PMID- 12759116 OWN - NLM STAT- MEDLINE DCOM- 20040107 LR - 20190712 IS - 0091-3057 (Print) IS - 0091-3057 (Linking) VI - 75 IP - 1 DP - 2003 Apr TI - Noradrenergic and serotonergic blockade inhibits BDNF mRNA activation following exercise and antidepressant. PG - 81-8 AB - Antidepressants and physical exercise have been shown to increase the transcription of hippocampal brain-derived neurotrophic factor (BDNF). Much evidence regarding the initial actions of antidepressant medications as well as exercise leads to the hypothesis that noradrenergic (NE) and/or serotonergic (5-HT) activation is a key element in the BDNF transcriptional elevation common to both interventions. Currently, we used short-term beta-adrenergic, 5-HT(1A), or 5-HT(2A/C) receptor blockade to characterize the influence of NE and 5-HT systems on BDNF transcription during physical exercise and antidepressant treatment. In situ hybridization revealed that beta-adrenergic blockade significantly blunted the BDNF mRNA elevations due to exercise, and also inhibited the modest elevations in the CA3 and dentate gyrus following short-term treatment with tranylcypromine. In contrast, 5-HT(2A/C) blockade only minimally altered exercise-induced BDNF mRNA levels, but inhibited up-regulation of BDNF transcription via tranylcypromine. Finally, 5-HT(1A) blockade did not inhibit exercise-induced BDNF mRNA elevations, but significantly enhanced levels above those achieved with exercise alone in the CA4. These results suggest that NE activation via beta-adrenergic receptors may be essential for both exercise and antidepressant-induced BDNF regulation. 5-HT(1A) and 5-HT(2A/C) activation, on the other hand, appear to be most important for antidepressant-induced BDNF regulation, but may also participate significantly in exercise-induced regulation in the CA4. FAU - Ivy, A S AU - Ivy AS AD - Department of Biological Sciences, California State University Los Angeles, 5151 State University Drive, Los Angeles, CA 90032, USA. FAU - Rodriguez, F G AU - Rodriguez FG FAU - Garcia, C AU - Garcia C FAU - Chen, M J AU - Chen MJ FAU - Russo-Neustadt, A A AU - Russo-Neustadt AA LA - eng GR - MH 59776/MH/NIMH 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 - United States TA - Pharmacol Biochem Behav JT - Pharmacology, biochemistry, and behavior JID - 0367050 RN - 0 (Adrenergic Antagonists) RN - 0 (Adrenergic beta-Antagonists) RN - 0 (Antidepressive Agents) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Piperazines) RN - 0 (Pyridines) RN - 0 (RNA, Messenger) RN - 0 (Serotonin Antagonists) RN - 3E3V44J4Z9 (Tranylcypromine) RN - 71IH826FEG (N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide) RN - 97F9DE4CT4 (Ketanserin) RN - 9Y8NXQ24VQ (Propranolol) RN - X4W3ENH1CV (Norepinephrine) SB - IM MH - Adrenergic Antagonists/*pharmacology MH - Adrenergic beta-Antagonists/pharmacology MH - Animals MH - Antidepressive Agents/*pharmacology MH - Biotransformation/drug effects MH - Brain-Derived Neurotrophic Factor/*biosynthesis MH - Hippocampus/drug effects/metabolism MH - In Situ Hybridization MH - Ketanserin/pharmacology MH - Male MH - Norepinephrine/*antagonists & inhibitors MH - Physical Exertion/*physiology MH - Piperazines/pharmacology MH - Propranolol/pharmacology MH - Pyridines/pharmacology MH - RNA, Messenger/biosynthesis MH - Rats MH - Rats, Sprague-Dawley MH - Running/physiology/psychology MH - Serotonin Antagonists/*pharmacology MH - Tranylcypromine/pharmacology MH - Up-Regulation/drug effects EDAT- 2003/05/22 05:00 MHDA- 2004/01/08 05:00 CRDT- 2003/05/22 05:00 PHST- 2003/05/22 05:00 [pubmed] PHST- 2004/01/08 05:00 [medline] PHST- 2003/05/22 05:00 [entrez] AID - S0091305703000443 [pii] AID - 10.1016/s0091-3057(03)00044-3 [doi] PST - ppublish SO - Pharmacol Biochem Behav. 2003 Apr;75(1):81-8. doi: 10.1016/s0091-3057(03)00044-3.