Changes in truncated trkB and p75 receptor expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment

Although numerous studies have examined the effects of neurotrophin treatme nt following spinal cord injury, few have examined the changes that occur i n the neurotrophin receptors following either such damage or neurotrophin t reatment. To determine what changes occur in neurotrophin receptor expressi on following spinal cord damage, adult rats received a midthoracic spinal c ord hemisection alone or in combination with intrathecal application of bra in-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). Using immun ohistochemical and in situ hybridization techniques, p75, trkA trkB, and tr kC receptor expression was examined throughout the spinal cord. Results sho wed that trkA, full-length trkB, and trkC receptors were not present in the lesion site but had a normal expression pattern ill uninjured parts of the spinal cord. In contrast, p75 receptor expression occurred on Schwann cell s throughout the lesion site. BDNF and NT-3 (but not saline) applied to the lesion site increased this expression. In addition, the truncated trkB rec eptor was expressed in the border between the lesion and intact spinal cord . Truncated trkB receptor expression was also increased throughout the whit e matter ipsilateral to the lesion and BDNF (but not NT-3 or saline) preven ted this increase. The study is the first to show changes in truncated trkB receptor expression that extend beyond the site of a spinal cord lesion an d is one of the first to show that BDNF and NT-3 affect Schwann cells and/o r p75 expression following spinal cord damage. These results indicate that changes in neurotrophin receptor expression following spinal cord injury co uld influence the availability of neurotrophins at the lesion site. In addi tion, neurotrophins may affect their own availability to damaged neurons by altering the expression of the p75 and truncated trkB receptor. (C) 2000 A cademic Press.