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Depolarization, exocytosis and amino acid release evoked by hyposmolarity from cortical synaptosomes
Author(s) -
Tuz Karina,
PeñaSegura Claudia,
Franco Rodrigo,
PasantesMorales Herminia
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.0953-816x.2004.03209.x
Subject(s) - taurine , glutamate receptor , depolarization , chelerythrine , exocytosis , chemistry , protein kinase c , synaptosome , tetrodotoxin , osmolyte , egta , veratridine , biochemistry , medicine , endocrinology , biology , amino acid , sodium , calcium , sodium channel , receptor , phosphorylation , organic chemistry , membrane , secretion
External osmolarity reduction (20%) led to labelled glutamate, GABA and taurine release from rat brain cortical synaptosomes. A Cl – ‐independent, Na + ‐dependent, La 3+ ‐sensitive and tetrodotoxin (TTX) reduced depolarization of synaptosomes occurred upon hyposmolarity, suggestive of Na + entry through nonselective cation channels. This depolarization, together with cytosolic Ca 2+ ([Ca 2+ ] I ) increase, resulted in exocytosis, monitored by FM1‐43. The release fraction resulting from these phenomena was estimated, by its decrease, by La 3+ , EGTA‐AM and tetanus toxin (TeTX), as 34–44% for glutamate, 21–29% for GABA and 18–22% for taurine. Protein kinase C (PKC) activation by phorbol‐12‐myristate‐13‐acetate (PMA) increased the hyposmolarity‐elicited exocytosis and this activation increased glutamate (80%), GABA (51%) and taurine (42%) hyposmotic efflux. Inhibition by chelerythrine reduced glutamate, GABA and taurine efflux by 64%, 50% and 24%, respectively. The Na + ‐dependence of amino acid release (glutamate 63%, GABA 46% and taurine 29%) may result from both, prevention of the depolarization‐exocytosis efflux, and blockade of the carrier reversal operation. Carrier blockade by dl ‐threo‐β‐benzyloxy aspartate (TBOA) and NO‐711 resulted in 37% and 28% reduction of glutamate and GABA release, respectively. Contribution of the osmolyte leak pathway to amino acid release, estimated by the influence of Cl – (NPPB) and tyrosine kinase (AG18) blocker, was up to 55% for taurine, but only 10–18% for GABA, with apparently no contribution for glutamate. The predominant osmolyte‐type mechanism of taurine release suggest its function in volume control in nerve endings, while glutamate and GABA respond to events concurrent with hyposmolarity by a neurotransmitter‐like release mechanism. The hyposmolarity‐induced amino acid efflux from nerve endings may have consequences for neuronal excitability during hyponatremia.