Effects of calcium antagonists nifedipine and flunarizine on phencyclidine-induced changes in the regional dopaminergic metabolism of the rat brain

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...

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Bibliographic Details
Published in:Biochemical pharmacology 1996-01, Vol.51 (1), p.83-86
Main Authors: Etou, K, Kuroki, T, Tatebayashi, Y, Tashiro, N, Hirano, M
Format: Article
Language:English
Subjects:
3,4-Dihydroxyphenylacetic Acid - metabolism
Animals
Biological and medical sciences
Brain - drug effects
Brain - metabolism
Brain Mapping
calcium antagonist
Calcium Channel Blockers - pharmacology
Dopamine - metabolism
dopaminergic neuron
flunarizine
Flunarizine - pharmacology
Hallucinogens - pharmacology
Homovanillic Acid - metabolism
Male
Medical sciences
Miscellaneous
Neuropharmacology
nifedipine
Nifedipine - pharmacology
Pharmacology. Drug treatments
phencyclidine
Phencyclidine - pharmacology
Rats
Rats, Inbred Strains
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Summary: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.
ISSN:0006-2952
1873-2968
DOI:10.1016/0006-2952(95)02127-2