title: Galectin-1 is involved in the potentiation of neuropathic pain in the dorsal horn.
abstract: Galectin-1 is one of the endogenous-galactoside-binding lectins, suggested to be involved in a variety of functions, such as neurite outgrowth, synaptic connectivity, cell proliferation and apoptosis. This protein is expressed in the dorsal root ganglion (DRG) and the spinal cord in the developing and adult rats, especially intensely in small DRG neurons. In the present study, we examined whether galectin-1 is colocalized with TrkA or c-Ret mRNA in small DRG neurons and the effect of axotomy on the expression of galectin-1 in the spinal cord. About 20% of the DRG neurons showed intense galectin-1-immunoreactivity (IR). Of the intensely galectin-1-IR DRG neurons, 93.9% displayed c-Ret mRNA positive signals. On the other hand, only 6.8% displayed TrkA mRNA positive signals. Galectin-1-IR was increased in the dorsal horn at 1 to 2 weeks after axotomy. Intrathecal administration of anti-recombinant human galectin-1 antibody (anti-rhGAL-1 Ab) partially but significantly attenuated the upregulation of substance P receptor (SPR) in the spinal dorsal horn and the mechanical hypersensitivity induced by the peripheral nerve injury. These data suggest that endogenous galectin-1 may potentiate neuropathic pain after the peripheral nerve injury at least partly by increasing SPR in the dorsal horn.
authors.affiliation: Department of Anatomy and Neurobiology, Wakayama Medical University, Kimiidera 811-1, Wakayama 640-0012, Japan. imika@js9.so-net.ne.jp
authors.forename: Hiroki
authors.initials: H
authors.lastname: Imbe
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Okamoto
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Kadoya
authors.forename: Hidenori
authors.initials: H
authors.lastname: Horie
authors.forename: Emiko
authors.initials: E
authors.lastname: Senba
mesh_terms: D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D019771:Axotomy / Q000379:methods; D001522:Behavior, Animal; D015153:Blotting, Western / Q000379:methods; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D002452:Cell Count; D007839:Functional Laterality; D037483:Galectin 1 / Q000276:immunology / Q000502:physiology*; D005727:Ganglia, Spinal / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization / Q000379:methods; D008026:Ligation / Q000379:methods; D008124:Locomotion / Q000502:physiology; D008161:Lumbosacral Region; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D010146:Pain / Q000378:metabolism* / Q000503:physiopathology; D017288:Pain Threshold / Q000187:drug effects; D020671:Posterior Horn Cells / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism; D051096:Proto-Oncogene Proteins c-ret; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics / Q000378:metabolism; D020917:Receptor, trkA; D012584:Sciatic Nerve / Q000293:injuries / Q000378:metabolism / Q000503:physiopathology; D013116:Spinal Cord / Q000166:cytology* / Q000378:metabolism; D018709:Statistics, Nonparametric; D013373:Substance P / Q000378:metabolism; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D000906:Antibodies; D002352:Carrier Proteins; D037483:Galectin 1; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D013373:Substance P; D051096:Proto-Oncogene Proteins c-ret; D020794:Receptor Protein-Tyrosine Kinases; D020917:Receptor, trkA; C495001:Ret protein, rat