Effects of calcium antagonists nifedipine and flunarizine on phencyclidine-induced changes in the regional dopaminergic metabolism of the rat brain.
K Etou, T Kuroki, Y Tatebayashi, N Tashiro, M Hirano
Biochemical Pharmacology January 12, 1996 DOI: 10.1016/0006-2952(95)02127-2 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal experiment Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | Nifedipine Flunarizine Phencyclidine (PCP) |
| Key findings | PCP significantly increased dopamine metabolite levels in the prefrontal cortex, nucleus caudatus putamen, and amygdala. Nifedipine, but not flunarizine, significantly antagonized these PCP-induced increases. The authors suggest nifedipine attenuates PCP-induced dopaminergic hyperactivity and may have antipsychotic properties. |
Abstract
To elucidate the psychotropic actions of calcium (Ca) antagonists, we investigated the effect of the voltage-dependent Ca channel antagonists, nifedipine and flunarizine, on phencyclidine (PCP)-induced changes in the monoamine metabolism in the regional brain areas of rats. The results indicate that the administration of nifedipine alone attenuated dopamine (DA) metabolism in the nucleus caudatus putamen while enhancing serotonin (5-HT) metabolism. By contrast, flunarizine increased DA metabolism. PCP significantly increased DA metabolite levels in the prefrontal cortex, the nucleus caudatus putamen, and the amygdala. The PCP-induced increases in DA metabolism in these regions were significantly antagonized by nifedipine, but not by flunarizine. These results indicate that nifedipine attenuates the PCP-induced hyperactivity of the dopaminergic neurons, suggesting antipsychotic properties for this drug.