INHIBITION OF ENDOGENOUS GLUTAMATE RELEASE FROM HIPPOCAMPAL TISSUE BYCA2+ CHANNEL TOXINS

The pharmacology of voltage-dependent Ca2+ channels involved in the re lease of endogenous neurotransmitter amino acids was measured from sma ll tissue slices of rat hippocampal CA1 region. Application of 50 mM K Cl induced large increases in Ca2+-dependent overflow of endogenous gl utamate, aspartate and gamma-aminobutyric acid (GABA). Pretreatment of tissues with the funnel-web spider toxin omega-Aga-IVA (200 nM) reduc ed KCl-induced overflow of all three amino acids. Pretreatment with th e cone snail toxin omega-CgTx-GVIA (2 muM) 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.