{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T03:22:04Z","timestamp":1761016924103,"version":"3.38.0"},"reference-count":29,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2011,12,23]],"date-time":"2011-12-23T00:00:00Z","timestamp":1324598400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Lysophosphatidic acid (<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>), an initiator of neuropathic pain, causes allodynia. However, few studies have evaluated the pharmacological profile of<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010induced pain. In this study, a<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010induced pain model was developed and pharmacologically characterized with clinically relevant drugs used for neuropathic pain, including antiepileptics, non\u2010steroidal anti\u2010inflammatory agents, analgesics, local anaesthetics\/antiarrhythmics and antidepressants. Gabapentin (1\u201330\u2009mg\/kg, p.o.) significantly reversed<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010induced allodynia, but neither indomethacin (30\u2009mg\/kg, p.o.) nor morphine (0.3\u20133\u2009mg\/kg, s.c.) did, which indicates that<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010induced pain consists mostly of neuropathic rather than inflammatory pain. Both pregabalin (0.3\u201310\u2009mg\/kg, p.o.) and \u03c9\u2010<jats:styled-content style=\"fixed-case\">CgTX MVIIA<\/jats:styled-content>(0.01\u20130.03\u2009\u03bcg\/mouse, i.t.) completely reversed<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010induced allodynia in a dose\u2010dependent manner. Lidocaine (1\u201330\u2009mg\/kg, s.c.), mexiletine (1\u201330\u2009mg\/kg, p.o.) and carbamazepine (10\u2013100\u2009mg\/kg, p.o.) significantly ameliorated<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010induced allodynia dose dependently. Milnacipran (30\u2009mg\/kg, i.p.) produced no significant analgesic effect in<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010induced allodynia. In<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010injected mice, expression of the \u03b12\u03b41 subunit of the voltage\u2010gated calcium channel (<jats:styled-content style=\"fixed-case\">VGCC<\/jats:styled-content>) was increased in the dorsal root ganglion (<jats:styled-content style=\"fixed-case\">DRG<\/jats:styled-content>) and spinal dorsal horn. Furthermore, the<jats:styled-content style=\"fixed-case\">VGCC<\/jats:styled-content>current was potentiated in both the<jats:styled-content style=\"fixed-case\">DRG<\/jats:styled-content>from<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010injected mice and<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>(1\u2009<jats:styled-content style=\"fixed-case\">\u03bcM<\/jats:styled-content>)\u2010treated<jats:styled-content style=\"fixed-case\">DRG<\/jats:styled-content>from saline\u2010injected mice, and the potentiated<jats:styled-content style=\"fixed-case\">VGCC<\/jats:styled-content>current was amended by treatment with gabapentin (100\u2009<jats:styled-content style=\"fixed-case\">\u03bcM<\/jats:styled-content>). The<jats:styled-content style=\"fixed-case\">LPA<\/jats:styled-content>\u2010induced pain model described here mimics aspects of the neuropathic pain state, including the sensitization of<jats:styled-content style=\"fixed-case\">VGCC<\/jats:styled-content>, and may be useful for the early assessment of drug candidates to treat neuropathic pain.<\/jats:p>","DOI":"10.1002\/j.1532-2149.2011.00096.x","type":"journal-article","created":{"date-parts":[[2011,12,25]],"date-time":"2011-12-25T00:09:17Z","timestamp":1324771757000},"page":"994-1004","source":"Crossref","is-referenced-by-count":11,"title":["Pharmacological characterization of lysophosphatidic acid\u2010induced pain with clinically relevant neuropathic pain drugs"],"prefix":"10.1002","volume":"16","author":[{"given":"K.","family":"Ogawa","sequence":"first","affiliation":[{"name":"Pain and Neurology, Discovery Research Laboratories Shionogi &amp; Co., Ltd Shiga Japan"},{"name":"Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences Kanazawa University Graduate School of Natural Science and Technology Ishikawa Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Takasu","sequence":"additional","affiliation":[{"name":"Pain and Neurology, Discovery Research Laboratories Shionogi &amp; Co., Ltd