INCREASED EXPRESSION OF BDNF AND TRKB MESSENGER-RNA IN RAT FACIAL MOTONEURONS AFTER AXOTOMY

Motoneurons of the adult survive after axotomy even though they are de prived of putative target derived trophic factors. Alternative sources of trophic support may substitute. In this study we test the hypothes is that the immediate environment of the motoneuronal cell body or the cell body itself increases the production of trophic factors after ax onal injury. Using in situ hybridization (ISH) and reverse transcripti on-polymerase chain reaction (RT-PCR), we report that after axotomy, r at facial motoneurons increase the expression of mRNA for brain-derive d neurotrophic factor (BDNF) and its receptor trkB. After transection of the facial nerve, we measured a 2- to 4-fold increase in BDNF mRNA expression which had its onset between 3 and 8 h after injury. The BDN F mRNA levels peaked at similar to 1-2 days and gradually declined the reafter to return to contralateral levels within 7 days of injury. Wes tern blotting revealed a several-fold increase in BDNF as early as 24 h, which subsequently reached a maximum in similar to 5-7 days and was still sustained at 2 weeks post-axotomy. Using exon-specific primers, we determined that the increase in BDNF mRNA is largely due to an inc reased expression from the promoters of exons IV and III, and to a les ser extent from exons I and II. Analysing the mRNA expression for the BDNF receptor, trkB, we found a 2- to 3-fold increase in full-length t rkB mRNA expression starting 2 days after axotomy which lasted for 2-3 weeks. These findings suggest that BDNF might act locally on axotomiz ed motoneurons in an autocrine fashion, providing support for axotomiz ed motoneurons during the first weeks after axotomy.