Des-tyrosine(1) dynorphin A-(2-13) improves carbon monoxide-induced impairment of learning and memory in mice

The effects of des-tyrosine(1) dynorphin A-(2-13) (dynorphin A-(2-13)) on carbon monoxide (CO)-induced impairment of learning and memory in mice were investigated using a Y-maze task and a passive avoidance test. The lower percentage alternation and shorter step-down latency of the CO-exposed group indicated that learning and/or memory impairment occurred in mice 5 and 7 days after CO exposure, respectively. Administration of dynorphin A-(2-13) (1.5 and/or 5.0 nmol/mouse, intracerebroventricularly (i.c.v.)) 30 min before behavioral tests improved the CO-induced impairment in alternation performance and the CO-induced shortened step-down latency. We previously reported that dynorphin A-(1-13) improved the impairment of learning and/or memory via kappa opioid receptor mediated mechanisms. To determine whether the effect of dynorphin A-(2-13) was also mediated via kappa opioid receptors, we attempted to block its action using a selective kappa opioid receptor antagonist, nor-binaltorphimine (nor-BNI). Nor-BNI (4.9 nmol/mouse, i.c.v.) did not block the effects of dynorphin A-(2-13) on the CO-induced impairment of learning and/or memory. These results indicate that dynorphin A-(2-13) improves impairment of learning and/or memory via a non-opioid mechanism.