{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,25]],"date-time":"2025-10-25T12:07:19Z","timestamp":1761394039659},"reference-count":41,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2011,5,25]],"date-time":"2011-05-25T00:00:00Z","timestamp":1306281600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2011,7]]},"abstract":"<jats:sec><jats:label \/><jats:p><jats:italic>J. Neurochem.<\/jats:italic>(2011)<jats:bold>118<\/jats:bold>, 256\u2013265.<\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>We have previously demonstrated that lysophosphatidic acid (LPA) production in the spinal cord following partial sciatic nerve injury (SCNI) and its signaling initiate neuropathic pain. In order to examine whether LPA production depends on the intense nociceptive signal, we have attempted to see suppression by pre\u2010emptive treatment with centrally administered morphine, which mainly inhibits nociceptive signal at the level of spinal cord. In the present study, we developed a quantitative mass spectrometry assay to simultaneously analyze several species of lysophosphatidyl choline (LPC). The levels of 16:0\u2010, 18:0\u2010 and 18:1\u2010LPC in the spinal cord and dorsal root were maximally increased at 75\u2003min after SCNI and then declined, as LPC is converted to LPA by autotaxin (ATX). In<jats:italic>atx<\/jats:italic><jats:sup><jats:italic>+\/\u2212<\/jats:italic><\/jats:sup>\u2010mice, on the other hand, these levels were similar to wild\u2010type mice at 75\u2003min, but maximal at 120\u2003min, suggesting that this difference is partly due to the low conversion of LPC to LPA in<jats:italic>atx<\/jats:italic><jats:sup><jats:italic>+\/\u2212<\/jats:italic><\/jats:sup>\u2010mice. When morphine was centrally administered before SCNI, the injury\u2010induced increase of LPC was completely abolished. These results suggest that LPC (or LPA) is produced by injury\u2010induced nociceptive signal, which is effectively and pre\u2010emptively suppressed by central morphine, possibly through known descending anti\u2010nociceptive pathways.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1471-4159.2011.07297.x","type":"journal-article","created":{"date-parts":[[2011,5,4]],"date-time":"2011-05-04T09:04:26Z","timestamp":1304499866000},"page":"256-265","source":"Crossref","is-referenced-by-count":15,"title":["Pre\u2010emptive morphine treatment abolishes nerve injury\u2010induced lysophospholipid synthesis in mass spectrometrical analysis"],"prefix":"10.1111","volume":"118","author":[{"given":"Jun","family":"Nagai","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Ueda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2011,5,25]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbalip.2008.06.005"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/cne.901870304"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1139\/y59-099"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.010909.105753"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1124\/pr.110.003111"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/B0-443-07287-6\/50012-6"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1044-0305(03)00064-3"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm1060"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-4-6"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2008.05725.x"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2010.03.056"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.prostaglandins.2009.02.002"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2009.05987.x"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-5-64"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2010.06955.x"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.109.164830"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3959(98)00045-1"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2533"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1002\/rcm.4484"},{"key":"e_1_2_7_21_1","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-6-78"},{"key":"e_1_2_7_22_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cca.2009.04.025"},{"key":"e_1_2_7_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pneurobio.2007.06.005"},{"key":"e_1_2_7_24_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2008.11.010"},{"key":"e_1_2_7_25_1","doi-asserted-by":"publisher","DOI":"10.1002\/mas.10061"},{"key":"e_1_2_7_26_1","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-1-19"},{"key":"e_1_2_7_27_1","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(93)91284-S"},{"key":"e_1_2_7_28_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(71)90122-1"},{"key":"e_1_2_7_29_1","doi-asserted-by":"publisher","DOI":"10.1038\/nn1992"},{"key":"e_1_2_7_30_1","doi-asserted-by":"publisher","DOI":"10.1158\/1055-9965.1185.13.7"},{"key":"e_1_2_7_31_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jchromb.2006.03.006"},{"key":"e_1_2_7_32_1","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.D400010-JLR200"},{"key":"e_1_2_7_33_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M605142200"},{"key":"e_1_2_7_34_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1388-1981(02)00133-6"},{"key":"e_1_2_7_35_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5541-09.2010"},{"key":"e_1_2_7_36_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2005.06.003"},{"key":"e_1_2_7_37_1","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-4-11"},{"key":"e_1_2_7_38_1","doi-asserted-by":"publisher","DOI":"10.2217\/clp.10.88"},{"key":"e_1_2_7_39_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jasms.2010.03.038"},{"key":"e_1_2_7_40_1","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.jbchem.a021715"},{"key":"e_1_2_7_41_1","doi-asserted-by":"crossref","first-page":"259","DOI":"10.1016\/S1016-8478(23)10716-3","article-title":"A synaptic model for pain: long\u2010term potentiation in the anterior cingulate cortex","volume":"23","author":"Zhuo M.","year":"2007","journal-title":"Mol. 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