Caudate-Putamen in Hyperactive Behavior in Rats
Institution
Morehead State University
Faculty Advisor/ Mentor
Ilsun M. White
Abstract
Previous neurophysiological studies indicated that in rats amphetamine produced hyperactivity and also excited neurons in the caudateputamen (the dorsal striatum). The present study further examined the involvement of the caudate-putamen (CPu) in amphetamine-induced hyperactivity in rats, using CPu lesions and direct infusions of amphetamine into CPu. In Experiment 1, rats received either NMDA or sham lesions in CPu. In Experiment 2, rats were implanted with bilateral cannulae, aimed at the dorsal CPu. Our hypothesis was that CPu lesions would suppress amphetamineinduced hyperactivity, and that direct infusions of amphetamine into the CPu would produce hyperactivity. Activity of each animal was measured by distance traveled in an open-field. Data were recorded every 5 min for a 60 min period, during habituation, vehicle, and amphetamine sessions, occurring on different days. During habituation, distance traveled did not differ between lesioned rats and the controls. Following systemic amphetamine injection (1mg/kg, i.p.), rats with CPu lesions and the control rats showed comparable markedly enhanced behavioral activity. We also found that amphetamine (10mg/ml, 0.6ml/site) infusions into CPu failed to produce hyperactivity. Our data suggest that CPu lesions failed to block amphetamine-induced hyperactivity, and that amphetamine-induced hyperactivity is not directly mediated by excess dopamine within CPu. Our hypothesis was not supported by the present findings. Given that amphetamine infusions into the nucleus accumbens (the ventral striatum) reliably produce hyperactivity, future research on regional specificity within the striatum in psychostimulant-related behavior is warranted.
Caudate-Putamen in Hyperactive Behavior in Rats
Previous neurophysiological studies indicated that in rats amphetamine produced hyperactivity and also excited neurons in the caudateputamen (the dorsal striatum). The present study further examined the involvement of the caudate-putamen (CPu) in amphetamine-induced hyperactivity in rats, using CPu lesions and direct infusions of amphetamine into CPu. In Experiment 1, rats received either NMDA or sham lesions in CPu. In Experiment 2, rats were implanted with bilateral cannulae, aimed at the dorsal CPu. Our hypothesis was that CPu lesions would suppress amphetamineinduced hyperactivity, and that direct infusions of amphetamine into the CPu would produce hyperactivity. Activity of each animal was measured by distance traveled in an open-field. Data were recorded every 5 min for a 60 min period, during habituation, vehicle, and amphetamine sessions, occurring on different days. During habituation, distance traveled did not differ between lesioned rats and the controls. Following systemic amphetamine injection (1mg/kg, i.p.), rats with CPu lesions and the control rats showed comparable markedly enhanced behavioral activity. We also found that amphetamine (10mg/ml, 0.6ml/site) infusions into CPu failed to produce hyperactivity. Our data suggest that CPu lesions failed to block amphetamine-induced hyperactivity, and that amphetamine-induced hyperactivity is not directly mediated by excess dopamine within CPu. Our hypothesis was not supported by the present findings. Given that amphetamine infusions into the nucleus accumbens (the ventral striatum) reliably produce hyperactivity, future research on regional specificity within the striatum in psychostimulant-related behavior is warranted.