Alterations in BDNF and trkB mRNA levels in the cerebral cortex following experimental brain trauma in rats

Recent studies have suggested that brain-derived neurotrophic factor (BNDF) and its receptor, trkB, may provide neuroprotection following injury to th e central nervous system. Conversely, other studies have implicated BDNF as a contributing factor to neurodegenerative events that occur following inj ury. In order to further investigate the role of BDNF in neuroprotection, w e subjected adult rats to a lateral fluid percussion (FP) injury of moderat e severity (2.0-2.1 atm) or sham injury. After survival periods of 1, 3, 6, 24, or 72 h, the brains were processed for the in situ hybridization local ization of BDNF and trkB mRNAs using S-35-labeled cRNA probes. Hybridizatio n levels were compared between injured and sham animals for regions of the cortex that were located within, adjacent to, and remote from the site of t he cortical contusion. BDNF mRNA levels were significantly decreased in the injured cortex at 72 h, increased in adjacent cortical areas at 3 h, and i ncreased bilaterally in the piriform cortex from 3 to 24 h post-FP injury. Expression of trkB mRNA was significantly decreased at all postinjury time- points in the injured cortex and at 24 h in the adjacent cortex. These resu lts demonstrate that, following lateral FP injury, BDNF and trkB mRNA level s are decreased in cortical regions that contain degenerating neurons, gene rally unchanged in adjacent regions, and increased in remote areas. Thus, i njury-induced decreases in the expression of BDNF and trkB may confer vulne rability to neurons within the cortical contusion.