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.

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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.

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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.

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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

Abstract

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.