Seminars & Events
Monday, February 11, 2013: Dr. Daphne Soares (University of Maryland College Park) will speak on "The Sensory World of Cavefishes" at 4:45 pm in Goodpaster Hall 195.
Monday, March 4, 2013: Dr. Joe Cheer (University of Maryland Baltimore) will speak on "Endogenous Cannabinoids and the Pursuit of Reward" at 4:45 pm in Goodpaster Hall 195.
Friday, April 12, 2013: Dr. Jill McGaughy (University of New Hampshire) will speak on "The Role of Cortical Norepinephrine in the Ontogeny of Executive Function" at 3:00 pm in Schaefer Hall 106.
Dr. Erin Johnson '02 recently received her Ph.D. in Neuroscience from the University of Rochester School of Medicine, and was inducted as an alumni member of Nu Rho Psi.
Ron Saul, "Chronic activation of the substantia nigra nociceptin/orphanin receptor induces motor deficits similar to Parkinson's disease," 2008. Saul, the 2008 winner of the Neuroscience Award, infused a drug into the substantia nigra of rats and measured the resulting motor behaviors, mood disturbances, and cognitive abilities.
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.