Lack of expression of long-term potentiation in the dentate gyrus but not in the CA1 region of the hippocampus of μ-opioid receptor-deficient mice

Henry Matthies, Helmut Schroeder, Axel Becker, Horace Loh, Volker Höllt, Manfred Krug

Research output: Contribution to journalArticlepeer-review

35 Scopus citations

Abstract

The possible involvement of the μ-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 μ-opioid receptor-deficient mutant mice. In transversal hippocampal slices from mice lacking the μ- 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 μ-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 μM 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. (C) 2000 Elsevier Science Ltd.

Original languageEnglish (US)
Pages (from-to)952-960
Number of pages9
JournalNeuropharmacology
Volume39
Issue number6
DOIs
StatePublished - May 1 2000

Keywords

  • Binding assay
  • Funaltrexamine
  • Hippocampus
  • Long-term potentiation
  • Synaptic plasticity
  • μ-opioid receptor
  • μ-opioid-deficient mutant mice

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