PMID- 10993692 OWN - NLM STAT- MEDLINE DCOM- 20001026 LR - 20091119 IS - 0014-4886 (Print) IS - 0014-4886 (Linking) VI - 165 IP - 2 DP - 2000 Oct TI - Changes in truncated trkB and p75 receptor expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment. PG - 327-41 AB - Although numerous studies have examined the effects of neurotrophin treatment following spinal cord injury, few have examined the changes that occur in the neurotrophin receptors following either such damage or neurotrophin treatment. To determine what changes occur in neurotrophin receptor expression following spinal cord damage, adult rats received a midthoracic spinal cord hemisection alone or in combination with intrathecal application of brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). Using immunohistochemical and in situ hybridization techniques, p75, trkA, trkB, and trkC receptor expression was examined throughout the spinal cord. Results showed that trkA, full-length trkB, and trkC receptors were not present in the lesion site but had a normal expression pattern in uninjured parts of the spinal cord. In contrast, p75 receptor expression occurred on Schwann cells throughout the lesion site. BDNF and NT-3 (but not saline) applied to the lesion site increased this expression. In addition, the truncated trkB receptor was expressed in the border between the lesion and intact spinal cord. Truncated trkB receptor expression was also increased throughout the white matter ipsilateral to the lesion and BDNF (but not NT-3 or saline) prevented 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 and is one of the first to show that BDNF and NT-3 affect Schwann cells and/or p75 expression following spinal cord damage. These results indicate that changes in neurotrophin receptor expression following spinal cord injury could influence the availability of neurotrophins at the lesion site. In addition, neurotrophins may affect their own availability to damaged neurons by altering the expression of the p75 and truncated trkB receptor. CI - Copyright 2000 Academic Press. FAU - King, V R AU - King VR AD - Neuroscience Section, Division of Biomedical Sciences, Queen Mary and Westfield College, Mile End Road, London, E1 4NS, United Kingdom. FAU - Bradbury, E J AU - Bradbury EJ FAU - McMahon, S B AU - McMahon SB FAU - Priestley, J V AU - Priestley JV LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Exp Neurol JT - Experimental neurology JID - 0370712 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Neurotrophin 3) RN - 0 (RNA, Messenger) RN - 0 (Receptor, Nerve Growth Factor) RN - EC 2.7.10.1 (Receptor, trkB) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/pharmacology/therapeutic use MH - Male MH - Neurotrophin 3/pharmacology/therapeutic use MH - RNA, Messenger/drug effects/metabolism MH - Rats MH - Rats, Wistar MH - Receptor, Nerve Growth Factor/drug effects/*metabolism MH - Receptor, trkB/drug effects/*metabolism MH - Spinal Cord/drug effects/*metabolism MH - Spinal Cord Injuries/drug therapy/*metabolism EDAT- 2000/09/20 11:00 MHDA- 2001/02/28 10:01 CRDT- 2000/09/20 11:00 PHST- 2000/09/20 11:00 [pubmed] PHST- 2001/02/28 10:01 [medline] PHST- 2000/09/20 11:00 [entrez] AID - S0014-4886(00)97480-6 [pii] AID - 10.1006/exnr.2000.7480 [doi] PST - ppublish SO - Exp Neurol. 2000 Oct;165(2):327-41. doi: 10.1006/exnr.2000.7480.