Gwendolyn G. Calhoon

Gwendolyn G. Calhoon

Visiting Assistant Professor of Neuroscience

Associations

Neuroscience

Hathorn Hall, Room 105

207-786-6091gcalhoon@bates.edu

About

Education

  • BA, Psychology, St. Mary’s College of Maryland (2006)
  • PhD, Neuroscience, University of Maryland, Baltimore (2013)
  • Postdoctoral Fellowship, Oak Ridge Institute for Science and Education,  National Institute of Diabetes and Digestive and Kidney Diseases (2014)
  • Certification, Kaufman Teaching Certificate Program, Massachusetts Institute of Technology (2016)
  • Postdoctoral Fellow, Picower Institute for Learning and Memory, Massachusetts Institute of Technology (2018)

Courses Taught

  • NSPY 160 Introduction to Neuroscience
  • NSPY 250 Biological Basis of Motivation and Emotion
  • NSPY 362 Psychopharmacology
  • NSPY 363 Physiological Psychology

Research Interests

More than a third of American adults are obese, and an additional third are overweight. This added poundage has led to over $100 billion in direct and indirect health care costs, which by some estimates eclipses the cost of smoking. Distributed neural networks control our intake of calorically dense foods. Among the nodes driving feeding, the nucleus accumbens (NAc) is known to detect the hedonic value of rewards and to invigorate motivated reward seeking behavior. Alterations to the NAc are implicated in numerous psychiatric illnesses, including substance use disorders, impulse control disorders, and mood disorders, many of which count changes in appetite among their symptoms. This relationship implies that signaling in NAc circuits is impacted in the non-homeostatic feeding that leads to obesity. While the impacts of obesity and high fat diet upon the mesolimbic dopamine system are well studied, comparatively little is known about changes to glutamatergic signaling in the NAc. In my research program, I use optogenetic, chemogenetic, behavioral, and electrophysiological strategies in rodents to interrogate the role of NAc circuits in diet-induced obesity, addressing questions such as:

  • What neuroplastic changes are caused by an obesogenic diet in the NAc?
  • How long do diet-induced changes in the NAc persist after return to a normal diet and normal weight?
  • Are NAc circuit changes sufficient to drive long-term changes in body weight or feeding behavior?
  • Can we intervene in compulsive feeding behavior by manipulating NAc signaling?

Selected Publications

  1. Calhoon, G. G., Sutton, A. K., Chang, C.-J., Libster, A. M., Glober, G. F., Leveque, C. L., Murphy, G. D., Namburi, P., Leppla, C. A., Siciliano, C. A., Wildes, C. P., Kimchi, E. Y., Beyeler, A., & Tye, K. M. (2018). Acute food deprivation rapidly modifies valence-coding microcircuits in the amygdala. bioRxiv, doi: https://doi.org/10.1101/285189.
  2. Chatterjee, S., Sullivan, H. A., MacLennan, B. J., Xu, R., Hou, Y., Lavin, T. K., Lea, N. E., Michalski, J. E., Babcock, K. R., Dietrich, S., Matthews, G. A., Beyeler, A., Calhoon, G. G., Glober, G., Whitesell, J. D., Yao, S., Cetin A., Harris, J. A., Zeng, H., Tye, K. M., Reid, R. C., & Wickersham, I. R. (2018). Nontoxic, double-deletion-mutant rabies viral vectors for retrograde targeting of projection neurons. Nature Neuroscience, 21 (4): 638-646.
  3. Beyeler, A., Namburi, P., Glober, G. F., Simonnet, C., Calhoon, G. G., Conyers, G. F., Luck, R., Wildes, C. P., & Tye, K. M. (2016). Divergent routing of positive and negative information from the amygdala during memory retrieval. Neuron, 90 (2): 348-361.
  4. Namburi, P., Beyeler, A., Yorozu, S., Calhoon, G. G., Halbert, S. A., Wichmann, R., Holden, S. S., Mertens, K. L., Anahtar, M., Felix-Ortiz, A. C., Wickersham, I. R., Gray, J. M., & Tye, K. M. (2015). A circuit mechanism for differentiating positive and negative associations. Nature, 520: 675-678.
  5. Cabungcal, J. H., Counotte, D. S., Lewis, E. M., Tejeda, H. A., Piantadosi, P., Pollock, C., Calhoon, G. G., Sullivan, E. M., Presgraves, E., Kil, J., Hong, L. E., Cuenod, M., Do, K. Q., & O’Donnell, P. (2014). Juvenile antioxidant treatment prevents adult deficits in a developmental model of schizophrenia. Neuron, 85 (5): 1073-84.
  6. Calhoon, G. G. & O’Donnell, P. (2013). Closing the gate in the limbic striatum: prefrontal suppression of hippocampal and thalamic inputs. Neuron, 78 (1): 181-90.
  7. Stalnaker, T. A., Calhoon, G. G., Ogawa, M., Roesch, M. R., & Schoenbaum, G. (2012). Reward prediction error signaling in posterior dorsomedial striatum is action-specific. The Journal of Neuroscience, 32 (30): 10296-305.
  8. McDannald, M. A., Whitt, J. P., Calhoon, G. G., Piantadosi, P. T., Karlsson, R. M., O’Donnell, P., & Schoenbaum, G. (2011). Impaired reality testing in an animal model of schizophrenia. Biological Psychiatry, 70 (12): 1122-6.
  9. Gruber, A. J., Calhoon, G. G., Shusterman, I., Schoenbaum, G., Roesch, M. R., & O’Donnell, P. (2010). More is less: A disinhibited prefrontal cortex impairs cognitive flexibility. The Journal of Neuroscience, 30 (50): 17102-17110.
  10. Stalnaker, T. A., Calhoon, G. G., Ogawa, M., Roesch, M. R., & Schoenbaum, G. (2010). Neural correlates of stimulus-response and response-outcome associations in dorsolateral versus dorsomedial striatum. Frontiers in Integrative Neuroscience, 4: 12. doi:89/fnint.2010.00012.