电磁辐射（EMF）具有神经行为损伤效应，但机理不明，且难于防护。课题组前期研究发现：热习服可减轻EMF诱导的抑郁样行为，并可能与其调节海马神经发生有关。由于热习服可诱导小胶质细胞M2型活化，而CX3CR1又是小胶质细胞M2型活化分子标志物，与神经发生密切相关。据此我们推测：热习服可能通过调节小胶质细胞M2型活化高表达CX3CR1，促进海马神经发生，从而改善EMF导致的抑郁样行为。为进一步验证假设并探讨机理，本项目主要研究①热习服调节小胶质细胞M2型活化、促进海马神经发生与EMF诱导抑郁样行为的相关性；②CX3CR1作为小胶质细胞M2型活化关键分子在热习服调节EMF损伤海马神经发生中的关键作用；③CX3CR1及CREB相关信号通路调节小胶质细胞分泌IGF-1、BDNF改善海马神经发生的机理。本项目不仅可揭示热习服保护EMF损伤神经行为的作用机制，而且有望为EMF暴露职业人群提供有效防护措施。

Electromagnetic fields (EMF) exposure could initiate the central neverous system (CNS) injury. But the mechanism is not so clear and it is hard to prevent. Our recently studies found that heat acclimation (HA) attenuates depressive behavior, this protective linked to potential effects on hippocampal neurogenesis. Considering the expression of M2 active marker CX3CR1 and the linkage of neurogenesis in M2 activation of microglia induced by HA, we hypothesis that CX3CR1 is robustly induced in HA-activated M2 microglia, leading to hippocampal neurogenesis, and thus ameliorate depressive behavior following EMF exposure. To validate this assumption, we plan to study: (1) The relationship between the enhancement of hippocampal neurogenesis and the amelioration of depressive behavior in HA-activated M2 microglia following EMF exposure. (2) CX3CR1, as a pivotal microglial M2 marker, have a potential protective role in the regulation of HA on EMF-impared hippocampal neurogenesis. (3) The mechanism of CX3CR1 pathway regulate the secretion IGF-1 and BDNF in the attenuation of depressive behavior. This study could explore the mechanism of neuroprotection of HA against EMF-induced nerve injury, and provide a effective and feasible method to protect occupational population against EMF injury.