Brain-Derived Neurotrophic Factor (BDNF) and Traumatic Brain Injury (Head and Spinal)

Neurotrophic factors. including brain-derived neurotrophic factor BDNF. may provide neuroprotection to the brain following injury. Previous studies have demonstrated that mRNA levels of BDNF and its receptor trkB are altered following experimental brain injury in the rat. The present study investigated whether these injury-induced alterations in BDNF and trkB mRNA levels lead to subsequent alterations in protein levels. In addition, activation of the BDNFtrkB signal transduction cascade was evaluated by measuring protein levels of a major downstream effector, extracellular signal regulate kinase, in its inactive ERK and activated form MAPK. Protein levels of BDNF, trkB, ERK, and MAPK were investigated in the cortex and hippocampus between 3 h and 5 d after lateral fluid percussion brain injury in the rat. BDNF protein levels were significantly increased in the bilateral hippocampus 48 h after injury. No significant alterations were observed in trkB, ERK, or MAPK protein levels after injury in either the cortex or hippocampus. These data suggest that the endogenous alterations in BDNF that occur after experimental brain injury are not activating the ERK pathway, but involvement of other pathways cannot be excluded.