N. Bradley Keele, Ph.D.
Interim Department Chair and Associate Professor of Psychology and Neuroscience
Psychology & Neuroscience
Education
Ph.D., Neuroscience, The University of Texas Medical Branch, Galveston, 1997
B.S., Psychology, Baylor University, 1990
Biography
Dr. Keele joined the Baylor faculty in 1998 as an assistant professor of psychology and neuroscience. Prior to coming to Baylor, he was a post-doctoral fellow at the National Institutes of Health in Bethesda, MD. He earned his B.S. degree in psychology from Baylor University before obtaining his Ph.D. in neuroscience from the University of Texas Medical Branch in Galveston. In his spare time, Dr. Keele enjoys travelling, dining out, and coaching youth soccer. He is an avid fan of the Dallas Cowboys, as well as Baylor football, baseball, softball and basketball.
Academic Interests and Research
Interests: The functional role of neuronal excitability in the limbic system.
My lab is primarily focused on the neurobiology of complex emotional behaviors such as fear and anxiety disorders and depression. We examine the contribution of epilepsy-like neuronal hyperexcitability in emotional behavior and psychopathology. This work is currently funded by the National Institute of Mental Health (NIMH).
We use animal models to study the functional changes of single nerve cells in the amygdala, a part of the brain important for controlling fear and aggression. Besides its role in emotion, the amygdala is also often the locus of abnormal electrical discharges that underlie epilepsy. We hypothesize that epilepsy-like mechanisms of cellular excitability in the amygdala contribute to the function and dysfunction of this important limbic nucleus. Presently we are engaged in dissecting the cellular and molecular changes in the amygdala that contribute to disturbed emotional behaviors. Our recent findings have shown that deficiencies in the neurotransmitter serotonin, which is important in controlling mood and anxiety, have several effects. First, low amygdala serotonin causes exaggerated fear learning in a clinically-relevant model of anxiety disorders. Also, low serotonin leads to heightened neuronal activity in the amygdala (increased action potential firing). The molecular mechanisms involve up-regulation of the AMPA subtype of glutamate receptor. We are also investigating the role of serotonin on a hyperpolarization-activated current recorded from single amygdala neurons that is important in controlling excitability. By understanding the cellular and molecular mechanisms that control behavior, these studies can provide important new information on the biological basis of complex behaviors and psychiatric disease.
Selected Publications:
Hughes, C. R. & Keele, N. B. (2006). Phenytoin normalizes exaggerated fear behavior in p-chlorophenylalanine (PCPA)-treated rats. Epilepsy & Behavior, 9, 557-563.
Keele, N. B. (2005). The role of serotonin in impulsive and aggressive behaviors associated with epilepsy-like neuronal hyperexcitability in the amygdala. Epilepsy & Behavior, 7, 325-335.
Keele, N. B. & Randall, D. R. (2003). Altered modulation of excitatory neurotransmission in the amygdala by serotonin in an animal model of impulsive aggression. Annals of the New York Academy of Sciences, 985, 528-532.
Keele, N. B. (2001). Phenytoin inhibits isolation-induced aggression specifically in rats with low serotonin. NeuroReport, 12, 1107-12.
Keele, N. B., Arvanov, V. L., & Shinnick-Gallagher, P. (1997). Quisqualate-preferring metabotropic glutamate receptor activates Na+-Ca2+ exchange in rat basolateral amygdala neurones. Journal of Physiology (London), 499, 87-104.
Complete list of publications at Google Scholar.
Courses taught at Baylor
- NSC 1306 - Introduction to Neuroscience
- PSY/NSC 3319 - Clinical Neuroscience
- PSY/NSC 3370 - Affective Neuroscience
- PSY/NSC 4330 - Behavioral Neuroscience
- NSC 5360 - Neurophysiology