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.


Alumni Highlight

Check out Jordan Gaines Lewis '11's award-winning blog, Gaines on Brains.




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.


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.