PMID- 12383240 OWN - NLM STAT- MEDLINE DCOM- 20021204 LR - 20220310 IS - 0953-816X (Print) IS - 0953-816X (Linking) VI - 16 IP - 6 DP - 2002 Sep TI - Differential effects of acute and chronic exercise on plasticity-related genes in the rat hippocampus revealed by microarray. PG - 1107-16 AB - Studies were performed to determine the effects of acute and chronic voluntary periods of exercise on the expression of hippocampal genes. RNAs from rodents exposed to a running wheel for 3, 7 and 28 days were examined using a microarray with 1176 cDNAs expressed primarily in the brain. The expression of selected genes was quantified by Taqman RT-PCR or RNase protection assay. The largest up-regulation was observed in genes involved with synaptic trafficking (synapsin I, synaptotagmin and syntaxin); signal transduction pathways (Ca2+/calmodulin-dependent protein kinase II, CaM-KII; mitogen-activated/extracellular signal-regulated protein kinase, MAP-K/ERK I and II; protein kinase C, PKC-delta) or transcription regulators (cyclic AMP response element binding protein, CREB). Genes associated with the glutamatergic system were up-regulated (N-methyl-d-aspartate receptor, NMDAR-2A and NMDAR-2B and excitatory amino acid carrier 1, EAAC1), while genes related to the gamma-aminobutyric acid (GABA) system were down-regulated (GABAA receptor, glutamate decarboxylase GAD65). Brain-derived neurotrophic factor (BDNF) was the only trophic factor whose gene was consistently up-regulated at all timepoints. These results, together with the fact that most of the genes up-regulated have a recognized interaction with BDNF, suggest a central role for BDNF on the effects of exercise on brain plasticity. The temporal profile of gene expression seems to delineate a mechanism by which specific molecular pathways are activated after exercise performance. For example, the CaM-K signal system seems to be active during acute and chronic periods of exercise, while the MAP-K/ERK system seems more important during long-term exercise. FAU - Molteni, Raffaella AU - Molteni R AD - Division of Neurosurgery, UCLA Brain Injury Research Center and Department of Physiological Science, UCLA, 621 Charles E. Young Drive Los Angeles California 90095, USA. FAU - Ying, Zhe AU - Ying Z FAU - Gomez-Pinilla, Fernando AU - Gomez-Pinilla F LA - eng GR - NS 38978/NS/NINDS NIH HHS/United States GR - NS 39522/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - France TA - Eur J Neurosci JT - The European journal of neuroscience JID - 8918110 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (DNA, Complementary) RN - 0 (Nerve Growth Factors) RN - 0 (Nerve Tissue Proteins) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/biosynthesis/genetics MH - DNA, Complementary/analysis/genetics MH - Gene Expression Regulation/*genetics MH - Genes, Regulator/genetics MH - Hippocampus/*metabolism MH - MAP Kinase Signaling System/genetics MH - Male MH - Nerve Growth Factors/biosynthesis/genetics MH - Nerve Tissue Proteins/*biosynthesis/genetics MH - Neuronal Plasticity/*genetics MH - Neurons/*metabolism MH - Oligonucleotide Array Sequence Analysis MH - *Physical Conditioning, Animal MH - Protein Transport/genetics MH - Rats MH - Rats, Sprague-Dawley MH - Reaction Time/genetics MH - Synaptic Vesicles/genetics/metabolism MH - Up-Regulation/*genetics EDAT- 2002/10/18 04:00 MHDA- 2002/12/05 04:00 CRDT- 2002/10/18 04:00 PHST- 2002/10/18 04:00 [pubmed] PHST- 2002/12/05 04:00 [medline] PHST- 2002/10/18 04:00 [entrez] AID - 2158 [pii] AID - 10.1046/j.1460-9568.2002.02158.x [doi] PST - ppublish SO - Eur J Neurosci. 2002 Sep;16(6):1107-16. doi: 10.1046/j.1460-9568.2002.02158.x.