Yao xue xue bao = Acta pharmaceutica Sinica · 2001
[The expression levels of GIRK1 and IRK1 in memory deficit rats].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Tong X Y, Wang X L
Аннотация
AIM: To study the expression level of GIRK1 and IRK1 in cerebral cortex after aggregated beta-amyloid peptide25-35 injection into the rat cerebral ventricle for different times.
METHODS: To test the spatial learning and memory in Morris water maze. To observe GIRK1 and IRK1 expression levels by RT-PCR.
RESULTS: In Morris water maze task, the latencies of beta-amyloid peptide treated rats were longer than those of the sham rars in the 4, 5, 8, 10 training periods ("student" t-test, P < 0.05). The expression levels of GIRK1 in beta-amyloid peptide injection day 1 and day 3 groups are decreased significantly compared with sham group (Tukey's test, P < 0.05) and there is no difference between beta-amyloid peptide injection day 17 group and sham group. IRK1 expression levels are no difference among the four groups.
CONCLUSION: Injection of aggregated beta-amyloid peptide25-35 into rat cerebral ventricles can induce memory and potassium channel expression changes. Beta-amyloid peptide induced inhibition of GIRK1 expression may have some relations with brain dysfunction.
METHODS: To test the spatial learning and memory in Morris water maze. To observe GIRK1 and IRK1 expression levels by RT-PCR.
RESULTS: In Morris water maze task, the latencies of beta-amyloid peptide treated rats were longer than those of the sham rars in the 4, 5, 8, 10 training periods ("student" t-test, P < 0.05). The expression levels of GIRK1 in beta-amyloid peptide injection day 1 and day 3 groups are decreased significantly compared with sham group (Tukey's test, P < 0.05) and there is no difference between beta-amyloid peptide injection day 17 group and sham group. IRK1 expression levels are no difference among the four groups.
CONCLUSION: Injection of aggregated beta-amyloid peptide25-35 into rat cerebral ventricles can induce memory and potassium channel expression changes. Beta-amyloid peptide induced inhibition of GIRK1 expression may have some relations with brain dysfunction.