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Infrasound (IS) is generated by the mechanical vibration of the object frequency of 0.0001 to 20 Hz the acoustic widely found in nature and the social environment. High-intensity infrasound on human health, and an important part of the production of noise and noise. Studies have shown that infrasound can be used as a source of stress caused by the body's stress response, causing changes in the nervous system and the endocrine system, especially the pituitary - adrenal system reaction. Infrasound can cause rat hypothalamic paraventricular nucleus (PVN) of adrenocorticotropic hormone-releasing hormone (CRH) mRNA expression increased significantly by corticotropin-releasing hormone, CRH receptor type 1 (CRH-R1) combine to play a role. Recent studies have found that infrasound can cause changes in neuronal function, but also affect the glial cells, such as 8 Hz, GT; 90dB sound by resting into the activated state can be induced PVN microglia (MI) and promote their infiltration to the lesion site. We also found that in the previous experiment, the infrasound exposure can cause MI prior to activation of astrocytes (AS). MI is a widely distributed in the central nervous system (CNS) has the dual function of immune and inflammatory microglia cells. Under normal circumstances is in the resting state, the form of performance for branch-like, small cell body, protrusions stretch in all directions. Resting MI function is unclear, the MI projections and AS, neuronal and vascular endothelial cells directly contact may release low levels of growth factors, suggesting close mutual contact exists between them. Resting MI susceptible to brain injury or disease of any type of activation, morphology showed protruding less short, round cell body, larger volume, was \excess secretion of cytokines, including nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta), these factors can cause the death of neurons. Promote the dual role of host defense and repair or the formation of brain damage due to the degree of activation, to stimulate different type and local factors, MI, which is attributed to its different synthesis and secretion of cytokines. Past that neurons are involved in the stress response of effector cells, and the stress is closely related to the CRH-R1 is only expressed in neurons, including a recent study found that factors such as toxins or hypoxia stimulation, however, activation of the MI higher CRH-R1 expression of added exogenous CRH MI activation MI can promote proliferation and secretion of TNF-alpha and other cytokines in vitro culture, the application of CRH-R1 antagonists can block this effect. These results suggest that MI may play an important role in the stress response. Then, infrasound as a source of stress can promote MI CRH-R1 expression by CRH-R1 involved in stress response to infrasound, has not yet been reported. Therefore, this experiment 16Hz 130dB high strength caused by infrasound rat brain and cultured in vitro MI damage observed MI on CRH-R1 expression changes, and observe the CRH-R1 antagonist antalarmin in which the role of MI in the sub- sound stress the role and mechanism. Experimental Objective To study the 16Hz 130dB times sound the rat PVN MI CRH-R1 expression changes. Methods SD rats were exposed to sound pressure level 16Hz 130dB times the sound compartment 2h at different time points after infrasound (0.5,2,6,12,24 h) rats were sacrificed, brain tissue OX42 immunohistochemistry fluorescent chemical staining, observed infrasound the rat PVN MI change and its CRH-R1 expression changes. Results the control rats PVN area MI small number, generally resting state. Infrasound at 0.5h after rat PVN MI activation, proliferation, CRH-R1 expression increased and reached a peak at 6h. The role of infrasound the rat PVN District AS form did not change significantly, CRH-R1 expression not as good as MI significant. Infrasound PVN CRH expression was significantly increased, but mainly expressed in neurons rather than MI. 16Hz 130dB times sound conclusions can cause increased activation of its CRH-R1 expression in the PVN MI. Experiment II Objective To study the expression changes of 16Hz 130dB times sound cultured rat MI CRH-R1. 16Hz 130dB infrasound role 0.5h, 1h, 2h in vitro culture of MI in the role at different time points (0.5,1,2,4,8,12,24 h) Application OX42 immunofluorescence staining of MI Activation of its CRH-R1 expression changes. The results with the infrasound exposure time, the the MI activation rate increased, increased expression of CRH-R1. Infrasound 0.5h MI CRH-R1 expression began to increase, 4h reached a peak 12 hours after the fall. With the the infrasound exposure time extension, CRH-R1 expression was significantly increased compared with the control group, the difference was significant (P lt; 0.01). Above in a time-and intensity-dependent. Conclusion infrasound can induce the MI activation in vitro, MI after the activation of a large number of expression of CRH-R1 prompt the MI expression of CRH-R1 is not or exogenous CRH-mediated. Experimental purposes study CRH-RL antagonist antalarmin 16Hz 130dB times sound the rat PVN MI CRH-R1 expression changes. The same way as the above method, but before infrasound 20min application of CRH-Rl antagonist antalarmin the immunofluorescence staining observe the CRH/CRH-R1 expression. Results with the antagonist antalarmin CRH-Rl, can significantly reduce the role of infrasound to cause PVN area MI on CRH-Rl and increased expression of CRH, but no obvious effect on MI activation induced by infrasound. Conclusion CRH-RL antagonists can significantly reduce the expression of CRH-RL of MI, suggesting having anti infrasound stress the role.
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