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.


Tracy, M., Turek, K.C., Bailey, A.M., Brady, A.M., Vinish, M., Milstein, J., and Frost, D.O. (2011, November). The effects of adolescent exposure on behavior in the neonatal ventral hippocampal lesion model of schizophrenia.

Poster presented at the Society for Neuroscience Annual Meeting, Washington, DC.


The neonatal ventral hippocampal lesion (NVHL) model of schizophrenia has previously produced animals with deficits in sensory-motor gating, increased locomotor activity, hypersensitivity to stimulant drugs, and decreased social interaction. Antipsychotic drugs are typically used to lessen the symptoms in humans suffering from schizophrenia. We aimed here to test the long-lasting effects of adolescent exposure to antipsychotic drugs (olanzapine) in the NVHL model. Long-Evans rats received bilateral infusions of ibotenic acid (NVHL group) or artificial CSF (sham group) into the ventral hippocampus at postnatal day (PD) 7. During PD28 - PD49 (adolescence), animals were administered either 120 mL of olanzapine in 0.001 M acetic acid with a target dose of 7.5 mg/kg per day (NVHL n=16; sham n=12) or a vehicle solution of 0.001 M acetic acid in water (NVHL n=16; sham n=12). During the adolescent period, social interaction with a cage-mate was measured twice (PD 38 & PD 48) in a 60 x 60 x 28 cm open field. NVHL animals demonstrated significantly fewer play attacks and evasive behavior when compared to sham animals (p < .05). Adolescent sham animals given olanzapine also showed significantly fewer play attacks and evasive behavior compared to shams given vehicle. At PD 90 all animals were tested for pre-pulse inhibition (PPI), spontaneous locomotion, amphetamine-induced locomotion, and for adult social interaction with a novel partner. There were no differences in PPI in NVHL and sham animals. In addition, olanzapine exposure during adolescence did not alter adult measurements of PPI in either NVHL or sham animals. All animals showed a decrease in locomotor behavior across time, but there were no differences in ambulatory counts between the NVHL and sham animals. The relationship between early play behavioral differences, olanzapine exposure and adult social interactions will be discussed.