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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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Formato: | Texto |
Lenguaje: | English |
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Springer Netherlands
2006
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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. |
format | Text |
id | pubmed-2096647 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
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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