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PubMed1977

Evidence for a noradrenergic mechanism in the grooming produced by (+)-amphetamine and 4, alpha-dimethyl-m-tyramine (H 77/77) in rats.

Rats were kept on a 12-h light-dark cycle. One hour after the light was switched on, physiological saline, (+)-amphetamine 1 mg/kg, and H 77/77 5 mg/kg were injected s.c.; the number of groomings was counted 1-2 h after the treatments. (+)-Amphetamine and H 77/77 produced increased grooming which was antagonized by the tyrosine hydroxylase inhibitor H 44/68 (250 mg/kg), the dopamine-beta-hydroxylase inhibitor FLA 63 (40), the neuroleptics haloperidol (0.1 and 0.5), and clozapine (1 and 5). The (+)-amphetamine-induced grooming was also antagonized by the NA-receptor blocker aceperone (10) but not by the sedative phenothiazines mepazine (10) and diphenhydramine (20) nor diazepam (1). These results indicate that NA-release is involved in the mediation of (+)-amphetamine- and H 77/77-induced grooming. The inhibition of haloperidol and clozapine is presumably due to NA-receptor blockade.

Amphetamine↗
PubMed1978

Influence of the new 5-HT-uptake inhibitor paroxetine on hypermotility in rats produced by p-chloroamphetamine (PCA) and 4,alpha-dimethyl-7-tyramine (H 77/77).

Two different forms of hypermotility produced by the amphetamine derivatives PCA and H 77/77, 5 mg/kg of each, was studied in rats treated s.c. with the new 5-HT uptake inhibitor paroxetine. The substance inhibited the effect of PCA but did not influence that of H 77/77. The 5-HT-uptake inhibitors paroxetine, imipramine, and chlorimipramine were also administered p.o. at various times before PCA. The three substances inhibited PCA-induced hypermotility. Paroxetine 0.5-2 mg/kg, was active at intervals of 1-4 h and 4 mg/kg was active at 18-h interval. Imipramine and chlorimipramine 25-30 mg/kg showed PCA inhibition at treatment intervals of 1-2h, but 80-100 mg/kg or more was required to inhibit PCA at intervals of 4 and 18 h. Previous results have shown that PCA-induced hypermotility is antagonized by substances inhibiting 5-HT synthesis and uptake, whereas H 77/77-induced hypermotility is inhibited by substances blocking NA synthesis, uptake, and receptors. The previous and present results indicate that paroxetine is a selective 5-HT-uptake inhibitor. After oral administration paroxetine presumably produces a more potent and long-lasting 5-HT-uptake inhibition than imipramine and chlorimipramine.

Amphetamines↗
PubMed1975

Inhibition of 4,alpha-dimethyl-m-tyramine (H 77/77)-induced hypermotility in rats by single and repeated administration of chloropromazine, haloperidol, clozapine and thioridazine.

The effect of H 77/77 (5 mg/kg s.c.) on motility of rats kept in a familiar cage was investigated. H 77/77 produced hypermotility, which was reduced by oral pretreatment with chlorpromazine, haloperidol, clozapine and thioridazine. The 4 neuroleptics were administered acutely and for a 14 day period. H 77/77 was given 30 min after the single or last dose of neuroleptc (chronic treatment) condition. After both single and repeated administration the neuroleptics showed H 77/77-antagonism in doses ranging from 0.1-2.0 mg/kg. The effect on H 77/77 activity did not change significantly after repeated treatment. Clozapine and thioridazine, which clinically produce only minor extrapyramidal side effects, exert a weak effect or none at all in tests commonly used for neuroleptic activity. These 2 neuroleptics were potent H 77/77-antagonists. Inhibition of H 77/77-hypermotility may possibly be used as a test for neuroleptics.

Adrenergic Agents↗