Facilitation of long-term potentiation and memory in mice lacking nociceptin receptors

Toshiya Manabe, Yukihiro Noda, Takayoshi Mamiya, Hiroyuki Katagiri, Takeshi Houtani, Miyuki Nishi, Tetsuo Noda, Tomoyuki Takahashi, Tetsuo Sugimoto, Toshitaka Nabeshima and Hiroshi Takeshima ()
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Toshiya Manabe: Faculty of Medicine, University of Tokyo
Yukihiro Noda: Nagoya University, School of Medicine
Takayoshi Mamiya: Nagoya University, School of Medicine
Hiroyuki Katagiri: Faculty of Medicine, University of Tokyo
Takeshi Houtani: Kansai Medical University
Miyuki Nishi: Faculty of Medicine, University of Tokyo
Tetsuo Noda: Cancer Institute, Kami-Ikebukuro
Tomoyuki Takahashi: Faculty of Medicine, University of Tokyo
Tetsuo Sugimoto: Kansai Medical University
Toshitaka Nabeshima: Nagoya University, School of Medicine
Hiroshi Takeshima: Faculty of Medicine, University of Tokyo

Nature, 1998, vol. 394, issue 6693, 577-581

Abstract: Abstract The peptide nociceptin (also named orphanin FQ) acts in the brain to produce various pharmacological effects, including hyperalgesia and hypolocomotion1,2. The nociceptin receptor uses guanine-nucleotide-binding proteins to mediate the inhibition of adenylyl cyclase, the activation of potassium channels and inhibition of calcium channels3. It has been shown using knockout mice that the nociceptin receptor is not required for regulation of nociceptive responses or locomotion activity, but modulates the auditory function4. Here we show that mice lacking the nociceptin receptor possess greater learning ability and have better memory than control mice. Histological analysis revealed the expression of both the nociceptin precursor and the nociceptin receptor in the hippocampus, thought to take part in aspects of learning and memory. Moreover, the receptor-deficient mice showed larger long-term potentiation in the hippocampal CA1 region than control mice, without apparent changes in presynaptic or postsynaptic electrophysiological properties. These results show that the loss of the nociceptin receptor results in a gain-of-function mutation in both the memory process and the long-term potentiation mechanism in CA1, perhaps as a result of altered intracellular signal transduction systems in neurons.

Date: 1998
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DOI: 10.1038/29073

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