title: Regulation of Trk receptors following contusion of the rat spinal cord.
abstract: Neurotrophins function through high-affinity tyrosine kinase (Trk) receptors to promote growth and survival of cells in the injured nervous system. To investigate the role of Trk receptors in the adult nervous system, we examined TrkA, TrkB, and TrkC mRNA expression in spinal cord and brain after spinal contusion. At 1 day postinjury, all Trk receptor transcripts were down regulated at and around the site of injury, a situation that persisted through the first week. By 42 days, Trk expression was absent only within the cavity. In addition, truncated TrkB expression was substantially increased in ependymal cells and astrocytes surrounding the lesion cavity of chronically injured spinal cords. Rostral and caudal to the injury site, TrkA, TrkB, and TrkC mRNA expression did not differ from that of uninjured control spinal cords. Furthermore, no changes were observed in TrkB or TrkC expression in the axotomized corticospinal and rubrospinal neurons. These studies suggest that loss of Trk receptors at the injury site may contribute to the early progressive cellular loss in injured spinal cords, while increased presence of truncated TrkB receptors in the chronic injured spinal cord may sequester and restrict BDNF availability to support axonal regeneration and neuronal survival. The persistence of Trk receptors on supraspinal neurons suggests that neurotrophin application can support growth and survival in the acute and chronic injury states.
authors.affiliation: Center for Developmental Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, Texas 75235-9133, USA. dliebl@miami.edu
authors.forename: D J
authors.initials: DJ
authors.lastname: Liebl
authors.forename: W
authors.initials: W
authors.lastname: Huang
authors.forename: W
authors.initials: W
authors.lastname: Young
authors.forename: L F
authors.initials: LF
authors.lastname: Parada
mesh_terms: D000818:Animals; D001921:Brain / Q000166:cytology / Q000378:metabolism; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D017403:In Situ Hybridization; D009414:Nerve Growth Factors / Q000096:biosynthesis / Q000235:genetics; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000378:metabolism; D051381:Rats; D020318:Rats, Long-Evans; D020917:Receptor, trkA / Q000235:genetics / Q000378:metabolism*; D020813:Receptor, trkB / Q000235:genetics / Q000378:metabolism*; D020812:Receptor, trkC / Q000235:genetics / Q000378:metabolism*; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology
chemical_list: D009414:Nerve Growth Factors; D012333:RNA, Messenger; D020917:Receptor, trkA; D020813:Receptor, trkB; D020812:Receptor, trkC