The effects of dynorphin A-(1–13) on carbon monoxide (CO)-induced amnesia in mice were investigated using a step-down type passive avoidance task. Memory deficiency occurred in mice when training commenced 7 days after CO exposure although it was not produced 1 day after CO exposure. The median step-down latency in the retention test of the CO-exposed group was significantly shorter than that of the control group. Administration of dynorphin A-(1–13) (1.5 nmol/mouse i.c.v.) 15 min before the first training session prolonged the step-down latency in the CO-exposed group. Dynorphin A-(1–13) administered immediately after the first training session or administered 15 min before the retention test also prolonged the step-down latency in the CO-exposed group. To determine whether this effect of dynorphin A-(1–13) was mediated via κ-opioid receptors, we attempted to block its action using a κ-opioid receptor antagonist (nor-binaltorphimine). Nor-binaltorphimine (5.44 nmol/mouse i.c.v.) blocked the effect of dynorphin A-(1–13) on delayed amnesia. However, dynorphin A-(1–13) (0.5, 1.5 and 5.0 nmol/mouse) did not facilitate the acquisition of memory in normal mice. These results suggest that dynorphin A-(1–13) modulates the κ-opioid receptor-mediated opioid neuronal system, and that it ameliorates the disruptive effect of CO on acquisition, consolidation and/or recall of memory.
European Journal of Pharmacology – Elsevier
Published: Aug 25, 1995
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