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Acta Biochim Biophys Sin (Shanghai). 2015 Aug;47(8):647-53. doi: 10.1093/abbs/gmv049. Epub 2015 Jun 9.

Involvement of cannabinoid receptors in infrasonic noise-induced neuronal impairment.

Author information

1
Department of Neurology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
2
Department of Specific Diagnosis, PLA 323 Hospital, Xi'an 710032, China.
3
Fourth Military Medical University, Xi'an 710032, China.
4
Department of Radiation Medicine and Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an 710032, China kangchu@fmmu.edu.cn biomidas@fmmu.edu.cn.
5
Department of Neurology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China kangchu@fmmu.edu.cn biomidas@fmmu.edu.cn.

Abstract

Excessive exposure to infrasound, a kind of low-frequency but high-intensity sound noise generated by heavy transportations and machineries, can cause vibroacoustic disease which is a progressive and systemic disease, and finally results in the dysfunction of central nervous system. Our previous studies have demonstrated that glial cell-mediated inflammation may contribute to infrasound-induced neuronal impairment, but the underlying mechanisms are not fully understood. Here, we show that cannabinoid (CB) receptors may be involved in infrasound-induced neuronal injury. After exposure to infrasound at 16 Hz and 130 dB for 1-14 days, the expression of CB receptors in rat hippocampi was gradually but significantly decreased. Their expression levels reached the minimum after 7- to 14-day exposure during which the maximum number of apoptotic cells was observed in the CA1. 2-Arachidonoylglycerol (2-AG), an endogenous agonist for CB receptors, reduced the number of infrasound-triggered apoptotic cells, which, however, could be further increased by CB receptor antagonist AM251. In animal behavior performance test, 2-AG ameliorated the infrasound-impaired learning and memory abilities of rats, whereas AM251 aggravated the infrasound-impaired learning and memory abilities of rats. Furthermore, the levels of proinflammatory cytokines tumor necrosis factor alpha and interleukin-1β in the CA1 were upregulated after infrasound exposure, which were attenuated by 2-AG but further increased by AM251. Thus, our results provide the first evidence that CB receptors may be involved in infrasound-induced neuronal impairment possibly by affecting the release of proinflammatory cytokines.

KEYWORDS:

cannabinoid receptors; infrasound; neuronal impairment; proinflammatory cytokines; vibroacoustic disease

PMID:
26058582
DOI:
10.1093/abbs/gmv049
[Indexed for MEDLINE]

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