title: Lack of expression of long-term potentiation in the dentate gyrus but not in the CA1 region of the hippocampus of mu-opioid receptor-deficient mice.
abstract: The possible involvement of the mu-opioid receptor subtype in mechanisms of long-term potentiation (LTP) of the lateral perforant pathway to the dentate gyrus neurons, as well as of the Schaffer collateral-commissural input of CA1 neurons, was investigated using mu-opioid receptor-deficient mutant mice. In transversal hippocampal slices from mice lacking the mu-opioid receptor (MOR) only a short potentiation in the dentate gyrus after tetanization of the lateral perforant pathway was found. In contrast, the loss of the mu-opioid receptor in the CA1 region did not affect the potentiation of the field potentials induced by tetanization of the Schaffer collaterals. In parallel experiments, the application of 10 microM of the selective MOR-antagonist, funaltrexamine, decreased LTP in the dentate gyrus of wild-type mice but again did not alter the potentiation of the field potentials in the CA1. The loss of MOR-binding in the hippocampus was accompanied by a reduction in D2-binding sites indicating a possible compensatory role of the dopaminergic system. The D1- and glutamate binding was not affected. These observations confirm earlier results with pharmacological blockade of opioid receptors in the dentate gyrus and demonstrate an essential role of MOR activation for the generation of LTP in the dentate gyrus of the mouse but not necessarily in the CA1 region.
authors.affiliation: Institute of Pharmacology and Toxicology, Faculty of Medicine, Otto-von-Guericke University, Leipziger Strasse 44, 39120, Magdeburg, Germany. henry.matthies@medizin.uni-magdeburg.de
authors.forename: H
authors.initials: H
authors.lastname: Matthies
authors.forename: H
authors.initials: H
authors.lastname: Schroeder
authors.forename: A
authors.initials: A
authors.lastname: Becker
authors.forename: H
authors.initials: H
authors.lastname: Loh
authors.forename: V
authors.initials: V
authors.lastname: Höllt
authors.forename: M
authors.initials: M
authors.lastname: Krug
mesh_terms: D000200:Action Potentials; D000818:Animals; D003342:Corpus Striatum / Q000378:metabolism / Q000648:ultrastructure; D018891:Dentate Gyrus / Q000502:physiology*; D005260:Female; D006624:Hippocampus / Q000033:anatomy & histology / Q000502:physiology*; D066298:In Vitro Techniques; D017774:Long-Term Potentiation; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D009271:Naltrexone / Q000031:analogs & derivatives / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D017447:Receptors, Dopamine D1 / Q000378:metabolism; D017448:Receptors, Dopamine D2 / Q000378:metabolism; D017470:Receptors, Glutamate / Q000378:metabolism; D017450:Receptors, Opioid, mu / Q000172:deficiency / Q000235:genetics*; D013570:Synaptic Membranes / Q000378:metabolism
chemical_list: D009292:Narcotic Antagonists; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D017470:Receptors, Glutamate; D017450:Receptors, Opioid, mu; D009271:Naltrexone; C024524:beta-funaltrexamine