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CNS effects of calcium channel blocking drugs
Author(s) -
Govoni S.,
Battaini F.,
Trabucchi M.,
Paoletti R.
Publication year - 1985
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(85)90135-2
Subject(s) - pharmacognosy , library science , pharmacology , medicine , chemistry , computer science , biological activity , in vitro , biochemistry
Calcium entry blockers have originally been used as cardiovascular drugs useful in angina and arrhythmia. Recent data indicate that some derivatives may have a selective action on cerebral tissues. However, in Front of the vast literature on the vascular and on the protective effects of calcium entry blockers in hypoxia,redatively little is knawnon their direct CNS action in normal conditions. This is somewhat surprising since the brain is very rich in calcium antagonist binding sites and neurotransmitter release is believed to be dependent on calcium entry within the nerve endings. In the present investigation the effect of calcium entry blockers (CEBs) on neurotransmitter release was studied in rat striatus either after in viva treatment or following in vitro addition of nifedipine, verapamil 2nd flunarizine. In particular. the release of endogenous dopamine (DA), measured by HPLC with electrochemical detection, and the release of met-enkephalin immunoreactive material (ME-IR). measured by RIA. here evaluated. The results indicate the CLBs inhibii ,;iriatal DA and ME-IR release. Enkephalin seems to be more susceptible than ilA to this inhibitory action after in viva CEBr treatment. The effect was apparently independent from the vascular action of these drugs inaicating the possibility of so far unexplored direct influences on CNS activity in control, well oxygenated, rats. On this line receptor studies using tritiated CEBs during development and after pharmacological manipulation will help to clarify the relevance of calcium channel blocking to neurotransnission.