A variety of drugs were screened to determine which were capable of blocking the behavioral stimulation produced in mice by acute administration of phencyclidine (PCP). Chlorpromazine and clozapine blocked PCP-induced stimulation, while haloperidol, reserpine, and alpha-methyl-p-tyrosine did not. The GABA receptor agonists imidazole acetic acid and muscimol blocked PCP, but other drugs that influence GABA, such as dipropylacetic acid, baclofen, and diazepam, were ineffective. Yohimbine and methysergide also blocked PCP in high dosages, but other drugs with comparable alpha-noradrenergic and serotonergic blocking properties (phentolamine, cyproheptadine, and cinnanserin) were ineffective. Cholinergic and anticholinergic drugs, beta-noradrenergic and opiate antagonists and nonspecific sedatives and convulsants were also ineffective. These findings suggest that chlorpromazine, clozapine, yohimbine, and methysergide may share a property that is unlike their primary known modes of action on dopaminergic, alpha-noradrenergic, and serotonergic neurotransmitter systems, and that this property accounts for their ability to block PCP. However, the effectiveness of GABA agonists appears to be mediated through direct activation of GABA receptors. It is suggested that chlorpromazine and imidazole acetic acid should be considered as possible drug treatments for PCP toxicity.
reduction was observed 4 to 9 hours later. "When calcitonin was given 1, 3, or 22 hours before, feeding was not substantially decreased." Increasing the period between the ingestion ofa flavor and the induction of sickness decreases the conditioned taste aversion subsequently displ.ayed (6). Delaying the injection of lithium chloride from 1.5 hours to 4.5 hours produced a fourfold decrease in the effectiveness of the injection as measured by intake suppression (7). Therefore, an amount of lithium chloride producing a similar decrease in food intake should have been injected at least 4 to 5 hours after a novel flavor had been presented. Should such a test still show no taste aversion, the conclusion that no sickness was present to cause the reduction in food intake would be made more plausible. However, some doubt would still remain because we do not know how the speed of onset of sickness influences the formation of conditioned taste aversion. Gradualness of onset may militate against the efficiency of a learned association.
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