| BackgroundAs accelerating process of population aging, age-related diseases including cognitivedecline have been attracting people’s attention. It was obviously expressed in learningand memory impairment in the early stage of age-related cognitive decline. Althoughthere were so many researches, the underlying neuromechanism of the age-relatedimpairment of learning and memory is not yet clear. Nowadays, it is thought that thedestruction of synaptic integrity may lead to the age-related decline in learning andmemory. Complexin regulates exocytosis at neuronal presynaptic active zone byreversiblely combining with SNARE complexes and changing the structure. Syntaxin1,the prototype family of SNARE proteins, is a protein enriched in presynaptic terminal.Syntaxin1associated with SNAP-25to form the t-SNARE heterodimer, which is anacceptor for subsequent synaptobrevin engagement. This process does mediate synapticvesicle docking and neurotransmitter releasing. Several researches have proved that thetwo proteins are related to learning and memory: In complexin knock-out mouse,learnig and memory impairment was obvious; Rats with learning memory tasks showedan increase in the expression of syntaxin1in three subregions of the hippocampus.However, the change of the complexin and syntaxin1in normal aging are still notclarified.Objective①To explore the effects of age on the levels of complexin and syntaxin1in differenthippocampal stratums.②To explore the correlation between spatial learning and memory functions and the levels of complexin and syntaxin1in these hippocampalstratums.MethodsThree age groups in the SAMP8mice (4.5month-old group,8month-old group and13month-old group) were used. The ability of spatial learning and memory wasevaluated by six-arm radial water maze (RAWM) and the complexin and syntaxin1inhippocampus were detected by immunohistochemistry (mean optical density wasviewed as the relative content of the two proteins). The article contains repeatedmeasures analysis of variance, single factor analysis of variance, rank sum test andspearman’s rank correlation.Results①For the SAMP8mice, the average number of errors and latency during learning andmemory periods were higher in the13-month-old group than those in the8month-oldand4.5month-old groups, and the8month-old group was higher than4.5month-oldgroup.②Compared to the4.5-month mice, the13-month mice had significantly lowerlevel of complexin1/2in the polymorphic layer and outer molecular layer of dentategyrus and the stratum radiatum of CA1subfield, so had the8-month-old mice in theouter molecular layer of dentate gyrus and the stratum radiatum of CA1subfield. Inaddition, complexin1/2relative amount of the13-month-old mice was significant lowerthan that of the8-month-old mice in CA3stratum lucidum.③Compared to the4.5-month mice, the13-month mice had significantly higher level of syntaxin1inhippocampus except DG polymorphic layer and CA3stratum lucidum, so did the8-month-old mice in DG stratum moleculare, CA1stratum moleculare, CA1stratumradiatum, CA1stratum oriens and CA3pyramidal layer; And in DG granular layer,CA1pyramidal layer, CA1stratum oriens, syntaxin1relative amount of13month-oldmice was higher than that of8month-old mice.④In SAMP8mice，positivecorrelation was confirmed between the relative amount of the complexin1/2in CA1stratum radiatum and the number of errors and latency during learning and memory periods, while in CA1subregion, CA3stratum oriens and DG stratum molecularenegative correlation was discovered between the syntaxin1relative amount and thenumber of errors and latency during learning and memory.ConclusionAge-related impairment of spatial learning and memory was confirmed in SAMP8mice.During the mice aging, in hippocampus the level of complexin1/2expression inhippocampus appeared a circuit-specific reduction while the amount of the syntaxin1increased in most stratums. The changes may associate to the age-related spatiallearning and memory impairment. |
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