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Rech RH. 
“Brain Lesions and Psychostimulant Drugs”. 
Psychopharmacol.Bull.. 1978;14(4):35-38.
The effects of brain lesions on psychostimulant drug activity are reviewed. Avoidance activity of poor-performance Sprague-Dawley rats was improved by d-amphetamine (AM), atropine or scopolamine. Massive caudate or septal lesions had no effect on, while nucleus accumbens lesions decreased the AM improvement of poor performers. AM was ineffective in reversing deficits in shuttle-box avoidance induced by small electrolytic caudate nucleus lesions. In rats, 6-hydroxydopamine, intraventricularly, produced a marked deficit in one-way avoidance responding which was reversed by intraventricular dopamine or norepinenephrine, by systemic apomorphine or l-dopa, and clonidine. AM stereotypy was blocked only in striatal-lesioned rats. Medial forebrain lesions that lowered telencephalic serotonin showed a correlated increase in the AM stimulation of VI-60 sec operant behavior for water reinforcement. Locomotor activity stimulation by AM was potentiated by prior p-chlorophenylalanine or 5,6dihydroxytryptamine treatment. LSD did not affect FR-32 operaoperant responding for water reinforcement in rats, but after pretreatment with intraventricular, 5,7-dihydroxytryptamine (TR) it disrupted the response. p-Chloroamphetamine pretreatment did not potentiate the LSD effect. Electrical stimulation of the dorsal raphe nucleus suppressed rat amygdala unit activity; pretreatment with p-chlorophenylalanine or TR prevented this effect. 5-Hydroxytryptophan administration reversed the effect of p-chlorophenylanine. Near-threshold stimulation of dorsal raphe cells, to suppress amygdala units, was blocked by LSD. AM or 2,5-dimethoxy-5-methylamphetamine (MP) increased the rate of radioactivity efflux from the lateral ventricle of rat brain following pulse labelling with l4C-catecholamine. Pretreatment with intraventricular 6-hydroxydopamine prevented the effect of AM or MP. 6-Hydroxy-dopa or MK-486 reduced the efflux of radioactivity over the whole time course of release by AM, but after MP treatment initial efflux was as in non-lesioned subjects, while in the latter phase efflux was at baseline levels. AM appears to release both dopamine and noradrenaline while MP apparently selectively releases dopamine during the early phases of activity and noradrenaline in the later phase.
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