PMID- 17610355 OWN - NLM STAT- MEDLINE DCOM- 20071129 LR - 20151119 IS - 0897-7151 (Print) IS - 0897-7151 (Linking) VI - 24 IP - 7 DP - 2007 Jul TI - Time window for voluntary exercise-induced increases in hippocampal neuroplasticity molecules after traumatic brain injury is severity dependent. PG - 1161-71 AB - We recently found that an exercise-induced increase in hippocampal brain-derived neurotrophic factor (BDNF) is dependent when exercise is initiated after traumatic brain injury (TBI). When voluntary exercise was delayed by 2 weeks after a mild fluid-percussion injury (FPI) in rats, an increase in BDNF and an improvement in behavioral outcome were observed. This suggests that following FPI there is a therapeutic window for the implementation of voluntary exercise. To determine if more severely injured animals require more time after TBI before voluntary exercise can increase neuroplasticity, adult male rats with a moderate lateral FPI or sham injury were housed with or without access to a running wheel from post-injury-day (PID) 0-6, 14-20 or 30-36. Rats with a mild injury only had access to the running wheel from PID 0-6 or 14-20. Rats were sacrificed at PID 7, 21, or 37. BDNF, synapsin I, and cyclic AMP response element binding protein (CREB) were analyzed within the ipsilateral hippocampus. Whereas BDNF levels significantly increased with exercise in the mild FPI rats that were exercised from PID 14 to 20, the moderate FPI rats only showed significant increases in BDNF when exercised from PID 30 to 36. In addition, moderate FPI rats that were allowed to exercise from PID 30 to 36 also exhibited significant increases in synapsin I and CREB. These results indicate that the time window for exercise-induced increases in BDNF, synapsin I, and CREB is dependent on injury severity. FAU - Griesbach, Grace S AU - Griesbach GS AD - Division of Neurosurgery, University of California-Los Angeles (UCLA), Los Angeles, California, USA. ggriesbach@mednet.ucla.edu FAU - Gomez-Pinilla, Fernando AU - Gomez-Pinilla F FAU - Hovda, David A AU - Hovda DA LA - eng GR - NS048535/NS/NINDS NIH HHS/United States GR - NS27544/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PL - United States TA - J Neurotrauma JT - Journal of neurotrauma JID - 8811626 RN - 0 (Biomarkers) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Cyclic AMP Response Element-Binding Protein) RN - 0 (Nerve Tissue Proteins) RN - 0 (Synapsins) SB - IM MH - Animals MH - Biomarkers/metabolism MH - Brain Injuries/metabolism/physiopathology/*rehabilitation MH - Brain-Derived Neurotrophic Factor/metabolism MH - Cyclic AMP Response Element-Binding Protein/metabolism MH - Exercise Therapy/*methods/standards MH - Hippocampus/*metabolism/physiopathology MH - Male MH - Nerve Regeneration/physiology MH - Nerve Tissue Proteins/*metabolism MH - Neuronal Plasticity/*physiology MH - Physical Conditioning, Animal/*physiology MH - Rats MH - Rats, Sprague-Dawley MH - Synapsins/metabolism MH - Time Factors MH - Treatment Outcome MH - Up-Regulation/physiology EDAT- 2007/07/06 09:00 MHDA- 2007/12/06 09:00 CRDT- 2007/07/06 09:00 PHST- 2007/07/06 09:00 [pubmed] PHST- 2007/12/06 09:00 [medline] PHST- 2007/07/06 09:00 [entrez] AID - 10.1089/neu.2006.0255 [doi] PST - ppublish SO - J Neurotrauma. 2007 Jul;24(7):1161-71. doi: 10.1089/neu.2006.0255.