Altered trkB neurotrophin receptor activation does not influence the N-methyl-D-aspartate receptor antagonist-mediated neurotoxicity in mouse posterior cingulate cortex.

摘要

Non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists produce toxic effects in the limbic cortex of rodent brain. NMDA antagonists also increase the expression of brain-derived neurotrophic factor (BDNF) mRNA in the same brain areas. The aim of this study was to investigate whether increased BDNF signalling plays a role in the NMDA-mediated toxic effect by using transgenic mice with modified BDNF signalling and HSP-70 expression as an indicator of toxicity. Neither the enhanced nor the reduced trkB activity influenced MK-801-induced neurotoxic effects in the posterior cingulate cortex of mouse brain, which indicates that increased BDNF production neither protects nor exacerbates neurotoxic effects of NMDA receptor antagonists.