PMID- 22527999 OWN - NLM STAT- MEDLINE DCOM- 20120907 LR - 20211021 IS - 1573-7365 (Electronic) IS - 0885-7490 (Print) IS - 0885-7490 (Linking) VI - 27 IP - 2 DP - 2012 Jun TI - Developmental traumatic brain injury decreased brain derived neurotrophic factor expression late after injury. PG - 167-73 LID - 10.1007/s11011-012-9309-7 [doi] AB - Pediatric traumatic brain injury (TBI) is a major cause of acquired cognitive dysfunction in children. Hippocampal Brain Derived Neurotrophic Factor (BDNF) is important for normal cognition. Little is known about the effects of TBI on BDNF levels in the developing hippocampus. We used controlled cortical impact (CCI) in the 17 day old rat pup to test the hypothesis that CCI would first increase rat hippocampal BDNF mRNA/protein levels relative to SHAM and Naive rats by post injury day (PID) 2 and then decrease BDNF mRNA/protein by PID14. Relative to SHAM, CCI did not change BDNF mRNA/protein levels in the injured hippocampus in the first 2 days after injury but did decrease BDNF protein at PID14. Surprisingly, BDNF mRNA decreased at PID 1, 3, 7 and 14, and BDNF protein decreased at PID 2, in SHAM and CCI hippocampi relative to Naive. In conclusion, TBI decreased BDNF protein in the injured rat pup hippocampus 14 days after injury. BDNF mRNA levels decreased in both CCI and SHAM hippocampi relative to Naive, suggesting that certain aspects of the experimental paradigm (such as craniotomy, anesthesia, and/or maternal separation) may decrease the expression of BDNF in the developing hippocampus. While BDNF is important for normal cognition, no inferences can be made regarding the cognitive impact of any of these factors. Such findings, however, suggest that meticulous attention to the experimental paradigm, and possible inclusion of a Naive group, is warranted in studies of BDNF expression in the developing brain after TBI. FAU - Schober, Michelle Elena AU - Schober ME AD - University of Utah, Salt Lake City, USA. michelle.schober@hsc.utah.edu FAU - Block, Benjamin AU - Block B FAU - Requena, Daniela F AU - Requena DF FAU - Hale, Merica A AU - Hale MA FAU - Lane, Robert H AU - Lane RH LA - eng GR - K12 HD001410/HD/NICHD NIH HHS/United States PT - Journal Article DEP - 20120425 PL - United States TA - Metab Brain Dis JT - Metabolic brain disease JID - 8610370 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Nerve Tissue Proteins) RN - 0 (RNA, Messenger) RN - 63231-63-0 (RNA) SB - IM MH - Animals MH - Brain/*growth & development MH - Brain Injuries/genetics/*metabolism MH - Brain-Derived Neurotrophic Factor/*biosynthesis/genetics MH - Hippocampus/injuries/metabolism MH - Male MH - Nerve Tissue Proteins/biosynthesis MH - RNA/biosynthesis/isolation & purification MH - RNA, Messenger/biosynthesis/genetics MH - Rats MH - Rats, Sprague-Dawley MH - Real-Time Polymerase Chain Reaction MH - Stereotaxic Techniques PMC - PMC3383795 MID - NIHMS376910 COIS- Disclosure of Conflict Of Interest The authors declare that they have no conflict of interest. EDAT- 2012/04/25 06:00 MHDA- 2012/09/08 06:00 PMCR- 2013/06/01 CRDT- 2012/04/25 06:00 PHST- 2011/12/10 00:00 [received] PHST- 2012/04/15 00:00 [accepted] PHST- 2012/04/25 06:00 [entrez] PHST- 2012/04/25 06:00 [pubmed] PHST- 2012/09/08 06:00 [medline] PHST- 2013/06/01 00:00 [pmc-release] AID - 10.1007/s11011-012-9309-7 [doi] PST - ppublish SO - Metab Brain Dis. 2012 Jun;27(2):167-73. doi: 10.1007/s11011-012-9309-7. Epub 2012 Apr 25.