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.
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.