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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The role of the electrogenic sodium pump in the glutamate afterhyperpolarization of frog spinal cord.</title><author><name sortKey="Padjen, A L" sort="Padjen, A L" uniqKey="Padjen A" first="A L" last="Padjen">A L Padjen</name></author><author><name sortKey="Smith, P A" sort="Smith, P A" uniqKey="Smith P" first="P A" last="Smith">P A Smith</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">6308228</idno><idno type="pmc">1198976</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1198976</idno><idno type="RBID">PMC:1198976</idno><date when="1983">1983</date><idno type="wicri:Area/Pmc/Corpus">000208</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000208</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The role of the electrogenic sodium pump in the glutamate afterhyperpolarization of frog spinal cord.</title><author><name sortKey="Padjen, A L" sort="Padjen, A L" uniqKey="Padjen A" first="A L" last="Padjen">A L Padjen</name></author><author><name sortKey="Smith, P A" sort="Smith, P A" uniqKey="Smith P" first="P A" last="Smith">P A Smith</name></author></analytic><series><title level="j">The Journal of Physiology</title><idno type="ISSN">0022-3751</idno><idno type="eISSN">1469-7793</idno><imprint><date when="1983">1983</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Drug responses of isolated hemisected frog spinal cords were examined by means of the sucrose-gap technique. The glutamate-induced depolarizations (glu-d) of motoneurones (recorded from ventral roots), and primary afferents (recorded from dorsal roots), were followed by an afterhyperpolarization (glu-a.h.). The depolarization induced by DL-homocysteic acid (DLH) was only occasionally followed by an afterhyperpolarization (DLH-a.h.). The glu-a.h. on both roots persisted in the presence of tetrodotoxin (TTX, 0.1-1 microM), or Ringer solution containing 10 mM-Mg2+; 0.1 mM-Ca2+ or 2 mM-Mn2+; 0.2 mM-Ca2+. This indicated that the response was neither due to the release of endogenous neurally active substances nor to the activation of a Ca2+-sensitive K+ conductance. The glu-a.h. was reduced or blocked by K+-free Ringer solution, 3-acetylstrophanthin (3-Ac-Str; 1 microM) or Li+ ions, and was therefore attributed to the activity of the electrogenic Na+ pump. The duration of depolarization induced by glu or DLH was increased in the presence of K+-free Ringer solution, 1 microM 3-Ac-Str or Li ions. It is therefore suggested that the electrogenic Na+ pump may play a role in limiting the duration of depolarization induced by the action of excitatory amino acids. The re-admission of K+ ions to preparations which had been incubated in K+-free Ringer solution produced a transient hyperpolarization (K-a.h.) of the membrane potential of ventral roots which is also attributable to the activation of the electrogenic Na+ pump. Both the K-a.h. and the glu-a.h. were enhanced in Ca2+-free Ringer solution. It is therefore suggested that the Ca2+ ions may modulate the activity of the electrogenic pump in central nervous tissue.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Physiol</journal-id><journal-title>The Journal of Physiology</journal-title><issn pub-type="ppub">0022-3751</issn><issn pub-type="epub">1469-7793</issn></journal-meta><article-meta><article-id pub-id-type="pmid">6308228</article-id><article-id pub-id-type="pmc">1198976</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>The role of the electrogenic sodium pump in the glutamate afterhyperpolarization of frog spinal cord.</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Padjen</surname><given-names>A L</given-names></name></contrib><contrib contrib-type="author"><name><surname>Smith</surname><given-names>P A</given-names></name></contrib></contrib-group><pub-date pub-type="ppub"><month>3</month><year>1983</year></pub-date><volume>336</volume><fpage>433</fpage><lpage>451</lpage><abstract><p>Drug responses of isolated hemisected frog spinal cords were examined by means of the sucrose-gap technique. The glutamate-induced depolarizations (glu-d) of motoneurones (recorded from ventral roots), and primary afferents (recorded from dorsal roots), were followed by an afterhyperpolarization (glu-a.h.). The depolarization induced by DL-homocysteic acid (DLH) was only occasionally followed by an afterhyperpolarization (DLH-a.h.). The glu-a.h. on both roots persisted in the presence of tetrodotoxin (TTX, 0.1-1 microM), or Ringer solution containing 10 mM-Mg2+; 0.1 mM-Ca2+ or 2 mM-Mn2+; 0.2 mM-Ca2+. This indicated that the response was neither due to the release of endogenous neurally active substances nor to the activation of a Ca2+-sensitive K+ conductance. The glu-a.h. was reduced or blocked by K+-free Ringer solution, 3-acetylstrophanthin (3-Ac-Str; 1 microM) or Li+ ions, and was therefore attributed to the activity of the electrogenic Na+ pump. The duration of depolarization induced by glu or DLH was increased in the presence of K+-free Ringer solution, 1 microM 3-Ac-Str or Li ions. It is therefore suggested that the electrogenic Na+ pump may play a role in limiting the duration of depolarization induced by the action of excitatory amino acids. The re-admission of K+ ions to preparations which had been incubated in K+-free Ringer solution produced a transient hyperpolarization (K-a.h.) of the membrane potential of ventral roots which is also attributable to the activation of the electrogenic Na+ pump. Both the K-a.h. and the glu-a.h. were enhanced in Ca2+-free Ringer solution. It is therefore suggested that the Ca2+ ions may modulate the activity of the electrogenic pump in central nervous tissue.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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