Effects of dynorphin fragments on learning and memory impairment induced by carbon monoxide exposure and β-amyloid peptide (25-35) in mice

The anti-amnesic effects of dynorphins on beta-amyloid peptide-(25-35)- and carbon monoxide (CO)-induced impairment of learning and/or memory in mice were investigated using a Y-maze task and a passive avoidance rest. Administration of beta-amyloid peptide-(25-35) or CO intoxication induced a decrease in both alternation behavior and latency in passive avoidance tests. Dynorphin A-(1-13) and A-(2-13) (0.5 and/or 1.5 nmol/mouse, i.c.v.) improved the beta-amyloid peptide-(25-35)- and GO-induced impairment of alternation performance and shortened the step-down latency. Nor-binaltorphimine (nor-BNI) (4.9 nmol/mouse, i.c.v.) partially blocked the effects of dynorphin A-(1-13), but did not block the effects of dynorphin A-(2-13) on the beta-amyloid peptide-(25-35)- and GO-induced impairment of learning and/or memory. These results indicate that dynorphin fragments improve delayed amnesia induced by beta-amyloid peptide-(25-35) and CO via not only kappa opioid receptors, but also "non-opioid" mechanisms.