RESUMO
Objective To explore whether chronic forced swimming stress could improve whole brain radiation induced cognitive dysfunction and possible mechanism. Methods Thirty-nine one month old male Sprague-Dawley rats were randomized into sham control group ( C ) , swimming group ( C-S ) , radiation group( R) , and radiation plus swimming group( R-S) . Radiation groups were given a single dose of 20 Gy on whole-brain. Rats in the swimming groups were trained with swimming of 15 min/d, 5 d/w. Rat behavior was performed 3 months after radiation in an order of free activity in an open field and the Morris water maze test including the place navigation and spatial probe tests. Then, the protein expressions of BDNF, P-ERK, T-ERK, P-CREB and T-CREB in the rat hippocampus tissue were assayed by Western blot. Results On the day 2, in the place navigation test of Morris water maze, the latency of swimming group was significantly shorter than that of sham group, the latency of sham group was significantly shorter than that of radiation group, and the latency of radiation swimming group was significantly shorter than that of radiation group(P0?05). Western blot assay showed that the expressions of BDNF and its downstream signals including P-ERK and P-CREB were markedly reduced by radiation ( P < 0?05 ) , but this reduction was attenuated by the chronic forced swimming stress. Conclusion The chronic forced swimming stress could improve whole brain radiation induced cognitive dysfunction by up-regulating the expressions of BDNF and its downstream signal molecules of P-ERK and P-CREB in hippocampus.
RESUMO
Objective To observe the changes of behavior, intracellular free calcium and the expression of calmodulin dependent protein kinase Ⅱ(CaMKⅡ) in the hippocampal neurons of chronic forced swimming stress rats. Methods Male Wistar rats were randomly divided into control group and chronic forced swimming stress group. The behavior was examined using sucrose preference test, open-filed test and Morris water maze. The intracellular free calcium was examined by fluorescence spectrophotometer. The expression of CaMKⅡ was detected using colloidal gold immunoelectron microscopy technique, Western blotting and RT-PCR. Results The consumption of sucrose and erect quantity of chronic forced swimming stress group were lower than those of control group(P<0.01, P<0.05). The escape latency time in Morries water maze test of chronic forced swimming stress group was higher than that of control group(P<0.01). The intracellular free calcium level and the expression of CaMKⅡ in the hippocampus was higher than that of control group(P<0.01).Conclusion The lasting dysfunction of Ca~(2+)/CaMKⅡ signaling cascades in hippocampus may play important roles in the pathogenesis of chronic forced swimming stress rats.