{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T17:31:29Z","timestamp":1760203889501},"reference-count":44,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2009,2,2]],"date-time":"2009-02-02T00:00:00Z","timestamp":1233532800000},"content-version":"vor","delay-in-days":1920,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2003,11]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Whole\u2010cell patch recordings were made from substantia gelatinosa (SG) neurons in transverse lumbar spinal cord slices of 15\u2010 to 30\u2010day\u2010old rats.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Endomorphin 1 (EM\u20101) or EM\u20102 (10 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) hyperpolarized or induced an outward current in 26 of the 66 SG neurons. The <jats:italic>I<\/jats:italic>\u2013<jats:italic>V<\/jats:italic> relationship showed that the peptide activates an inwardly rectifying K<jats:sup>+<\/jats:sup> current.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>EM\u20101 or EM\u20102 (0.3\u201310 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) suppressed short\u2010latency excitatory postsynaptic currents (EPSCs) and long\u2010latency inhibitory postsynaptic currents (IPSCs) in nearly all SG neurons tested or short\u2010latency IPSCs in six of the 10 SG neurons. [Met<jats:sup>5<\/jats:sup>] enkephalin or [<jats:sc>D<\/jats:sc>\u2010Ala<jats:sup>2<\/jats:sup>, <jats:italic>N<\/jats:italic>\u2010Me\u2010Phe<jats:sup>4<\/jats:sup>, Gly<jats:sup>5<\/jats:sup>\u2010ol]\u2010enkephalin (DAMGO) (1\u201310 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) depressed EPSCs and IPSCs. EM\u20101 or EM\u20102 depressed synaptic responses without causing a significant change in holding currents or inward currents induced by glutamate.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Glutamate also evoked a short\u2010latency outward current in five SG neurons or a biphasic current in two neurons; the outward current was blocked by tetrodotoxin (TTX, 0.3 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) or bicuculline (10 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>). EM\u20101 or DAMGO (1 or 5 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) attenuated the glutamate\u2010evoked outward or biphasic currents in four of the seven SG neurons.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>EM\u20101 (1 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) reduced the frequency, but not the amplitude of miniature EPSCs or miniature IPSCs.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Naloxone (1 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) or the selective <jats:italic>\u03bc<\/jats:italic>\u2010opioid receptor antagonist <jats:italic>\u03b2<\/jats:italic>\u2010funaltrexamine (<jats:italic>\u03b2<\/jats:italic>\u2010FNA, 25 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) antagonized the action of EM; EM\u2010induced hyperpolarizations persisted in the presence of the <jats:italic>\u03ba<\/jats:italic>\u2010opioid receptor antagonist (nor\u2010binaltorphimine dihydrochloride, 1 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) and\/or <jats:italic>\u03c3<\/jats:italic>\u2010opioid receptor antagonist (naltrindole hydrochloride, 1 <jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>It may be concluded that EM acting on <jats:italic>\u03bc<\/jats:italic>\u2010opioid receptors hyperpolarizes a population of SG neurons by activating an inwardly rectifying K<jats:sup>+<\/jats:sup> current, and attenuates excitatory and inhibitory synaptic currents evoked in a population of SG neurons, probably by a presynaptic site of action.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2003) <jats:bold>140<\/jats:bold>, 1088\u20131096. doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0705534\">10.1038\/sj.bjp.0705534<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0705534","type":"journal-article","created":{"date-parts":[[2003,11,12]],"date-time":"2003-11-12T20:52:59Z","timestamp":1068670379000},"page":"1088-1096","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Effects of endomorphin on substantia gelatinosa neurons in rat spinal cord slices"],"prefix":"10.1111","volume":"140","author":[{"given":"Su\u2010Ying","family":"Wu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshitaka","family":"Ohtubo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G Cristina","family":"Brailoiu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nae J","family":"Dun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2009,2,2]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0165-3806(90)90128-L"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(91)91134-M"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(90)91519-M"},{"key":"e_1_2_7_5_1","first-page":"717","article-title":"The substantia gelatinosa of the spinal cord","volume":"103","author":"CERVERO F.","year":"1980","journal-title":"J. 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