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.
Kircher, D.M., and Brady, A.M. (2010, November). An investigation of the behavioral effects of perinatal bisphenol-A exposure in comparison to disruptions observed in animal models of schizophrenia.
Poster presented at the Society for Neuroscience Annual Meeting, San Diego, CA.
The endocrine disrupting chemical Bisphenol-A (BPA) found in many products including bottles and food containers, can cross the placental barrier and potentially produce changes in offspring. In mice perinatal BPA treatment decreases dopamine D3 receptor density and increases D1 receptor production in adulthood. Similar disruptions in dopaminergic function have also been observed in the neonatal vental hippocampal lesion (NVHL) animal model of schizophrenia. To assess the potential similarities between BPA exposure and developmental animal models of schizophrenia, the present study examined the effects of perinatal BPA treatment on several behaviors known to be disrupted in the NVHL and other models. Pregnant Sprague Dawley females were treated with a low dose of BPA (20 µg/kg/day) or corn oil vehicle from embryonic day (ED) 13 until weaning at postnatal day (PD) 21. Upon reaching adulthood (PD 56) male offspring (BPA, n= 11; vehicle, n = 10) underwent behavioral testing. Pre-pulse inhibition (PPI) of the startle response was measured in acoustic startle chambers. Perinatal BPA exposure did not alter PPI (p = .832). Locomotion in response to a novel (stressful) environment was assessed using an automated activity chamber. Animals perinatally exposed to BPA had increased locomotion as time in the chamber progressed compared to vehicle treated animals (p = .047). Social interaction was assessed by placing animals into the open field with a novel partner of the same treatment and recording nonaggressive social, aggressive social, and nonsocial/individual behavior. Perinatal BPA exposure lead to decreases in sniffing/grooming of the partner animal in adulthood (p = .006). A decrease in total nonaggressive social behaviors in BPA exposed-animals approached significance (p = .09). Spatial memory was assessed using the Morris Water Maze. Escape latency and time spent in the quadrant during a probe trial was recorded for all animals. Perinatal BPA exposure did not alter escape latency during four days of acquisition (p = .994) however, BPA exposure decreased time spent in the target quadrant on the probe test (p = .001). Finally perinatal BPA exposure did not alter the number of dopamine cells in the SN, assessed via tyrosine hydroxolase immunohistochemistry (p = .395). Exposure to a low dose of BPA produces mild deficits in adulthood on behaviors that are also disrupted in animal models of schizophrenia.