{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T00:42:12Z","timestamp":1789432932377,"version":"build-2803163510"},"reference-count":34,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,3,6]],"date-time":"2012-03-06T00:00:00Z","timestamp":1330992000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Research Grants Council of Hong Kong","award":["HKBU260008"],"award-info":[{"award-number":["HKBU260008"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2012,4]]},"abstract":"Abstract<\/jats:title>\n \n Visceral hyperalgesia is a multifactorial gastrointestinal disorder which featured with alterations of abdominal motility and\/or gut sensitivity, and is believed to be triggered by environmental stressor or psychological factors. However, its etiology remains incompletely understood. In this study, we aimed to investigate whether nerve growth factor (\n NGF<\/jats:styled-content>\n )\u2010mediated neuronal plasticity is involved in neonatal maternal separation (\n NMS<\/jats:styled-content>\n )\u2010induced visceral hypersensitivity in adult rats, and whether\n NGF<\/jats:styled-content>\n antagonist can attenuate or block such development. In our experiments, animals subjected to\n NMS<\/jats:styled-content>\n were developed with visceral hyperalgesia at age of 8 weeks. The threshold for visceral pain among these\n NMS<\/jats:styled-content>\n rats was remarkably lowered than that of the normal handling (\n NH<\/jats:styled-content>\n ) rats; however, the expression levels of\n NGF<\/jats:styled-content>\n ,\n c\u2010fos<\/jats:italic>\n , calcitonin gene\u2010related peptide (\n CGRP<\/jats:styled-content>\n ),\n S<\/jats:styled-content>\n ubstance\n P<\/jats:styled-content>\n , and tyrosine kinases\n A<\/jats:styled-content>\n (\n T<\/jats:styled-content>\n rk\n A<\/jats:styled-content>\n ) were notably elevated in lumbosacral spinal cord and\/or dorsal root ganglion (\n DRG<\/jats:styled-content>\n ) when comparing to those of the\n NH<\/jats:styled-content>\n rats. Further, as intra\u2010peritoneal administration of\n NGF<\/jats:styled-content>\n (10\u2009\u03bcl at 1\u2009\u03bcg\/kg\/day) was given to\n NH<\/jats:styled-content>\n rats during neonatal period, effects that comparable to\n NMS<\/jats:styled-content>\n induction were observed in the adulthood. In contrast, when\n NMS<\/jats:styled-content>\n rats were treated with\n NGF<\/jats:styled-content>\n antagonist\n K<\/jats:styled-content>\n 252a (10\u2009\u03bcl\/day from postnatal days 2\u201314), which acts against tyrosine kinases, the neonatal stress\u2010induced down\u2010shifted visceral pain threshold was restored and neuronal activation, specifically\n NGF<\/jats:styled-content>\n and neuropeptide production, was attenuated. In conclusion, our data strongly suggest that\n NGF<\/jats:styled-content>\n triggers neuronal plasticity and plays a crucial role in\n NMS<\/jats:styled-content>\n \u2010induced visceral hypersensitivity in which\n NGF<\/jats:styled-content>\n antagonism provides positive inhibition via blocking the tyrosine phosphorylation of\n T<\/jats:styled-content>\n rk\n A<\/jats:styled-content>\n .\n <\/jats:p>","DOI":"10.1016\/j.ejpain.2011.07.005","type":"journal-article","created":{"date-parts":[[2011,8,18]],"date-time":"2011-08-18T22:56:57Z","timestamp":1313708217000},"page":"463-472","source":"Crossref","is-referenced-by-count":36,"title":["Nerve growth factor\u2010mediated neuronal plasticity in spinal cord contributes to neonatal maternal separation\u2010induced visceral hypersensitivity in rats"],"prefix":"10.1002","volume":"16","author":[{"given":"S.W.","family":"Tsang","sequence":"first","affiliation":[{"name":"School of Chinese Medicine Hong Kong Baptist University Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Zhao","sequence":"additional","affiliation":[{"name":"School of Chinese Medicine Hong Kong Baptist University Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Wu","sequence":"additional","affiliation":[{"name":"Faculty of Medicine The Chinese University of Hong Kong Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.J.Y.","family":"Sung","sequence":"additional","affiliation":[{"name":"Faculty of Medicine The Chinese University of Hong Kong Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Z.\u2010X.","family":"Bian","sequence":"additional","affiliation":[{"name":"School of Chinese Medicine Hong Kong Baptist University Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,3,6]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(19)31674-9"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3959(02)00046-5"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2004.05.019"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2003.024174"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(90)90732-O"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(95)93922-K"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2007.03.047"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2007.07.055"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00240.2001"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-08-02933.1998"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.46.5.670"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1572-0241.2003.07156.x"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.72.121801.161629"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(02)00908-X"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.3306916"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ne.19.030196.001445"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.13-05-02136.1993"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1038\/337362a0"},{"issue":"5","key":"e_1_2_6_20_1","doi-asserted-by":"crossref","first-page":"1886","DOI":"10.4049\/jimmunol.144.5.1886","article-title":"The role of mast cell degranulation products in mast cell hyperplasia. 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