The role of psychobiology in understanding abnormal behaviors has become increasingly important over the past decade. My research focuses on the neurobiology of stress, a critical variable in the development and expression of many psychological disorders. By using simple animal models that permit the manipulation and control of stress and other relevant variables, I hope to understand the neural causes and consequences of abnormal behavior. I am using such models to characterize alterations in neural plasticity resulting from stress.
Stress has been hypothesized to play a major role in several disorders, and the neurotransmitter systems and brain structures that are altered by stress have been implicated in a variety of psychological disorders. Thus, assessment of the effects of stress on these neurotransmitter systems and structures may have important implications for the causes and prevention of these disorders. Prefrontal cortex is a target for hormones involved in the stress response and has been implicated in disorders such as schizophrenia and depression that are exacerbated or precipitated by stress. Thus, understanding the effects of stress on prefrontal cortex is critical for understanding the influence of stress on psychopathology.
My lab is examining the effects of chronic stress and stress hormones on behaviors mediated by prefrontal cortex, as well as the changes in neural pharmacology, physiology, and morphology that underlie these effects. We have demonstrated that both chronic stress and exposure to the stress hormone corticosterone reorganize dendrites of neurons in prefrontal cortex. We are now more fully characterizing these effects, assessing their functional significance, and elucidating mechanisms underlying them.
In collaboration with colleagues at the National Institute on Alcohol Abuse and Alcoholism, the National Institute for Mental Health, and the University of Southern California School of Pharmacology, we are also using transgenic mice to investigate the roles of alterations in the serotonergic and glutamatergic systems in increased risk for neuropsychiatric disorders as well as contributions of these neurotransmitter systems in stress-induced dendritic changes. These studies will provide data relevant for understanding the neurobiological mechanisms underlying both altered corticolimbic function and risk for mood disorders in the presence of environmental stressors.