Functional alteration of opioid receptor subtypes in the mice exhibited conditioned suppression in motility

Tsutomu Kameyama, Toshitaka Nabeshima, Hiroyuki Kamei, Kiyoshi Matsuno

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Mice exhibit a marked suppression of motility (conditioned suppression) when placed in the same environment in which they had previously received the electric footshock. The present study was designed to investigate the functional change of opioid receptor subtypes in the conditioned suppression group using an opioid binding assay technique. In the synaptic membrane of the conditioned suppression group, the binding capacities of [3H]naloxone at high and low affinity binding sites and of [3H]phencyclidine at high affinity binding site were significantly increased compared to those of the control group. On the other hand, the binding capacity of [3H]ethylketocyclazocine at both affinity binding sites in the conditioned suppression group was not changed. These results suggest that the binding function of different opioid receptor subtypes may be altered differently by stress.

Original languageEnglish
Pages (from-to)263-266
Number of pages4
JournalNeuroscience Letters
Volume53
Issue number3
DOIs
Publication statusPublished - 04-02-1985
Externally publishedYes

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Opioid Receptors
Binding Sites
Ethylketocyclazocine
Phencyclidine
Synaptic Membranes
Naloxone
Opioid Analgesics
Control Groups

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Kameyama, Tsutomu ; Nabeshima, Toshitaka ; Kamei, Hiroyuki ; Matsuno, Kiyoshi. / Functional alteration of opioid receptor subtypes in the mice exhibited conditioned suppression in motility. In: Neuroscience Letters. 1985 ; Vol. 53, No. 3. pp. 263-266.
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Functional alteration of opioid receptor subtypes in the mice exhibited conditioned suppression in motility. / Kameyama, Tsutomu; Nabeshima, Toshitaka; Kamei, Hiroyuki; Matsuno, Kiyoshi.

In: Neuroscience Letters, Vol. 53, No. 3, 04.02.1985, p. 263-266.

Research output: Contribution to journalArticle

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