Loading…

ATP-mediated synaptic transmission and the relationship with glutamatergic neurons in hippocampus

We have reported that ATP mediates synaptic transmission in rat cultured hippocampal neurons (Jap.J.Pharmacol.,61, 67p, 1993). Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics...

Full description

Saved in:
Bibliographic Details
Published in:Japanese Journal of Pharmacology 1994, Vol.64 (suppl.1), p.143-143
Main Authors: Kazuhide Inoue, Ken Nakazawa, Shuichi Koizumi, Akira Takanaka
Format: Article
Language:Japanese
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page 143
container_issue suppl.1
container_start_page 143
container_title Japanese Journal of Pharmacology
container_volume 64
creator Kazuhide Inoue
Ken Nakazawa
Shuichi Koizumi
Akira Takanaka
description We have reported that ATP mediates synaptic transmission in rat cultured hippocampal neurons (Jap.J.Pharmacol.,61, 67p, 1993). Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics (namely fast and slow currents). Slow currents were reversibly blocked by suramin (100μM), reactive blue 2 (100μM) and α,β-methylene ATP(100μM), all ATP receptor antagonists. Fast currents were reversibly blocked by CNQX(30μM), a non-NMDA receptor blocker. An increase of internal Ca (「Ca」i) was evoked by the application of ATP(100μM) or glutamate (10μM), and blocked by suramin or CNQX. The cells which had only ATP receptors showed great increases in 「Ca」i by the stimulation of glutamate in the absence of tetrodotoxin (TTX, 3μM). The response was blocked by suramin (100μM). These data suggest that glutamatergic neurons connect with purinergic neurons.
format article
fullrecord <record><control><sourceid>medicalonline</sourceid><recordid>TN_cdi_medicalonline_journals_cf6jjopl_1994_0064s1_357_0143_0143480321</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>cf6jjopl_1994_0064s1_357_0143_0143480321</sourcerecordid><originalsourceid>FETCH-medicalonline_journals_cf6jjopl_1994_0064s1_357_0143_01434803213</originalsourceid><addsrcrecordid>eNqtTUsKwjAUzEJBUe_wLiAkTavtUkRx6cJ9eLbRpqQvIUkRb28Qj-BmBuY7Y0vOC7GtRFMv2CZGc-cF38taFs2S4eF23Y66M5h0B_FN6JNpIQWkOJocdgRIHaReQ9AWUxZibzy8TOrhaaeEY66GZy6RnkJ2wRDkhHctjn6KazZ_oI168-MVO59Pt-Pl-9qidWQNaTW4KVD2VfvYDYPzVommKRXnuzIKJau94qKUXyhrLgsh_zb0AbjfW90</addsrcrecordid><sourcetype>Publisher</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>ATP-mediated synaptic transmission and the relationship with glutamatergic neurons in hippocampus</title><source>ScienceDirect Journals</source><creator>Kazuhide Inoue ; Ken Nakazawa ; Shuichi Koizumi ; Akira Takanaka</creator><creatorcontrib>Kazuhide Inoue ; Ken Nakazawa ; Shuichi Koizumi ; Akira Takanaka ; Natl.Inst.Health Sciences ; Div.Pharmacol</creatorcontrib><description>We have reported that ATP mediates synaptic transmission in rat cultured hippocampal neurons (Jap.J.Pharmacol.,61, 67p, 1993). Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics (namely fast and slow currents). Slow currents were reversibly blocked by suramin (100μM), reactive blue 2 (100μM) and α,β-methylene ATP(100μM), all ATP receptor antagonists. Fast currents were reversibly blocked by CNQX(30μM), a non-NMDA receptor blocker. An increase of internal Ca (「Ca」i) was evoked by the application of ATP(100μM) or glutamate (10μM), and blocked by suramin or CNQX. The cells which had only ATP receptors showed great increases in 「Ca」i by the stimulation of glutamate in the absence of tetrodotoxin (TTX, 3μM). The response was blocked by suramin (100μM). These data suggest that glutamatergic neurons connect with purinergic neurons.</description><identifier>ISSN: 0021-5198</identifier><language>jpn</language><publisher>The Japanese Pharmacological Society</publisher><ispartof>Japanese Journal of Pharmacology, 1994, Vol.64 (suppl.1), p.143-143</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010</link.rule.ids></links><search><creatorcontrib>Kazuhide Inoue</creatorcontrib><creatorcontrib>Ken Nakazawa</creatorcontrib><creatorcontrib>Shuichi Koizumi</creatorcontrib><creatorcontrib>Akira Takanaka</creatorcontrib><creatorcontrib>Natl.Inst.Health Sciences</creatorcontrib><creatorcontrib>Div.Pharmacol</creatorcontrib><title>ATP-mediated synaptic transmission and the relationship with glutamatergic neurons in hippocampus</title><title>Japanese Journal of Pharmacology</title><description>We have reported that ATP mediates synaptic transmission in rat cultured hippocampal neurons (Jap.J.Pharmacol.,61, 67p, 1993). Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics (namely fast and slow currents). Slow currents were reversibly blocked by suramin (100μM), reactive blue 2 (100μM) and α,β-methylene ATP(100μM), all ATP receptor antagonists. Fast currents were reversibly blocked by CNQX(30μM), a non-NMDA receptor blocker. An increase of internal Ca (「Ca」i) was evoked by the application of ATP(100μM) or glutamate (10μM), and blocked by suramin or CNQX. The cells which had only ATP receptors showed great increases in 「Ca」i by the stimulation of glutamate in the absence of tetrodotoxin (TTX, 3μM). The response was blocked by suramin (100μM). These data suggest that glutamatergic neurons connect with purinergic neurons.</description><issn>0021-5198</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNqtTUsKwjAUzEJBUe_wLiAkTavtUkRx6cJ9eLbRpqQvIUkRb28Qj-BmBuY7Y0vOC7GtRFMv2CZGc-cF38taFs2S4eF23Y66M5h0B_FN6JNpIQWkOJocdgRIHaReQ9AWUxZibzy8TOrhaaeEY66GZy6RnkJ2wRDkhHctjn6KazZ_oI168-MVO59Pt-Pl-9qidWQNaTW4KVD2VfvYDYPzVommKRXnuzIKJau94qKUXyhrLgsh_zb0AbjfW90</recordid><startdate>1994</startdate><enddate>1994</enddate><creator>Kazuhide Inoue</creator><creator>Ken Nakazawa</creator><creator>Shuichi Koizumi</creator><creator>Akira Takanaka</creator><general>The Japanese Pharmacological Society</general><scope/></search><sort><creationdate>1994</creationdate><title>ATP-mediated synaptic transmission and the relationship with glutamatergic neurons in hippocampus</title><author>Kazuhide Inoue ; Ken Nakazawa ; Shuichi Koizumi ; Akira Takanaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-medicalonline_journals_cf6jjopl_1994_0064s1_357_0143_01434803213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>jpn</language><creationdate>1994</creationdate><toplevel>online_resources</toplevel><creatorcontrib>Kazuhide Inoue</creatorcontrib><creatorcontrib>Ken Nakazawa</creatorcontrib><creatorcontrib>Shuichi Koizumi</creatorcontrib><creatorcontrib>Akira Takanaka</creatorcontrib><creatorcontrib>Natl.Inst.Health Sciences</creatorcontrib><creatorcontrib>Div.Pharmacol</creatorcontrib><jtitle>Japanese Journal of Pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kazuhide Inoue</au><au>Ken Nakazawa</au><au>Shuichi Koizumi</au><au>Akira Takanaka</au><aucorp>Natl.Inst.Health Sciences</aucorp><aucorp>Div.Pharmacol</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ATP-mediated synaptic transmission and the relationship with glutamatergic neurons in hippocampus</atitle><jtitle>Japanese Journal of Pharmacology</jtitle><date>1994</date><risdate>1994</risdate><volume>64</volume><issue>suppl.1</issue><spage>143</spage><epage>143</epage><pages>143-143</pages><issn>0021-5198</issn><abstract>We have reported that ATP mediates synaptic transmission in rat cultured hippocampal neurons (Jap.J.Pharmacol.,61, 67p, 1993). Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics (namely fast and slow currents). Slow currents were reversibly blocked by suramin (100μM), reactive blue 2 (100μM) and α,β-methylene ATP(100μM), all ATP receptor antagonists. Fast currents were reversibly blocked by CNQX(30μM), a non-NMDA receptor blocker. An increase of internal Ca (「Ca」i) was evoked by the application of ATP(100μM) or glutamate (10μM), and blocked by suramin or CNQX. The cells which had only ATP receptors showed great increases in 「Ca」i by the stimulation of glutamate in the absence of tetrodotoxin (TTX, 3μM). The response was blocked by suramin (100μM). These data suggest that glutamatergic neurons connect with purinergic neurons.</abstract><pub>The Japanese Pharmacological Society</pub></addata></record>
fulltext fulltext
identifier ISSN: 0021-5198
ispartof Japanese Journal of Pharmacology, 1994, Vol.64 (suppl.1), p.143-143
issn 0021-5198
language jpn
recordid cdi_medicalonline_journals_cf6jjopl_1994_0064s1_357_0143_0143480321
source ScienceDirect Journals
title ATP-mediated synaptic transmission and the relationship with glutamatergic neurons in hippocampus
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-25T06%3A27%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-medicalonline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ATP-mediated%20synaptic%20transmission%20and%20the%20relationship%20with%20glutamatergic%20neurons%20in%20hippocampus&rft.jtitle=Japanese%20Journal%20of%20Pharmacology&rft.au=Kazuhide%20Inoue&rft.aucorp=Natl.Inst.Health%20Sciences&rft.date=1994&rft.volume=64&rft.issue=suppl.1&rft.spage=143&rft.epage=143&rft.pages=143-143&rft.issn=0021-5198&rft_id=info:doi/&rft_dat=%3Cmedicalonline%3Ecf6jjopl_1994_0064s1_357_0143_0143480321%3C/medicalonline%3E%3Cgrp_id%3Ecdi_FETCH-medicalonline_journals_cf6jjopl_1994_0064s1_357_0143_01434803213%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/&rfr_iscdi=true