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Inhibition of endogenous glutamate release from hippocampal tissue by Ca2+ channel toxins

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Abstract

The pharmacology of voltage-dependent Ca2+ channel involved in the release of endogenous neurotransmitter amino acids was measured from small tissue slices of rat hippocampal CA1 region. Application of 50 mM KCl induced large increases in Ca2+-dependent overflow of endogenous glutamate, aspartate and γ-aminobutyric acid (GABA)_. Pretreatment of tissues with the funnel-web spider toxin ω-Aga-IVA (200 nM) reduced KCl-induced overflow of all three amino acids. Pretreatment with the cone snail toxin ω-CgTx-GVIA (2 μM) caused similar but smaller reductions in amino acid overflow (aspartate overflow was not reduced significantly). These results indicate that P-type Ca2+ channels, and to a lesser extent, N-type Ca2+ channels, are involved in the release of transmitter amino acids under these conditions.

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    These TBCs consisted of three HEX type TBCs and the unclassified type TBC. HVA-Ca2+ channels residing in the terminals of mammalian central and peripheral neurons are essential in releasing neurotransmitters [7,24,32,44,46,47]. It is thus likely that ∼20%, at maximum, of the TBCs in mouse soft palates can release transmitters to taste nerve endings with chemical synapses, and that these presynaptic TBCs are of the HEX type.

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