Seminars & Events
Thursday, September 11, 2014: Dr. Bevil Conway (Wellesley College) will speak on his research in visual neuroscience and color at 4:30 pm in Goodpaster Hall 195.
Monday, October 27, 2014: Dr. Todd Gould (University of Maryland Baltimore) will speak on "Genes to behaviors to treatments in bipolar disorder" at 4:45 pm in Goodpaster Hall 195.Friday, December 5, 2014: Dr. Brian Mathur (University of Maryland Baltimore) will speak on "Braking bad: Aberrant inhibitory neurotransmission in addiction" at 3:00 pm in Goodpaster Hall 195.
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.