ABSTRACT
OBJECTIVE@#To evaluate the effect of prenatal mobile phone exposure on the expression of proliferating cell nuclear antigen (PCNA) and doublecortin (DCX) in dentate gyrus of offspring rats.@*METHODS@#The rat model of prenatal mobile phone exposure was established and there were three groups including control group, short term maternal exposure group and long term maternal exposure group(=6). From pregnant day 1 to day 17, pregnant rats in long term and short term maternal exposure group were exposed to an mobile phone in talking mode for 6 h/d and 24 h/d, respectively. Length of pregnancy, maternal body weight gain, litter size and pup's body weight were observed. The cell morphology in dentate gyrus of offspring rats at the age of 1 month was studied by cresyl violet staining. The immunohistochemical expression of PCNA and DCX in dentate gyrus of rat offspring were detected, and the expression of DCX and brain derived neurotrophic factor (BDNF) in hippocampus of rat offspring were evaluated by Western blot.@*RESULTS@#There was no difference in length of pregnancy, maternal body weight gain, litter size and pup's body weight among three groups. The morphological changes of pyramidal cells in the polymorphic layer and DCX-positive cells in the dentate gyrus were obvious in rat offspring of long term maternal exposure group. There were less PCNA-positive cells in dentate gyrus and decreased expression of DCX and BDNF in hippocampus by Western blot in long term maternal exposure group compared with control and short term maternal exposure group (all <0.05).@*CONCLUSIONS@#Long term prenatal mobile phone exposure might inhibit the expression of PCNA and DCX in dentate gyrus of rat offspring by down-regulating BDNF.
Subject(s)
Animals , Female , Pregnancy , Rats , Brain-Derived Neurotrophic Factor , Metabolism , Cell Phone , Dentate Gyrus , Metabolism , Hippocampus , Metabolism , Microtubule-Associated Proteins , Metabolism , Neuropeptides , Metabolism , Prenatal Exposure Delayed Effects , Proliferating Cell Nuclear Antigen , Metabolism , Radio WavesABSTRACT
<p><b>OBJECTIVE</b>To evaluate the effects of prenatal stress on neurological functions after middle cerebral artery occlusion (MCAO) in adult offspring rats.</p><p><b>METHODS</b>Pregnant rats were randomly assigned to prenatal stress treatment, which was exposed to restraint three times daily in the last week of pregnancy, and no prenatal stress treatment. Adult male offspring rats were subjected to transient focal cerebral ischemia by MCAO. They were randomly divided into four groups: sham group, prenatal stress + sham group, MCAO group and prenatal stress + MCAO group (n = 10). After 24 hours of reperfusion, the neurological deficits were evaluated. The infarct size, cell apoptosis and expression of Caspase 3, cleaved Caspase 3 and Bcl-2 were detected.</p><p><b>RESULTS</b>Compared with MCAO group, the neurological deficits, infarct size and apoptotic cells in prenatal stress + MCAO group were increased significantly (all P < 0.05). The expressions of Caspase 3 and cleaved Caspase 3 were much greater in prenatal stress + MCAO group than those of MCAO group, while the expression of Bcl-2 was significantly decreased in prenatal stress + MCAO group compared with MCAO group (all P < 0.05).</p><p><b>CONCLUSION</b>Prenatal stress might exacerbate neuroloeical deficits in the offspring rats after MCAO by increasing cell apoptosis.</p>