ArticleNeurochemical research1995
Characterization of the type of calcium channel primarily regulating GABA exocytosis from brain nerve endings.
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 5 papers.
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5 citing papers in PubMed, 14 citations in OpenAlex.
- Astrocyte-Mediated Neuromodulatory Regulation in Preclinical ALS: A Metadata Analysis.Frontiers in cellular neuroscience · 2018Article
- Effects of Levetiracetam, Carbamazepine, Phenytoin, Valproate, Lamotrigine, Oxcarbazepine, Topiramate, Vinpocetine and Sertraline on Presynaptic Hippocampal Na(+) and Ca(2+) Channels Permeability.Neurochemical research · 2016Article
- Dihydropiridines mechanism of action in striatal isolated nerve endings: comparison with omega-agatoxin IVA.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
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2 authors at 1 institution in 1 country.
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Abstract
In an attempt to further characterize the type of Ca2+ channels primarily regulating GABA exocytosis, the effects of increasing concentrations of omega CTx MVIIC,-omega-Aga IVA and other Ca2+ channel blockers (nitrendipine, Cd2+ and Ni2+), commonly used for pharmacologically discerning among the various types of Ca2+ channels, were tested on the dissected Ca2+ dependent fraction of the depolarization evoked release of GABA from mouse brain synaptosomes. Our results show that omega-CTx MVIIC inhibits GABA exocytosis with a calculated IC50 of 3 microM and omega-Aga IVA with a calculated IC50 of 50 nM. The divalent cation Cd2+ only diminishes GABA exocytosis at 70 microM, but does not modify this response at lower concentrations (i.e. 1 and 10 microM). Neither nitrendipine (10 microM) nor Ni2+ (100 microM and 500 microM) modified GABA exocytosis. The failure of nitrendipine at a high concentration to inhibit GABA exocytosis discards L-type Ca2+ channels as the main regulators of this response; likewise that of Ni2+ discards Ca2+ channels of the N-type, and the failure of nM concentrations of omega-CTx MVIIC or 500 microM Ni2+, also discards alpha 1A/Q-type Ca2+ channels as the main regulators of the GABA response. On the basis of these results and in particular of the higher potency of omega-Aga IVA than omega-CTx MVIIC, it is concluded that the type of Ca2+ channels that primarily determine the exocytosis of GABA belong to a P-like type of Ca2+ channels.
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