| Sleep is one kind of complicated physiological processes under the meticulous adjustment of central nerve system, which occupys one third of our life. In order to know its physiological function, scientists have done a lot of studies on sleep in human or animals by sleep deprivation . From Cohen's small-pedestal sleep deprivation model, simultaneously using home cage control group and large pedestal sleep deprivation group as control, we have found that sleep deprivation could induce neuron apoptosis in rat hippocampus of PSD group, which was mainly located in hippocampal CA1 and CAS areas, while no markedly positive cells could be seen in each hippocampal area of the control groups. The neuron apoptosis between the PSD group and control groups has significant difference. These results suggest that sleep deprivation induce neuron apoptosisin rat hippocampus. But what is the mechanism of this phenomenon? What is the possible signal transduction ways of this phenomenon? There are still not so much deep researches on it. In the present work, we observed the expression of MAPKs and c-Jun by -liquid scintillation counting, Western Blot and Immunocytochemistry in neuron apoptosis after sleep deprivation in rat hippocampus.32 health adult male SD rats with weighted 200g?20g were divided into three groups randomly. Each group had eight rats, they were (1) rapid eye movement sleep deprivation group (or paradoxical sleep deprivation, PSD),small pedestal diameter 7cm (2) large pedestal control group(LC), pedestal diameter 13cm (3) home cage control group(HC). The group (1) was named as experimental group, group (2) and (3) as control group. Each rat was deprived of sleep for 72 hours, which was begined at 8:OOAm of experimental day. The normal control rats stayed within their home cage throughout the experiment keeping their normal sleep-awake cycle. Animals were perfused with paraformaldehyte following normal serum after test, then removed the brain and took out double hippocampus. Western Blot was used for analysis of INK. P -liquid scintillation counting was used for analysis of ERK and immunocytochemistry was used for the analysis of c-Jun. All the data were analyzed withstatistical treatment. The results were showed as follows:1. HE staining: Apoptosis neuron became smaller. Nucleus was condensed. Chromatin was edged and some appeared semi-moon shape and nucleus broken, but the membrane was completely. Apoptosis neurons were mainly located in hippocampal CA1 and CA3 areas of PSD group, while no markedly positive cells could be seen in each hippocampal area of the two control groups and the CA2, CA4 areas of PSD group.2. $ -liquid scintillation counting: ERK basic activities had been found in the two control groups. The scores were 6582.38 ?2605.70 and 6204.13 + 2212.40.There had no obvious difference between them(P>0.05).While ERK activity was obviously lowered in the PSD group which score was only 807.88 + 1326.76.The expression of ERK in PSD group showed significant difference between the two control groups(P<0.05).3. Western Blot: The expression of JNK was obviously stronger in PSD group than in the two control groups. The JNK activity had increased 75% than HC group and 62.5% than LC group respectively. There were significant difference between PSD group and the two control groups(P<0.05),no significant difference between the two control groups.4. Immunocytochemistry: The c-Jun positive cell nuclei appeared brownish granules. No markedly c-Junpositive signals could be observed in the hippocampus of the two control groups. The distribution of c-Jun positive cells expressed in PSD group was consistent with that of apoptotic cells in HE staining. The expression of c-Jun was much stronger in CA1 and CAS areas than those in CA2 and CA4 areas of PSD group, which showed siganificant difference(P<0.05).Between hippocampal CA1 and CA3 area,CA2 and CA4 area there was no significant difference(P>0.05).Conclusions:(1) Sleep deprivation could induce neuron apoptosis in r...
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