An examination of parkinsonian versus anhedonia contributions to self-stimulation impairments induced by dopamine dysfunction.
Interference with brain dopamine neurotransmission can severely impair brain stimulation reward behavior. The significance of this impairment in reward behavior, however, has been a problematic issue. That is, it has been difficult to determine whether the dopamine dysfunction has attenuated the reward effect of the stimulation or has merely rendered the animal less able to generate the behavior required to obtain reinforcement. To experimentally re-assess this issue, the present studies examine the effect of unilateral 6-hydroxydopamine lesions of forebrain dopamine neurons on brain stimulation reward in animals. In general, these studies highlight the substantial motoric deficits produced by the lesion treatments. By combining lesion and neuroleptic drug treatments, however, it appeared that effects on reward could be detected.
D000818:Animals; D001921:Brain / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D006892:Hydroxydopamines / Q000494:pharmacology; D008297:Male; D016627:Oxidopamine; D010300:Parkinson Disease / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012201:Reward; D012653:Self Stimulation / Q000502:physiology*; D013378:Substantia Nigra / Q000502:physiology; D009435:Synaptic Transmission; D013681:Tegmentum Mesencephali / Q000502:physiology
D006892:Hydroxydopamines; D016627:Oxidopamine; D004298:Dopamine