George “Gef” Farmer, Ph.D.
I 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.
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.
Alexander J. (AJ) Rosenberg, Ph.D.
I am a postdoctoral fellow in the Department of Physiology and Anatomy. I am working under the supervision of Dr. Caroline Rickards in the Cerebral and Cardiovascular Physiology Laboratory. My research interests focus on minimizing cardiovascular health disparities in our aging population, with a particular interest in cerebrovascular physiology and cognitive health.
I received my M.S. and Ph.D. in Kinesiology, Nutrition and Rehabilitation Science at the University of Illinois at Chicago (UIC). I am also a certified strength and conditioning coach by the National Association of Strength and Conditioning. During my Ph.D., I was involved in a wide range of applied physiology projects where we sought to understand how the cardiovascular system responds to different physical and physiological stressors, and ultimately how these responses impact human health and function. I gained extensive experience in working with special populations, including individuals with Down Syndrome, Multiple Sclerosis, Parkinson’s Disease, heart failure, chronic kidney disease, and aged individuals (both healthy and diseased). My dissertation work focused on the association between arterial stiffness, systemic flow/pressure pulsatility, and cerebral hemodynamics with aging. The association between arterial stiffness and cerebral flow pulsatility may, in part, explain the relationship between elevated pressure fluctuations and end-organ disease in older adults. My dissertation project established a foundation for my current work as a postdoctoral fellow in Dr. Rickards’ laboratory at UNTHSC. In my primary postdoctoral study, I will be establishing a functional bioassay for early risk assessment of cerebrovascular dysfunction using a “reactive hyperemic” stimulus. Furthermore, I will be exploring cerebral vascular dynamics between males and females (both young and older adults) to determine the implication of sex differences in the detection, treatment and prevention of cerebrovascular disease and the connection to cognitive decline observed with aging.
Rosenberg, AJ., Lane, AD., Wee, SO., White, DW., Hilgenkamp, T., Fernhall, B., Baynard, T. Healthy Aging and Carotid Performance: Strain Measures and Beta-Stiffness Index. Hypertension Research. In-press: Accepted 2/18/2018.
Schroeder, EC., Rosenberg, AJ., Hilgenkamp, TI., White, DW., Baynard, T., Fernhall, B. Effect of Upper Body Position on Arterial Stiffness: Influence of Hydrostatic Pressure and Autonomic Function. J Hypertens. 2017. PMID: 28704262
Rosenberg, A.J., Wee, S.O., Schroeder, E., Bunsawat, K., Grigoriadis, G., Fernhall, B., Baynard, T. Effect of acute isokinetic resistance exercise on systemic arterial hemodynamics and cerebral blood flow dynamics: Is there a mismatch? [abstract]. Artery Research, Vol. 16, p101–102, 2016.
Kappus, RM., Bunsawat, K., Rosenberg, AJ., Fernhall, B. No Evidence of Racial Differences in Endothelial Function and Exercise Blood Flow in Young, Healthy Males Following Acute Antioxidant Supplementation. Int J Sports Med. 2017. PMID: 28219102.
Lei Wang, Ph.D.
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.
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 May 24, 2018