Indiana University Bloomington

Dr. Cara Wellman


Associate Professor of Psychology

 

 

 

 

Contact Information

Office: MSB-II 202
Office Phone: 812-855-4922
Lab: MSB-II 246
Lab Phone:812-855-1769
E-mail:
E-mail Cara Wellman

Web site: The Wellman Lab

 

Educational Background

  • 1986 B.A.- Ohio Wesleyan University
    Major: Psychology
    Minor: Chemistry
  • 1993 Ph.D.- Indiana University
    Double Major: Program in Neuroscience, Clinical Psychology (APA approved)

Areas of Study

  • Neural Science
  • Clinical Science

Research Topics

  • Stress effects on dendritic plasticity in prefrontal cortex
  • Stress effects on neurochemistry and function of prefrontal cortex
  • Age-related changes in neurochemistry and morphology of frontal cortex and associated behaviors
  • Mechanisms of age-related changes in cortical plasticity and behavior

Research Summary:

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 aging, pathology, and stress.

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 differential responses to injury or lesion suggest that plasticity is altered in the aged, which has important consequences for both 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.

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. 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 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 beginning to more fully characterize these effects and to assess their functional significance.

Representative Publications

Garrett, J.E., & Wellman, C.L. (2009). Chronic stress effects on dendritic morphology in medial prefrontal cortex: sex differences and estrogen dependence. Neuroscience, 162, 195Ð207.

Holmes, A., & Wellman, C.L. (2009). Stress-induced prefrontal reorganization and executive dysfunction in rodents. Neuroscience and Biobehavioral Reviews, 33, 773Ð783.

Wilber, A.A., & Wellman, C.L. (2009) Neonatal maternal separation-induced changes in glucocorticoid receptor expression in posterior interpositus interneurons but not projection neurons predict deficits in adult eyeblink conditioning. Neuroscience Letters, 460, 214-218.

Ball, K.T., Wellman, C.L., & Rebec, G.V. (2009). Sensitizing regimens of (±)3,4-methylenedioxymethamphetamine (ecstasy) elicit enduring and differential structural alterations in the brain motive circuit of the rat. Neuroscience, 160, 264Ð274.

Wilber, A.A., Southwood, C.J., & Wellman, C.L. (2009). Brief neonatal maternal separation alters extinction of conditioned fear and corticolimbic glucocorticoid and NMDA receptor expression in adult rats. Developmental Neurobiology, 69, 73-87.

Wellman, C.L., Izquierdo, A., Garrett, J.E., Martin, K.P., Carroll, J., Millstein, R., Murphy, D.L., Lesch, K.-P., & Holmes, A. (2007). Genetic inactivation of the serotonin transporter causes impairment of stress-coping and extinction-recall and medial prefrontal cortex abnormalities. Journal of Neuroscience, 27, 684-691.

Wilber, A.A., Southwood, C.J., Steinmetz, J.E., & Wellman, C.L. (2007). Neonatal maternal separation alters adult eyeblink conditioning and glucocorticoid receptor expression in the interpositus nucleus of the cerebellum. Developmental Neurobiology, 67, 1751-1764.

Miracle, A.D., Brace, M.F., Huyck, K.D., Singler, S.A., & 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., & 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, 5733Ð5738.

Kim, I., Wilson, R.E., & 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., & Wellman, C.L. (2005). Short-term, mild stress alters dendritic morphology in rat medial prefrontal cortex. Cerebral Cortex, 15, 1714-1722.

Works, S.J., Wilson, R.E., & 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., & Wellman, C.L. (2004). Chronic stress alters dendritic morphology in rat medial prefrontal cortex. Journal of Neurobiology, 60, 236-248.

Harmon, K.M., & 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.

Wellman, C.L. (2001). Dendritic reorganization in pyramidal neurons in medial prefrontal cortex after chronic corticosterone administration. Journal of Neurobiology, 49, 245-253.

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