PMID- 12921353 OWN - NLM STAT- MEDLINE DCOM- 20030926 LR - 20061115 IS - 1050-9631 (Print) IS - 1050-9631 (Linking) VI - 13 IP - 5 DP - 2003 TI - Rapid induction of BDNF expression in the hippocampus during immobilization stress challenge in adult rats. PG - 646-55 AB - Brain-derived neurotrophic factor (BDNF) is strongly expressed in the hippocampus, where it has been associated with memory processes. In the central nervous system, some learning processes, as well as brain insults, including stress, induce modifications in BDNF mRNA expression. Because stress and memory appear to share some neuronal pathways, we studied BDNF mRNA and BDNF peptide variations in response to short times of immobilization stress. Using an RNase protection assay, we demonstrated that short-time stress application induced a significant increase (at 60 min) in BDNF mRNA levels in the whole rat hippocampus. Changes in BDNF mRNA content appear to reflect increased expression of BDNF transcripts containing exons I, II, and III, that were also significantly modified at this time. The time course of stress-induced changes in BDNF transcript levels revealed that mRNA containing exon III was the first increased, significantly elevated by 15 min, attaining maximal levels at 60 min, as BDNF transcripts containing exons I and II. However, at longer times of stress (180 min), BDNF mRNA levels were decreased as well as mRNA containing exon IV. In situ hybridization analysis of discrete hippocampal layers demonstrated that BDNF mRNA expression increased as early as 15 min in most hippocampal regions, with no modification in the number of labeled cells. The same signal pattern, although less pronounced, was determined at 60 min, but at this time a significant increase in BDNF-positive cells was visualized in the CA3 layer. The peptide, measured by immunoassay, was significantly augmented after 180 min of stress exposure whereas at 300 min, levels were similar to those measured in control animals. These data suggest that rapid changes in BDNF expression may be part of a compensatory response to preserve hippocampal homeostasis or a form of neuronal plasticity to cope with new stimuli. FAU - Marmigere, Frederic AU - Marmigere F AD - Laboratoire de Plasticite Cerebrale, Universite de Montpellier, Montpellier, France. FAU - Givalois, Laurent AU - Givalois L FAU - Rage, Florence AU - Rage F FAU - Arancibia, Sandor AU - Arancibia S FAU - Tapia-Arancibia, Lucia AU - Tapia-Arancibia L LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Hippocampus JT - Hippocampus JID - 9108167 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (RNA, Messenger) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/*genetics/metabolism MH - Gene Expression Regulation/genetics MH - Hippocampus/cytology/*metabolism MH - Immunoassay MH - Male MH - Neurons/*metabolism MH - RNA, Messenger/metabolism MH - Rats MH - Rats, Sprague-Dawley MH - Reaction Time/*genetics MH - Restraint, Physical/psychology MH - Stress, Psychological/genetics/*metabolism MH - Up-Regulation/*genetics EDAT- 2003/08/19 05:00 MHDA- 2003/09/27 05:00 CRDT- 2003/08/19 05:00 PHST- 2003/08/19 05:00 [pubmed] PHST- 2003/09/27 05:00 [medline] PHST- 2003/08/19 05:00 [entrez] AID - 10.1002/hipo.10109 [doi] PST - ppublish SO - Hippocampus. 2003;13(5):646-55. doi: 10.1002/hipo.10109.