Alterations of spontaneous neuronal activity in the caudate-putamen, nucleus accumbens and amygdaloid complex of rats produced by D-amphetamine.
Changes in spontaneous neuronal activity in the caudate-putamen, accumbens nucleus and amygdaloid complex of immunobilized, locally anesthetized rats were recorded following intraperitoneal injection of 2.5 mg/kg d-amphetamine sulfate. In each site, d-amphetamine typically produced a prolonged depression of firing rate which, in most cases, occurred after an inital, brief potentiation of activity. However, the onset of the amphetamine-induced depression occurred signficantly later in the amygdala. Subsequent IP administration of either 5.0 mg/kg chlorpromazine or 2.0 mg/kg haloperidol reversed, to varying degrees, the amphetamine-induced depression of neuronal activity in each area. These results are discussed in terms of the known biochemical effects of amphetamine on catecholaminergic transmission and the alleged role of the nigro-neostriatal mesolimbic dopamine systems in the amphetamine behavioral response.
D000679:Amygdala / Q000187:drug effects; D000818:Animals; D001921:Brain / Q000187:drug effects*; D002421:Caudate Nucleus / Q000187:drug effects; D002746:Chlorpromazine / Q000494:pharmacology; D003913:Dextroamphetamine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D006220:Haloperidol / Q000494:pharmacology; D008297:Male; D009714:Nucleus Accumbens / Q000187:drug effects; D011699:Putamen / Q000187:drug effects; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects*
D006220:Haloperidol; D003913:Dextroamphetamine; D002746:Chlorpromazine