Regulation of Trk receptors following contusion of the rat spinal cord

Neurotrophins function through high-affinity tyrosine kinase (Trk) receptor s 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 exam ined TrkA, TrkB, and TrkC mRNA expression in spinal cord and brain after sp inal contusion. At 1 day postinjury, all Trk receptor transcripts were down regulated at and around the site of injury, a situation that persisted thr ough 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 chronica lly injured spinal cords. Rostral and caudal to the injury site, TrkA, TrkB , and TrkC mRNA expression did not differ from that of uninjured control sp inal cords. Furthermore, no changes were observed in TrkB or TrkC expressio n in the axotomized corticospinal and rubrospinal neurons. These studies su ggest that loss of Trk receptors at the injury site may contribute to the e arly progressive cellular loss in injured spinal cords, while increased pre sence of truncated TrkB receptors in the chronic injured spinal cord may se quester and restrict BDNF availability to support axonal regeneration and n euronal survival. The persistence of Trk receptors on supraspinal neurons s uggests that neurotrophin application can support growth and survival in th e acute and chronic injury states. (C) 2001 Academic Press.