K+depolarization evokes ATP, adenosine and glutamate release from glia in rat hippocampus: a microelectrode biosensor study

Heinrich, A. and Andó, R. D. and Túri, G. and Rózsa, B. and Sperlágh, B. (2012) K+depolarization evokes ATP, adenosine and glutamate release from glia in rat hippocampus: a microelectrode biosensor study. BRITISH JOURNAL OF PHARMACOLOGY, 167 (5). pp. 1003-1020. ISSN 0007-1188

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Abstract

ATP, adenosine and glutamate sensors exhibited transient and reversible current during depolarization with 25 mM K(+) , with distinct kinetics. The ecto-ATPase inhibitor ARL67156 enhanced the extracellular level of ATP and inhibited the prolonged adenosine efflux, suggesting that generation of adenosine may derive from the extracellular breakdown of ATP. Stimulation-evoked ATP, adenosine and glutamate efflux was inhibited by tetrodotoxin, while exposure to Ca(2+) -free medium abolished ATP and adenosine efflux from hippocampal slices. Extracellular elevation of ATP and adenosine were decreased in the presence of NMDA receptor antagonists, D-AP-5 and ifenprodil, whereas non-NMDA receptor blockade by CNQX inhibited glutamate but not ATP and adenosine efflux. The gliotoxin fluoroacetate and P2X7 receptor antagonists inhibited the K(+) -evoked ATP, adenosine and glutamate efflux, while carbenoxolone in low concentration and probenecid decreased only the adenosine efflux.

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