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.
Dr. Gwen Calhoon '06 recently received her Ph.D. in Neuroscience from the University of Maryland Baltimore, and was inducted into Nu Rho Psi.
Kallarackal, A. (2005, December). The Effect of Apamin, a Small Conductance Calcium-activated Potassium (SK) Channel Blocker, in a Mouse Model of Neurofibromatosis1.
Mentor: Dr. Aileen Bailey
Neurofibromatosis 1 (NF1) is a common genetic disorder known to cause a variety of physiological symptoms such as the formation of both benign and malignant tumors, and is also known to cause visuospatial learning deficits. A large component of the learning deficits in NF1 patients is difficulty in visuospatial tasks. The astrocytes of Nf1+/- mice exhibit an increased outward K+ current which is apamin (a specific blocker of small conductance calcium activated potassium (SK) channels) sensitive. SK channels appear to play a role in regulating long term potentiation (LTP), a mechanism of learning which has been shown to be impaired Nf1+/- mice. We found a significant upregulation of SK1 channels in Nf1+/- mouse brains in comparison to WT brains through western blot analysis. Immunohistochemistry showed that the upregulation is localized to the hippocampus and olfactory tract. We tested 32 mice and administered a 0.4mg/kg dose of apamin either through i.p injection or micro-osmotic pump to Nf1+/- mice and found that the apamin treated Nf1+/- mice significantly improved performance on the water maze task in comparison to saline treated Nf1+/- mice on the third day of training. We also tested Nf1+/- mice in the Barnes maze, another test of hippocampal dependent learning and found that Nf1+/- mice had higher escape latencies than normal control mice, however this was not significant. In this study we demonstrate a possible mechanism for the learning deficits seen in Nf1+/- mice and a possible drug therapy for rescuing these deficits. We also demonstrate a potentially novel learning deficit in Nf1+/- mice in the Barnes maze task.