Cara L. Wellman
B.A., Ohio Wesleyan University, 1986
Ph.D., Indiana University at Bloomington, 1993
Postdoctoral Fellow, Amgen,Inc.,
Thousand Oaks, CA, 1993-95
Email address: wellmanc(at)indiana.edu
(see also www.iub.edu/~caralab)
The role of psychobiology in understanding abnormal behaviors has become increasingly important over the past decade. My research focuses on the neurobiology of aging and stress, two critical variables in the development and expression of behavioral pathology. By using simple animal models that permit the manipulation and control of these variables, I hope to understand the neural causes and consequences of abnormal behavior. I am using two such models to characterize alterations in neural plasticity resulting from stress, aging, and pathology.
Stress, Prefrontal Cortex, and Psychopathology
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. This 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 and morphology that underlie these effects. We have demonstrated that both chronic stress and exposure to the stress hormone corticosterone reorganize dendrite of neurons in prefrontal cortex. We are now beginning to more fully characterize these effects, assess their functional significance, and elucidate mechanisms underlying them..
Age-Related changes in Plasticity of Frontal Cortex
Neural plasticity underlies a variety of processes, including development, learning and memory, and recovery from injury. Plasticity persists throughout the lifespan, but evidence suggests that this plasticity may be reduced in aging. For instance, the behavioral effects of moderate head injuries are more pronounced in aged patients. Similarly, aging prolongs the behavioral consequences of traumatic brain injury in rats, and aged rats are differentially vulnerable to the effects of loss of input to the hippocampus. These diffenential responses to injury or lesion suggest that plasticity is altered in the aged, which has important consequences for successful aging and treatment of neural disorders in the elderly . I have used lesions of the nucleus basalis in rats to assess neurochemical and morphological plasticity in frontal cortex. This work has demonstrated altered plasticity in frontal cortex of aging rats-lesions produce greater dendritic atrophy and differential changes in the glutamatergic system in aged rats. A current focus of the lab is to assess the mechanisms that underlie age-related changes in plasticity of frontal cortex and to determine how these changes influence behaviors mediated by frontal cortex. In answering these questions, I hope to contribute to our understanding of the basic mechanisms of neural changes in aging, as well as the causes and treatment of age-related dementias.
Wellman, C.L. (2001). Dendritic reorganization in pyramidal neurons in medial prefrontal cortex after chronic corticosterone administration. Journal of Neurobiology, 49: 245-253.
Seib, L.M. and Wellman, C.L. (2003). Daily injections alter dendritic spines in rat medial prefrontal cortex. Neuroscience Letters, 337: 29-32.
Harmon, K.M. and Wellman, C.L. (2003). Differential effects of cholinergic lesions on dendritic spines in frontal cortex of young adult and aging rats. Brain Research, 992: 60-68.
Works, S.J., Wilson, R.E., and Wellman, C.L. (2004). Age-dependent effect of cholinergic lesion on dendritic morphology in rat frontal cortex. Neurobiology of Aging, 25: 963-974.
Cook, S.C. and Wellman, C.L. (2004). Chronic stress alters dendritic morphology in rat medial prefrontal cortex. Journal of Neurobiology, 60: 236-248.
Kim, I., Wilson, R.E., and Wellman, C.L. (2005). Aging and cholinergic deafferentation alter GluR1 expression in rat frontal cortex. Neurobiology of Aging, 26: 1073-1081.
Brown, S.M., Henning, S.L., and Wellman, C.L. (2005). Short-term, mild stress alters dendritic morphology in rat medial prefrontal cortex. Cerebral Cortex, 15: 1714-1722.
Miracle, A.D., Brace, M.F., Huyck, K.D., Singler, S.A., and Wellman, C.L. (2006). Chronic stress impairs recall of extinction of conditioned fear. Neurobiology of Learning and Memory, 85: 213-218.
Garrett, J.E., Kim, I., Wilson, R.E., and Wellman, C.L. (2006). Effect of N-methyl-D-aspartate receptor blockade on plasticity of frontal cortex after cholinergic deafferentation in rat. Neuroscience, 140: 57-66.
Izquierdo, A., Wellman, C.L., & Holmes, A. (2006). Rapid dendritic retraction in medial prefrontal neurons and impaired fear extinction following exposure to uncontrollable stress. Journal of Neuroscience, 26: 5733-5738.