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Excitatory effect of ATP on rat area postrema neurons

ATP-induced inward currents and increases in the cytosolic Ca(2+) concentration ([Ca](in)) were investigated in neurons acutely dissociated from rat area postrema using whole-cell patch-clamp recordings and fura-2 microfluorometry, respectively. The ATP-induced current (I(ATP)) and [Ca](in) increase...

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Autores principales: Sorimachia, Masaru, Wakamoria, Minoru, Akaikeb, Norio
Formato: Texto
Lenguaje:English
Publicado: Springer Netherlands 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2096647/
https://www.ncbi.nlm.nih.gov/pubmed/18404492
http://dx.doi.org/10.1007/s11302-006-9004-4
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author Sorimachia, Masaru
Wakamoria, Minoru
Akaikeb, Norio
author_facet Sorimachia, Masaru
Wakamoria, Minoru
Akaikeb, Norio
author_sort Sorimachia, Masaru
collection PubMed
description ATP-induced inward currents and increases in the cytosolic Ca(2+) concentration ([Ca](in)) were investigated in neurons acutely dissociated from rat area postrema using whole-cell patch-clamp recordings and fura-2 microfluorometry, respectively. The ATP-induced current (I(ATP)) and [Ca](in) increases were mimicked by 2-methylthio-ATP and ATP-γS, and were inhibited by P2X receptor (P2XR) antagonists. The current–voltage relationship of the I(ATP) exhibited a strong inward rectification, and the amplitude of the I(ATP) was concentration-dependent. The I(ATP) was markedly reduced in the absence of external Na(+), and the addition of Ca(2+) to Na(+)-free saline increased the I(ATP). ATP did not increase [Ca](in) in the absence of external Ca(2+), and Ca(2+) channel antagonists partially inhibited the ATP-induced [Ca](in) increase, indicating that ATP increases [Ca](in) by Ca(2+) influx through both P2XR channels and voltage-dependent Ca(2+) channels. There was a negative interaction between P2XR- and nicotinic ACh receptor (nAChR)-channels, which depended on the amplitude and direction of current flow through either channel. Current occlusion was observed at V(h)s between −70 and −10 mV when the I(ATP) and ACh-induced current (I(ACh)) were inward, but no occlusion was observed when these currents were outward at a V(h) of +40 mV. The I(ATP) was not inhibited by co-application of ACh when the I(ACh) was markedly decreased either by removal of permeant cations, by setting V(h) close to the equilibrium potential of I(ACh), or by the addition of d-tubocurarine or serotonin. These results suggest that the inhibitory interaction is attributable to inward current flow of cations through the activated P2XR- and nAChR-channels.
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spelling pubmed-20966472008-02-27 Excitatory effect of ATP on rat area postrema neurons Sorimachia, Masaru Wakamoria, Minoru Akaikeb, Norio Purinergic Signal Original Article ATP-induced inward currents and increases in the cytosolic Ca(2+) concentration ([Ca](in)) were investigated in neurons acutely dissociated from rat area postrema using whole-cell patch-clamp recordings and fura-2 microfluorometry, respectively. The ATP-induced current (I(ATP)) and [Ca](in) increases were mimicked by 2-methylthio-ATP and ATP-γS, and were inhibited by P2X receptor (P2XR) antagonists. The current–voltage relationship of the I(ATP) exhibited a strong inward rectification, and the amplitude of the I(ATP) was concentration-dependent. The I(ATP) was markedly reduced in the absence of external Na(+), and the addition of Ca(2+) to Na(+)-free saline increased the I(ATP). ATP did not increase [Ca](in) in the absence of external Ca(2+), and Ca(2+) channel antagonists partially inhibited the ATP-induced [Ca](in) increase, indicating that ATP increases [Ca](in) by Ca(2+) influx through both P2XR channels and voltage-dependent Ca(2+) channels. There was a negative interaction between P2XR- and nicotinic ACh receptor (nAChR)-channels, which depended on the amplitude and direction of current flow through either channel. Current occlusion was observed at V(h)s between −70 and −10 mV when the I(ATP) and ACh-induced current (I(ACh)) were inward, but no occlusion was observed when these currents were outward at a V(h) of +40 mV. The I(ATP) was not inhibited by co-application of ACh when the I(ACh) was markedly decreased either by removal of permeant cations, by setting V(h) close to the equilibrium potential of I(ACh), or by the addition of d-tubocurarine or serotonin. These results suggest that the inhibitory interaction is attributable to inward current flow of cations through the activated P2XR- and nAChR-channels. Springer Netherlands 2006-05-30 2006-09 /pmc/articles/PMC2096647/ /pubmed/18404492 http://dx.doi.org/10.1007/s11302-006-9004-4 Text en © Springer Science + Business Media B.V. 2006
spellingShingle Original Article
Sorimachia, Masaru
Wakamoria, Minoru
Akaikeb, Norio
Excitatory effect of ATP on rat area postrema neurons
title Excitatory effect of ATP on rat area postrema neurons
title_full Excitatory effect of ATP on rat area postrema neurons
title_fullStr Excitatory effect of ATP on rat area postrema neurons
title_full_unstemmed Excitatory effect of ATP on rat area postrema neurons
title_short Excitatory effect of ATP on rat area postrema neurons
title_sort excitatory effect of atp on rat area postrema neurons
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2096647/
https://www.ncbi.nlm.nih.gov/pubmed/18404492
http://dx.doi.org/10.1007/s11302-006-9004-4
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