2003
DOI: 10.1073/pnas.0936131100
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Nifedipine facilitates neurotransmitter release independently of calcium channels

Abstract: Nifedipine, a drug used for treatment of hypertension and angina, exerts its effect by calcium channel blockade and nitric oxide production. We report here a previously uncharacterized action of nifedipine on central synaptic transmission that may partially explain its side effects. Nifedipine causes a long-lasting facilitation of tetrodotoxin-insensitive spontaneous glutamate release. This effect is independent of its L-type calcium channel blocking effect, and is not mimicked by other dihydropyridines such a… Show more

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Cited by 46 publications
(42 citation statements)
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“…The activation of protein kinase A or C pathways has been shown to facilitate transmitter release, and both are possible candidates (18,19). However, the results of Hirasawa and Pittman (12) show that the nifedipine effect was independent of these pathways. Furthermore, because the effect of nifedipine was still observed after nicardipine treatment, it was thought to facilitate mEPSC frequency at a site different than the Ltype VDCC.…”
contrasting
confidence: 43%
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“…The activation of protein kinase A or C pathways has been shown to facilitate transmitter release, and both are possible candidates (18,19). However, the results of Hirasawa and Pittman (12) show that the nifedipine effect was independent of these pathways. Furthermore, because the effect of nifedipine was still observed after nicardipine treatment, it was thought to facilitate mEPSC frequency at a site different than the Ltype VDCC.…”
contrasting
confidence: 43%
“…DHPs also block L-type VDCCs in CNS neurons and have been used to implicate the channel in stimulus transcription coupling (14). Regarding the mechanism by which nifedipine increases miniature synaptic activity, Hirasawa and Pittman (12) clearly show that it is completely independent of calcium-induced changes in basal release probability. The nifedipine-induced stimulatory effect on mEPSC frequency was not blocked by several strategies that interfere with calcium elevation including thapsigargin, a Ca 2ϩ -ATPase inhibitor that depletes Ca 2ϩ stores, chelation of [Ca 2ϩ ] i with 1,2-bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetateacetoxymethyl ester (BAPTA-AM), or nonselective blockade of VDCCs with Cd 2ϩ .…”
mentioning
confidence: 99%
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