| Infrasound, the flexible mechanical longitudinal wave ranging from 10~4~20Hz, exists widely in industry, traffic, military affairs and natural environment. As one of the major components of noise pollution, it seriously hazards people's health. Therefore it's very important to reveal the mechanisms of its biological effects, not only for wartime but also ordinary time. Basically infrasound exerts its damages on the organs through resonance induced in vivo to trigger a serial of pathological reactions, among which the central nervous system(CNS) is one of the primary targets. However, until now, the molecular mechanisms of infrasound acting on CNS hasn't been clarified .As the richest excitatory neurotransmirter in CNS, it's reported that glutamate is markedly accumulated in brain to the level inducing excitatory nervous toxicity and making various pathological damages on neurons, due to excessive release and reabsorption disturbance of glutamate after brain injury. The excitatory toxicity of glutamate is exerted via both of the inotropic and metabotropic glutamate receptors(iGluRs and mGluRs) activated on the neurons, which mediate the damages by overloading intracellular calcium through some unclear passages. It's known that the mGluRs located in prososynapse and posterosynapse can induce both excitatory and inhibitory effect and modulate the levels of iGluRs. Various factors can activate both kinds of GluRs to provocate pathologicalreactions. There have been eight subtypes of mGluRs cloned in human. These subtypes are divided into three groups according to their homogeny, coupled receptors, and preferential agonists. Group I includes mGluRl and mGluRS, reinforcing the excitatory nervous toxicity when activated; Group II includes mGluR2 and mGluR3, mediating the protective effects; and Group III includes mGluR4, mGluR6. mGluRV and mGluRS, owning the similar features with Group II. Since the functions of mGluRs were deeply exploited and its pharmacological features were continually revealed, the agonists and antagonists of the mGluRs have been the investigative hot spots in the CNS injury. In the previous studies, it was shown some iGluR antagonists have some curative effects in brain injury but with serious psychological side effects, which limit their potential in clinic. We have found that MCPG, the competitive antagonist of Group I mGluRs, has some curative effects on the CNS injury induced by infrasound.In order to further clarify the molecular mechanisms of infrasonic brain injury and the potential drugs targeting mGluRs, the rat model was established with the system of infrasonic sound pressure cabin in this study. The alterations of Group I , II mGluRs mRNA expression and location were detected by in situ hybridization and observed under optical and electron microscope respectively. The agonist DCG-IV of Group II mGluRs were used to study its intervention on infrasonic brain injury.The rat model of infrasonic brain injury was stably established with infrasound at the frequencies of 8Hz and 130dB. No significant differences in neurological severity score (NSS) and injured neurons counting in the cerebal cortex were observed between the group exposed to the infrasound once and the control. However markedly increased levels of the parameters were observed in the groups exposed 7 and 14 times to infrasound than that of the control(P<0.01). The typical pathological changes in the microscopic and super-microscopic structures of neurons were detected with the histopathological analysis. Meanwhile the expression of group I mGluR mRNA increased in cortex neurons after infrasonic exposure, reaching the highest level in the 7-time exposedgroup(P<0.01), but reverting to the normal level in the 14-time exposed group. On the contrary, the expression of group II mGluR mRNA in cortex neurons decreased after infrasonic exposure to the lowest level in the 1-time group(P<0.01) and reverted to the normal level in the 7-time and 14-time groups. In the intervention experimental groups, no significant chan...
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