Change of cholinergic transmission and memory deficiency induced by injection of beta-amyloid protein into NBM of rats

The change of cholinergic transmission of beta -amyloid protein (beta -AP) treated rats was studied by intracerebral microdialysis sampling combined w ith HPLC analysis. beta -AP(1-40) was injected into nucleus basalis magnoce llularis (NBM). Passive avoidance response test (step-down test) and delaye d alternation task were used for memory testing. The impairment of memory a fter injection of beta -AP(1-40) into NBM exhibited mainly the deficiency o f short-term working memory. One week after injection of beta -AP(1-40) the release of acetylcholine (ACh) from frontal cortex of freely-moving rats d ecreased significantly, and the response of cholinergic nerve ending to the action of high [K+] solution was rather weak. In control animals the perce ntage of increase of ACh-release during behavioral performance was 57%, whi le in beta -AP(1-40)-treated rats it was 34%. The temporary increase of the ACh-release of the rat put into a new place was also significantly diminis hed in beta -AP(1-40)-treated rats. The results show that the injection of beta -AP(1-40) into NBM impairs the cholinergic transmission in frontal cor tex, and the impairment of cholinergic transmission may be the main cause o f the deficit of working memory.