Brain-Derived Neurotrophic Factor (BDNF) and Traumatic Brain Injury (Head and Spinal)
Abstract
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 BDNF/trkB 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.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 1999
- Accession Number
- ADB246206
Entities
People
- Ramona R. Hicks
Organizations
- University of Kentucky