A Research Of Expressions Of Glu,GABA, GluR₁ And GABAR_A In Hippocampus Of MHE Rats

Objective: 1.The animal model of MHE was established to explore itspathogenesis; 2. blood ammonia and serum endotoxin were observed toexplore their role in pathogenesis of MHE ;3.Glu,GABA,GluR1,and GABARAexpressions were studied by immunohistochemocal staining.4.To explore therole of Glu,GluR1,GABA,GABARA in the mechanism of MHE in order to offerexperimental gist for treating MHE.Methods: At first, Morris water maze and brainstem auditory evokedpotentials(BAEP) of all 50 rats were measured to establish the normalstandard; the next, 9 rats were randomized into control group ,the other 41 ratswere modeled to be of hepatic cirrhosis with CCL4 and high-lipid andlow-protein food .9th week ,Morris water maze ,BAEP, EEG were measuredagain, if eith Morris water maze or BAEP were abnormal meanwhile whoseEEG was normal ,then the rats were be MHE ,the model of MHE wereestablished .Nextly, 9 rats of MHE were randomized to wipe off CCL4 andalcohol for 4 weeks ,which was fatty infiltrated liver group. 13th week, bothMorris water maze and BAEP were measured the third time . Then, bloodammonia, serum endotoxin was performed ;Further more, the liver tissue wereobserved ;at the last , Glu.GABA.GluR1 and GABARA expressions ofhippocampus in rats were observed by immunohistochemocal staining.Results: The escape latency of Morris water maze was similar amongmodel group and control group before modeling; 9th week after modeling ,theescape latency of Morris water maze in MHE group prolonged remarkably ascompared with control group (P<0.01),there were 16/30 (53.3%) rats wereelected into MHE group; while, the 13th week ,the escape latency of rats withfatty infiltrated liver was shorter obviously as compared with MHE group(P<0.01),and similar with control group(P>0.05); 9th week , the peaklatency(PL) of BAEP in MHE group prolonged remarkably as compared withcontrol group (P<0.01),there were 19/30 (63.3%) rats were elected into MHEgroup; the 13th week ,the escape latency of rats with fatty infiltrated liver wasshorter obviously as compared with MHE group (P<0.01) ,and similar withcontrol group(P>0.05);in all, the MHE prevalence in hepatic cirrhosis rats was70.0%. in the MHE model group ,the concentrations of blood ammonia andserum endotoxin were higher as compared to the control group and fattyinfiltrated liver group ; Glu and GluR1 of hippocampus in rats of MHE groupwere significant decreased as compared to the control group; GABA andGABARA of hippocampus in rats of MHE group were significantincreased(P<0.01) as compared to the control group(P<0.01). Glu, GluR1,GABA and GABARA of hippocampus in rats with fatty infiltrated liver weresimilar with control group(P>0.05).Conclusion : 1.An ideal animal model of MHE was made ;2. The increase ofblood ammonia and serum endotoxin is one pathogenesis of MHE . 3.Imbalance between Glu and GABA is another important pathogenesis ; 4.Thedecrease of Glu and GluR1 in hippocampus and the increase of GABA andGABARA in hippocampus may be one of the mechanisms for leaning,memory ,and space cognitive disturbance; 5.MHE was a reversible functionobstruction of cerebra and nerve system, if wipe off pathogeny, leaning,memory ,and space cognitive disturbance would be resumed.