ArticleNeurochemical research1995
omega-Aga IVA selectively inhibits the calcium-dependent fraction of the evoked release of [3H]GABA from synaptosomes.
Article in Neurochemical research, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Effects of Levetiracetam, Carbamazepine, Phenytoin, Valproate, Lamotrigine, Oxcarbazepine, Topiramate, Vinpocetine and Sertraline on Presynaptic Hippocampal Na(+) and Ca(2+) Channels Permeability.Neurochemical research · 2016Article
- Characterization of phenytoin, carbamazepine, vinpocetine and clorgyline simultaneous effects on sodium channels and catecholamine metabolism in rat striatal nerve endings.Neurochemical research · 2009Article
- Dihydropiridines mechanism of action in striatal isolated nerve endings: comparison with omega-agatoxin IVA.Neurochemical research · 2004Article
- Characterization of the participation of sodium channels on the rise in Na+ induced by 4-aminopyridine (4-AP) in synaptosomes.Neurochemical research · 2004Article
- Vinpocetine selectively inhibits neurotransmitter release triggered by sodium channel activation.Neurochemical research · 1999Article
- Effects of external pH variations on brain presynaptic sodium and calcium channels; repercussion on the evoked release of amino acid neurotransmitters.Neurochemical research · 1998Article
- Nigericin-induced Na+/H+ and K+/H+ exchange in synaptosomes: effect on [3H]GABA release.Neurochemical research · 1996Article
- Characterization of the type of calcium channel primarily regulating GABA exocytosis from brain nerve endings.Neurochemical research · 1995Article
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2 authors at 1 institution in 1 country.
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Abstract
The effect of omega-Aga IVA, a P-type Ca2+ channel blocker, on the release of the inhibitory neurotransmitter GABA and on the elevation of Cai induced by depolarization was investigated in [3H]GABA and fura-2 preloaded mouse brain synaptosomes, respectively. Two strategies (i.e. 20 mM external K+ and veratridine) that depolarize by different mechanisms the preparation were used. High K+ elevates Cai and induces [3H]GABA release in the absence of external Na+ and in the presence of TTX, conditions that abolish veratridine induced responses. The effect of omega-Aga IVA on the Ca2+ and Na+ dependent fractions of the depolarization evoked release of [3H]GABA were separately investigated in synaptosomes depolarized with high K+ in the absence of external Na+ and with veratridine in the absence of external Ca2+, respectively. The Ca2+ dependent fraction of the evoked release of [3H]GABA and the elevation of Ca2+ induced by high K+ are markedly inhibited (about 50%) in synaptosomes exposed to omega-Aga IVA (300 nM) for 3 min before depolarization, whereas the Na+ dependent, Ca2+ independent carrier mediated release of [3H]GABA induced by veratridine, which is sensitive to verapamil and amiloride, is not modified by omega-Aga IVA. Our results indicate that an omega-Aga IVA sensitive type of Ca2+ channel is highly involved in GABA exocytosis.
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