Seminars & Events

Friday, October 4, 2013: Dr. Laurie Ryan, SMCM '86 (National Institute on Aging) will speak on "Alzheimer's Disease: Targets and Treatments" at 3:00 pm in Goodpaster Hall 195.

Monday, October 21, 2013: Dr. Greg Elmer (University of Maryland Baltimore) will speak on "Domains and Constructs in Motivation: Where Does the Habenula Fit In?" at 4:45 pm in Goodpaster Hall 195

Friday, October 25, 2013:  Dr. Terry Davidson (American University) will speak on "Why We Overeat and Become Obese?  It Could be What We Think!" at 3:00 pm in Goodpaster Hall 195.


Alumni Highlight

Dr. Gwen Calhoon '06 recently received her Ph.D. in Neuroscience from the University of Maryland Baltimore, and was inducted into Nu Rho Psi.







SMP Spotlight

Katie Gluskin and Jeff Haus present their SMP
Katie Gluskin and Jeff Haus, "Entorhinal Cortex Lesions, Habituation, and Latent Inhibition," 2013. Gluskin and Haus, the 2013 co-winners of the Neuroscience Award, infused a neurotoxin into the entorhinal cortex of rats to induce a lesion, and measured the resulting habituation and latent inhibition behavior within a fear conditioning paradigm.


Cammarata, Erin (2011).  Temporoammonic excitation of CA1 cells in an animal model of depression. (Mentor: A. Bailey)


Depression is among the leading causes of mental disability in the world. The hippocampus plays an important role in depression. Patients with depression show hippocampal volume reductions shown by fMRI and hippocampal dysfunctions shown by deficits in spatial memory. Serotonin signaling in the hippocampus is thought to be impaired in patients with depression. Specifically, the TA-CA1 pathway connecting the hippocampus to the neocortex contains dense areas of 5HT1B receptors, and is involved in spatial memory function. Changes in serotonin’s potentiation of glutamatergic transmission at the TA pathway occur in animals with the CUS model of depression. Antidepressants, specifically fluoxetine, restore these changes to the potentiation at the TA pathway. According to this finding, animals with the CUS model of depression were predicted to have deficits in spatial memory because the TA pathway is linked to spatial memory functioning. In addition, it was hypothesized that fluoxetine would restore spatial memory function in animals with the CUS model of depression. This suggests that the activity of 5HT1B receptors at the TA pathway is involved in the etiology of depression, and that restoration of normal function to these synapses is critical to the therapeutic effects of antidepressants. The current study found significant evidence suggesting that CUS impaired spatial memory, but did not find any normalization of impairments mediated by fluoxetine.