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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 577/2/601    most recent jphysiol.2006.120386v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yang, C.-H. Articles by Hsu, K.-S. Search for Related Content PubMed PubMed Citation Articles by Yang, C.-H. Articles by Hsu, K.-S. Related Collections Neuroscience

¹ Department of Pharmacology
² Institute of Basic Medical Sciences, College of Medicine
³ Center for Gene Regulation and Signal Transduction Research, National Cheng Kung University, Tainan 701, Taiwan

Acute behavioural stress has been recognized as a strong influence on the inducibility of hippocampal long-term synaptic plasticity. We have reported previously that in adult male rats, acute behavioural stress impairs long-term potentiation (LTP) but enhances long-term depression (LTD) in the hippocampal CA1 region. In this study we report that the effects of stress on LTP and LTD were reversed when animals were introduced into a novel ‘stimulus-rich’ environment immediately after the stress. Novelty exploration-induced reversal of stress effects was prevented when the animals were given the NMDA receptor antagonist D-(–)-2-amino-5-phosphonopentanoic acid, the cholinergic antagonist atropine and the protein phosphatase (PP) 2B inhibitors cyclosporin A and cypermethrin, but not the ₁-adrenergic antagonist prazosin, the ß-adrenergic antagonist propranolol or the PP1/2A inhibitor okadaic acid, respectively before being subjected to the novel environment. In addition, the ability of novelty exploration to reverse the stress effects was mimicked by a direct application of the cholinergic agonist carbachol. Exposure to the novel environment following stress was accompanied by the activation of both PP2B and striatal-enriched tyrosine phosphatase (STEP). Taken together, these findings suggest that the activation of the cholinergic system and, in turn, the triggering of an NMDA receptor-mediated activation of PP2B to increase STEP activity appear to mediate the novelty exploration-induced reversal of stress-related modulation of hippocampal long-term synaptic plasticity.

(Received 3 September 2006; accepted after revision 21 September 2006; first published online 28 September 2006)
Corresponding author K.-S. Hsu: Department of Pharmacology, College of Medicine, National Cheng Kung University, No. 1, University Road, Tainan City 701, Taiwan. Email: richard{at}mail.ncku.edu.tw

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