The change of cholinergic transmission of p-amyloid protein (P-AP) treated rats was studied by intracerebral microdialysis sampling combined with HPLC analysis. β-AP1-40 was injected into nucleus basalis magnocellula...The change of cholinergic transmission of p-amyloid protein (P-AP) treated rats was studied by intracerebral microdialysis sampling combined with HPLC analysis. β-AP1-40 was injected into nucleus basalis magnocellularis (NBM). Passive avoidance response test (step-down test) and delayed alternation task were used for memory testing. The impairment of memory after injection of β-AP1-40 into NBM exhibited mainly the deficiency of short-term working memory. One week after injection of β-AP1-40 the release of acetylcholine (ACh) from frontal cortex of freely-moving rats decreased significantly, and the response of cholinergic nerve ending to the action of high [K+] solution was rather weak. In control animals the percentage of increase of ACh-release during behavioral performance was 57%, while in β-AP1-40-treated rats it was 34%. The temporary increase of the ACh-release of the rat put into a new place was also significantly diminished in β-AP1-40 -treated rats. The results show that the injection of β-AP1-40 into NBM impairs the cholinergic transmission in frontal cortex, and the impairment of cholinergic transmission may be the main cause of the deficit of working memory.展开更多
基金the National Natural Science Foundation of China (Grant Nos. 3699930140 & 39870733).
文摘The change of cholinergic transmission of p-amyloid protein (P-AP) treated rats was studied by intracerebral microdialysis sampling combined with HPLC analysis. β-AP1-40 was injected into nucleus basalis magnocellularis (NBM). Passive avoidance response test (step-down test) and delayed alternation task were used for memory testing. The impairment of memory after injection of β-AP1-40 into NBM exhibited mainly the deficiency of short-term working memory. One week after injection of β-AP1-40 the release of acetylcholine (ACh) from frontal cortex of freely-moving rats decreased significantly, and the response of cholinergic nerve ending to the action of high [K+] solution was rather weak. In control animals the percentage of increase of ACh-release during behavioral performance was 57%, while in β-AP1-40-treated rats it was 34%. The temporary increase of the ACh-release of the rat put into a new place was also significantly diminished in β-AP1-40 -treated rats. The results show that the injection of β-AP1-40 into NBM impairs the cholinergic transmission in frontal cortex, and the impairment of cholinergic transmission may be the main cause of the deficit of working memory.
