Effects of dynorphin A (1-13) on carbon monoxide-induced delayed amnesia in mice

M. Hiramatsu, M. Sasaki, Toshitaka Nabeshima, T. Kameyama

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

The effects of dynorphin A (1-13) on carbon monoxide (CO)-induced amnesia in mice were investigated. Memory deficiency was apparent during Y-maze testing 5 days after CO exposure (delayed amnesia). Percent alternation in the CO-exposed group was significantly lower than that in the control group. Administration of dynorphin A (1-13) (1.5 nmol, i.c.v.) 15 min before the Y-maze test session reversed the impairment of spontaneous alternation performance in the CO-exposed group. To determine whether this effect was mediated via kappa opioid receptors, we attempted to block the effect of dynorphin A using the kappa opioid receptor antagonist nor-binaltorphimine. Nor-binaltorphimine (5.44 nmol, i.c.v.) blocked the effect of dynorphin A (1-13) on delayed amnesia. Dynorphin A (1-13) did not affect the impairment of alternation induced by the blockade of NMDA-receptors by dizocilpine (MK-801), but significantly prevented the impairment induced by mecamylamine. These results suggest that dynorphin A (1-13) modulates the kappa receptor-mediated opioid neuronal system, and reverses the impairment of spontaneous alternation performance induced by CO exposure.

Original languageEnglish
Pages (from-to)73-79
Number of pages7
JournalPharmacology Biochemistry and Behavior
Volume56
Issue number1
DOIs
Publication statusPublished - 01-01-1996
Externally publishedYes

Fingerprint

Amnesia
Carbon Monoxide
kappa Opioid Receptor
Dizocilpine Maleate
Mecamylamine
Dynorphins
Narcotic Antagonists
N-Methyl-D-Aspartate Receptors
Opioid Analgesics
dynorphin (1-13)
Data storage equipment
Control Groups
Testing

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Toxicology
  • Pharmacology
  • Clinical Biochemistry
  • Biological Psychiatry
  • Behavioral Neuroscience

Cite this

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abstract = "The effects of dynorphin A (1-13) on carbon monoxide (CO)-induced amnesia in mice were investigated. Memory deficiency was apparent during Y-maze testing 5 days after CO exposure (delayed amnesia). Percent alternation in the CO-exposed group was significantly lower than that in the control group. Administration of dynorphin A (1-13) (1.5 nmol, i.c.v.) 15 min before the Y-maze test session reversed the impairment of spontaneous alternation performance in the CO-exposed group. To determine whether this effect was mediated via kappa opioid receptors, we attempted to block the effect of dynorphin A using the kappa opioid receptor antagonist nor-binaltorphimine. Nor-binaltorphimine (5.44 nmol, i.c.v.) blocked the effect of dynorphin A (1-13) on delayed amnesia. Dynorphin A (1-13) did not affect the impairment of alternation induced by the blockade of NMDA-receptors by dizocilpine (MK-801), but significantly prevented the impairment induced by mecamylamine. These results suggest that dynorphin A (1-13) modulates the kappa receptor-mediated opioid neuronal system, and reverses the impairment of spontaneous alternation performance induced by CO exposure.",
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Effects of dynorphin A (1-13) on carbon monoxide-induced delayed amnesia in mice. / Hiramatsu, M.; Sasaki, M.; Nabeshima, Toshitaka; Kameyama, T.

In: Pharmacology Biochemistry and Behavior, Vol. 56, No. 1, 01.01.1996, p. 73-79.

Research output: Contribution to journalArticle

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