Shiga Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Shinohara","sequence":"additional","affiliation":[{"name":"Pain and Neurology, Discovery Research Laboratories Shionogi &amp; Co., Ltd Shiga Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"Yoneda","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences Kanazawa University Graduate School of Natural Science and Technology Ishikawa Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Kato","sequence":"additional","affiliation":[{"name":"Pain and Neurology, Discovery Research Laboratories Shionogi &amp; Co., Ltd Shiga Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2011,12,23]]},"reference":[{"doi-asserted-by":"publisher","key":"e_1_2_5_2_1","DOI":"10.1097\/00000539-199812000-00027"},{"key":"e_1_2_5_3_1","doi-asserted-by":"crossref","first-page":"1243","DOI":"10.1016\/S0022-3565(25)21283-6","article-title":"Selective N\u2010type neuronal voltage\u2010sensitive calcium channel blocker, SNX\u2010111, produces spinal antinociception in rat models of acute, persistent and neuropathic pain","volume":"279","author":"Bowersox SS","year":"1996","journal-title":"J Pharmacol Exp Ther"},{"doi-asserted-by":"publisher","key":"e_1_2_5_4_1","DOI":"10.1093\/bja\/87.1.12"},{"doi-asserted-by":"publisher","key":"e_1_2_5_5_1","DOI":"10.1212\/WNL.44.5.857"},{"doi-asserted-by":"publisher","key":"e_1_2_5_6_1","DOI":"10.1016\/S0006-8993(00)01965-X"},{"doi-asserted-by":"publisher","key":"e_1_2_5_7_1","DOI":"10.1016\/S0304-3959(03)00253-7"},{"doi-asserted-by":"publisher","key":"e_1_2_5_8_1","DOI":"10.1038\/nm1060"},{"doi-asserted-by":"publisher","key":"e_1_2_5_9_1","DOI":"10.1016\/S0304-3959(96)03231-9"},{"doi-asserted-by":"publisher","key":"e_1_2_5_10_1","DOI":"10.1016\/j.neuroscience.2008.02.031"},{"doi-asserted-by":"publisher","key":"e_1_2_5_11_1","DOI":"10.1016\/j.pain.2006.04.022"},{"doi-asserted-by":"publisher","key":"e_1_2_5_12_1","DOI":"10.1016\/j.brainres.2010.03.010"},{"doi-asserted-by":"publisher","key":"e_1_2_5_13_1","DOI":"10.1111\/j.1471-4159.2009.05987.x"},{"doi-asserted-by":"publisher","key":"e_1_2_5_14_1","DOI":"10.1016\/j.jpain.2005.09.008"},{"doi-asserted-by":"publisher","key":"e_1_2_5_15_1","DOI":"10.1254\/jphs.09139FP"},{"doi-asserted-by":"publisher","key":"e_1_2_5_16_1","DOI":"10.1124\/jpet.103.050781"},{"doi-asserted-by":"publisher","key":"e_1_2_5_17_1","DOI":"10.1016\/j.neures.2010.07.2281"},{"doi-asserted-by":"publisher","key":"e_1_2_5_18_1","DOI":"10.1016\/j.pain.2010.12.004"},{"doi-asserted-by":"publisher","key":"e_1_2_5_19_1","DOI":"10.1097\/00000539-200212000-00046"},{"doi-asserted-by":"publisher","key":"e_1_2_5_20_1","DOI":"10.1124\/jpet.103.060582"},{"doi-asserted-by":"publisher","key":"e_1_2_5_21_1","DOI":"10.1254\/jphs.FPJ03087X"},{"doi-asserted-by":"publisher","key":"e_1_2_5_22_1","DOI":"10.1016\/S0304-3959(01)00436-5"},{"doi-asserted-by":"publisher","key":"e_1_2_5_23_1","DOI":"10.1212\/WNL.51.2.609"},{"doi-asserted-by":"publisher","key":"e_1_2_5_24_1","DOI":"10.1213\/ane.0b013e318167889a"},{"doi-asserted-by":"publisher","key":"e_1_2_5_25_1","DOI":"10.1016\/j.neures.2009.09.948"},{"doi-asserted-by":"publisher","key":"e_1_2_5_26_1","DOI":"10.1016\/j.neuropharm.2007.08.013"},{"doi-asserted-by":"publisher","key":"e_1_2_5_27_1","DOI":"10.1016\/j.pain.2008.11.019"},{"doi-asserted-by":"publisher","key":"e_1_2_5_28_1","DOI":"10.1186\/1744-8069-4-11"},{"doi-asserted-by":"publisher","key":"e_1_2_5_29_1","DOI":"10.1016\/S0304-3959(99)00197-9"},{"doi-asserted-by":"publisher","key":"e_1_2_5_30_1","DOI":"10.1016\/j.brainres.2009.01.029"}],"container-title":["European Journal of Pain"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1002%2Fj.1532-2149.2011.00096.x","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1002\/j.1532-2149.2011.00096.x","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,16]],"date-time":"2025-03-16T16:14:38Z","timestamp":1742141678000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1002\/j.1532-2149.2011.00096.x"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2011,12,23]]},"references-count":29,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2012,8]]}},"alternative-id":["10.1002\/j.1532-2149.2011.00096.x"],"URL":"https:\/\/doi.org\/10.1002\/j.1532-2149.2011.00096.x","archive":["Portico"],"relation":{},"ISSN":["1090-3801","1532-2149"],"issn-type":[{"type":"print","value":"1090-3801"},{"type":"electronic","value":"1532-2149"}],"subject":[],"published":{"date-parts":[[2011,12,23]]}}}