title: Involvement of microglial cells in infrasonic noise-induced stress via upregulated expression of corticotrophin releasing hormone type 1 receptor.
abstract: Infrasound is a kind of environmental noise and threatens the public health as a nonspecific biological stressor. Upregulated expression of corticotrophin releasing hormone (CRH) and its receptor CRH-R1 in the neurons of hypothalamic paraventricular nucleus (PVN) was reported to be responsible for infrasonic noise-induced stress and injuries. Recent studies revealed that CRH-R1 is expressed in activated microglial cells, lending support to the hypothesis that microglial cells may be also responsible for infrasonic noise-induced stress. In this work, we exposed Sprague-Dawley rats and in vitro cultured microglial cells to infrasound with a main frequency of 16 Hz and a sound pressure level of 130 dB for 2 h, and examined the changes in the expression of CRH-R1 at different time points after infrasound exposure by immunohistochemistry and semi-quantitative RT-PCR. We found that infrasound exposure resulted in a significant activation of microglia cells and upregulated their expression of CRH-R1 in the PVN in vivo. Upregulated expression of CRH-R1 can be blocked by antalarmin, a selective CRH-R1 antagonist. Our in vitro data further revealed that in the absence of neurons, infrasound can directly induce microglial activation and upregulate their CRH-R1 expression. These findings suggest that in addition to the PVN neurons, microglial cells are the effector cells for infrasound as well, and involve in the infrasound-induced stress through upregulated expression of CRH-R1.
authors.affiliation: Department of Neurology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, PR China.
authors.forename: F
authors.initials: F
authors.lastname: Du
authors.forename: L
authors.initials: L
authors.lastname: Yin
authors.forename: M
authors.initials: M
authors.lastname: Shi
authors.forename: H
authors.initials: H
authors.lastname: Cheng
authors.forename: X
authors.initials: X
authors.lastname: Xu
authors.forename: Z
authors.initials: Z
authors.lastname: Liu
authors.forename: G
authors.initials: G
authors.lastname: Zhang
authors.forename: Z
authors.initials: Z
authors.lastname: Wu
authors.forename: G
authors.initials: G
authors.lastname: Feng
authors.forename: G
authors.initials: G
authors.lastname: Zhao
mesh_terms: D000161:Acoustic Stimulation; D000162:Acoustics; D000818:Animals; D002478:Cells, Cultured; D005911:Gliosis / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D007031:Hypothalamus / Q000378:metabolism* / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D017628:Microglia / Q000378:metabolism*; D009622:Noise / Q000009:adverse effects*; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism / Q000503:physiopathology; D011743:Pyrimidines / Q000494:pharmacology; D011758:Pyrroles / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018019:Receptors, Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013312:Stress, Physiological / Q000502:physiology*; D015854:Up-Regulation / Q000502:physiology; D000099052:CRF Receptor, Type 1
chemical_list: D011743:Pyrimidines; D011758:Pyrroles; D018019:Receptors, Corticotropin-Releasing Hormone; C103016:antalarmin; D000099052:CRF Receptor, Type 1