, Taylor CT, de Kloet AD, Krause EG. Acute hypernatremia promotes anxiolysis and attenuates stress-induced activation of the hypothalamic-pituitary-adrenal axis in male mice. Physiol Behav. 2014.

de Kloet AD, Pati D, Wang L, Hiller H, Sumners C, Frazier CJ, Seeley RJ, Herman JP, Woods SC, Krause EG. Angiotensin type 1a receptors in the paraventricular nucleus of the hypothalamus protect against diet-induced obesity. J Neurosci. 2013.

 

 

This page was last modified on March 20, 2017