PMID- 11102572 OWN - NLM STAT- MEDLINE DCOM- 20010301 LR - 20190614 IS - 0006-8993 (Print) IS - 0006-8993 (Linking) VI - 885 IP - 2 DP - 2000 Dec 8 TI - Corticosterone inhibits generation of long-term potentiation in rat hippocampal slice: involvement of brain-derived neurotrophic factor. PG - 182-91 AB - In the present study, the effect of corticosterone (CORT) on the generation of long-term potentiation (LTP) and its underlying mechanism involving neurotrophin gene expression in CA1 synapses of rat hippocampal slice were examined. Our experimental results showed incubation of hippocampal slice with CORT for 3 h had no effect on either the slope or amplitude of excitatory postsynaptic potentials (EPSP) evoked in hippocampal CA1 pyramidal dentrites, indicating no marked change in basal synaptic transmission. However, when tetanic stimulation (100 pulses, 100 Hz) was delivered to the Schaffer collateral pathway, CORT application significantly attenuated the tetanus-induced increases of both EPSP slope and amplitude, demonstrating an inhibitory effect of CORT on LTP generation. In addition, CORT treatment significantly reduced both slope and amplitude ratios of the second evoked EPSP to the first one when paired-pulse facilitation (PPF) was established at different interpulse intervals from 20 to 40 ms, suggesting that a presynaptic mechanism may be involved in CORT-induced hippocampal synaptic plasticity. Reverse-transcription polymerase chain reaction (RT-PCR) analysis showed that CORT-treated hippocampal CA1 cells underwent a significant decrease in the expression of mRNA for nerve growth factor-beta (NGF-beta) and brain-derived neurotrophic factor (BDNF), but not for neurotrophin-3 (NT-3) compared with those in control. Moreover, BDNF co-applied with CORT significantly antagonized CORT-induced deficit in PPF. Taken together, the present results suggest that CORT-induced inhibition of LTP may be, at least to some extent, mediated by a presynaptic mechanism and decrease in the BDNF expression in rat hippocampal CA1 cells induced by CORT may partially account for this presynaptic mechanism. FAU - Zhou, J AU - Zhou J AD - Laboratory of Neuropharmacology, Beijing Institute of Pharmacology and Toxicology, Beijing 100850, PR China. jzhou@codon.nih.gov FAU - Zhang, F AU - Zhang F FAU - Zhang, Y AU - Zhang Y LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Netherlands TA - Brain Res JT - Brain research JID - 0045503 RN - 0 (Anti-Inflammatory Agents) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Neurotrophin 3) RN - 0 (RNA, Messenger) RN - 9061-61-4 (Nerve Growth Factor) RN - W980KJ009P (Corticosterone) SB - IM MH - Animals MH - Anti-Inflammatory Agents/*pharmacology MH - Brain-Derived Neurotrophic Factor/*drug effects/metabolism/pharmacology MH - Corticosterone/*pharmacology MH - Excitatory Postsynaptic Potentials/*drug effects/physiology MH - Gene Expression/drug effects/physiology MH - Hippocampus/*drug effects/physiology MH - Long-Term Potentiation/*drug effects/physiology MH - Male MH - Nerve Growth Factor MH - Neurotrophin 3/drug effects/metabolism MH - RNA, Messenger/drug effects/physiology MH - Rats MH - Rats, Sprague-Dawley EDAT- 2000/12/05 11:00 MHDA- 2001/03/07 10:01 CRDT- 2000/12/05 11:00 PHST- 2000/12/05 11:00 [pubmed] PHST- 2001/03/07 10:01 [medline] PHST- 2000/12/05 11:00 [entrez] AID - S0006-8993(00)02934-6 [pii] AID - 10.1016/s0006-8993(00)02934-6 [doi] PST - ppublish SO - Brain Res. 2000 Dec 8;885(2):182-91. doi: 10.1016/s0006-8993(00)02934-6.