title: Stress evoked by opiate withdrawal facilitates hippocampal LTP in vivo.
abstract: Stress impairs hippocampal long-term potentiation (LTP), but it is unknown whether the stress evoked by opiate withdrawal has the same effect. Here the authors report that opiate withdrawal for 4 days does not influence basal synaptic transmission, but results in a greatly increased LTP in hippocampal CA1 area in anesthetized rats. Elevated-platform stress enabled a large LTP in rats withdrawn for only 18 h, but the glucocorticoid receptor antagonist RU38486 (twice per day for 3 days) prevented the large LTP on 4 days withdrawal. Moreover, 4 days withdrawal enhanced the NMDAR-mediated EPSCs, in which the NR2A-containing NMDAR-mediated EPSC was increased but the NR2B-containing NMDAR-mediated EPSC was decreased. These results suggest that adaptive changes of the NMDAR and glucocorticoid receptor functions during 4 days of opiate withdrawal may enable stress to facilitate hippocampal LTP, potentially contributing to the opiate withdrawal experience-dependent modifications of hippocampal functions.
authors.affiliation: Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, People's Republic of China.
authors.forename: Zhifang
authors.initials: Z
authors.lastname: Dong
authors.forename: Weixia
authors.initials: W
authors.lastname: Zhong
authors.forename: Meng
authors.initials: M
authors.lastname: Tian
authors.forename: Huili
authors.initials: H
authors.lastname: Han
authors.forename: Jun
authors.initials: J
authors.lastname: Cao
authors.forename: Tianle
authors.initials: T
authors.lastname: Xu
authors.forename: Jianhong
authors.initials: J
authors.lastname: Luo
authors.forename: Lin
authors.initials: L
authors.lastname: Xu
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D004307:Dose-Response Relationship, Radiation; D004334:Drug Administration Schedule; D004347:Drug Interactions; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects* / Q000503:physiopathology; D006727:Hormone Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000187:drug effects* / Q000502:physiology / Q000528:radiation effects; D008297:Male; D015735:Mifepristone / Q000494:pharmacology; D009025:Morpholines / Q000008:administration & dosage*; D018408:Patch-Clamp Techniques / Q000379:methods; D010636:Phenols / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013315:Stress, Psychological / Q000503:physiopathology*; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology; D013997:Time Factors
chemical_list: D018691:Excitatory Amino Acid Antagonists; D006727:Hormone Antagonists; D009025:Morpholines; D010636:Phenols; D010880:Piperidines; C109643:Ro 25-6981; D015735:Mifepristone; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; C037574:morpholine