| Formaldehyde and benzene are the main indoor pollutants which will hazard to human beings including all age phases. It will not only hazard the pregnant women but also their offspring. Following the warming of global climate, the effect of hyperthermia on human beings is paid more attention. Heat stress caused by hyperthermia as a biotic affectoi impacts on the metabolism and physiological function of nerve cell to influence the formation of nervous system. However, it hasn't been reported whether exposure to hazardous indoor pollutants due to interior decoration combined with hyperthermia influences the nervous system of postnatal ratsAccording the above reason, firstly we exposured early pregnant rats to the analogous environment of interior decoration combined with hyperthermia. Then the effect of this environment on the morpha and function of hippocampal neurons of postnatal rats was researched by neuropathological and neurochemical technology. The neural development and neuroethology of postnatal rats were detected and we tried to explore the mechanism.Methods1. Cylindrical polymethyl methacrylate plastics toxiferous cabinet was used to simulate the environment of decor dwellings. And the environment temperature was set at 25℃,38.5℃,40℃and 42℃by its ceramic febrifacient tube. Then acetylacetone spectrophotometer was used to detect the concentration of formaldehyde of air in the cabinet. The concentration of benzene, methylbenzene and dimethyl benzene was detected by capillary atmosphere chromatography.2. By using the toxiferous and hyperthermal facilities, the rats were divided into four groups. Each group will be managed with two hours per day within ten days. Controlled group: the pregnant rats were in the cabinet for 2 hours without any pollutants. Intoxicated group: the pregnant rats were in the cabinet with pollutants of low concentration. Combined group: the pregnant rats were in the cabinet with pollutants of low concentration and temperature at 38.5℃. Hyperthermia group: the pregnant rats were in the cabinet with temperature at 38.5℃. In order to estimate the effect of different contaminative environment on morphology of embryonic nervous system, pathological stain and RT-PCR were used to observe the number and morphous of hippocampal neurons of postnatal rats and postnatal one month rats. And alteration of the NR1 subunit of NMDA receptor of hippocampal neurons was also detected.3. In order to estimate the effect of different contaminative environment on the function of embryonic nervous system,the observation on neuroethological development and MORRI'S water maze were used to detect the alteration of neuroethological development, study and cognition of four groups postnatal rats.Results1. Analogue hazardous indoor pollutants due to interior decoration at high, midrange and low concentration and 25℃,38.5℃,40℃and 42℃environment temperature which were consistent with the national standard. And we have been chosen the low concentration indoor pollutants and 38.5℃environment temperature as the parameter in this experiment.2. Low concentration pollutants and temperature at 38.5℃could respectively induce degeneration and apoptosis of hippocampal neurons. Low concentration indoor pollutants combined with temperature at 38.5℃could aggravate the injury of hippocampal neurons.3. With the RT-PCR examination, we found that the expression of mRNA of the NR1 subunit of NMDA receptor at the CA1 area of hippocampus differed obviously both in neonatal rat group and postnatal one month rats group .The expression of Combined group(P<0.01), Intoxicated group(P<0.05) and Hyperthermia group (P<0.05) were higher than that of Controlled group. And the expression of Combined group was higher than that of Intoxicated group and Hyperthermia group.(P<0.01).4. With auxanological examination, we observed that there was no morphological malformation of nervous system in four groups postnatal rats. The superficial turn over reflex (F=14.9, P<0.001),spacial turn over reflex(F=41.9, P<0.001)and negative tropism (F=9.5, P<0.001)of postnatal rats differed obviously among four groups. The response time of combined group, intoxicated group and hyperthermia group was obviously later than that of controlled group, but there was no obvious difference among combined group, intoxicated group and hyperthermia group. The anterior limb hanging time of postnatal 14 days (F=60.6, P<0.001)and 16 days(F=173.9, P<0.001)rats in intoxicated group and combined group were shorter than that of hyperthermia group and controlled group. And there was no obvious difference between intoxicated group and combined group. It indicated that pollutants and hyperthermia could delay the formation of pristine reflect.5. With behavioral examination, we observed that the times of passing through the platform differed obviously(P<0.001). The times of combined group were obviously less than those of controlled group, intoxicated group and hyperthermia group. And the times of intoxicated group and hyperthermia group were evidently less than that of controlled group(P<0.05). It indicated showed that pollutants and hyperthermia could damage the study and memory function of postnatal rats.[Conclusion]1. The combination of low concentration indoor pollutants and 38.5℃hyperthermia will be better to simulate the situation of damaged organism that caused by indoor pollutants and hyperthermal environment.2. Although by launching low concentration indoor pollutants and 38.5℃hyperthermia at early pregnant period would not bring in morphological malformation of nervous system in offspring, but it could result in degeneration and necrosis of hippocampal neurons in rats.3. The formation of early reflex in offspring rats was delayed by low concentration indoor pollutants combined with 38.5℃hyperthermia ,moreover, the damage to spacial exploration of rat is more remarkable.4. The low concentration indoor pollutants combined with 38.5℃hyperthermia increased the expression of NR1 subunit in NMDAR ,and caused overloading of calcium ions, which may be one of the mechanism inducing damage to morphology and function in hippocampal neurons of offspring rats.
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