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The effects of nomifensine maleate (HOE 984) were evaluated using two behavioral tasks. The drug produced dose related increases in both psychomotor activity and operant responding for brain stimulation reward. These results may point to possible psychostimulant properties for the drug.
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The author's recollections of the events leading to the discovery of rewarding brain stimulation at McGill University in 1953, with a history of his subsequent attempts to find a learning theory congruent with the phenomenon.
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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.
The pulse-pair paradigm was used to behaviorally assess the absolute and relative refractory periods of neurons subserving brain-stimulation reward. The amplitude of the second pulse was either equal to, 41% greater than, or 73% greater than the amplitude of the first pulse. In the equal amplitude condition, recovery from refractoriness began as early as 0.4 msec and did not asymptote until as late as 3.5 msec. A 41% increase in the intensity shortened the time course of recovery in five out of six cases. In only one of these five cases did a 73% increase in the intensity of the second pulse produce further changes in time course. Neither increase in the amplitude of the second pulse affected the time course of recovery in one subject. The absolute refractory periods of the directly stimulated reward-relevant neurons appear to be less than 1.5 msec and as short as 0.4 msec; some of these neurons have relative refractory periods that range between 1.0 and 3.5 msec.