Effect of Vagus Nerve Stimulation on Wake-promoting and Expression of γ-aminobutyric Acid b1 Receptor in Prefrontal Cortex of Coma Rats post Traumatic Brain Injury
10.3969/j.issn.1006-9771.2017.09.010
- VernacularTitle:迷走神经电刺激对脑外伤昏迷大鼠意识及前额叶皮质γ-氨基丁酸b1受体表达的影响
- Author:
Chengcheng LIAO
;
Zhen FENG
;
Feifei HUANG
;
Qin CHEN
- Keywords:
traumatic brain injury;
coma;
vagus nerve stimulation;
wake-promoting;
γ-aminobutyric acid b1 receptor;
rats
- From:
Chinese Journal of Rehabilitation Theory and Practice
2017;23(9):1037-1042
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the wake-promoting effect of vagus nerve stimulation (VNS) on coma rats after traumatic brain in-jury (TBI), and the related mechanism. Methods A total of 168 healthy Sprague-Dawley rats were randomly divided into blank group, TBI group, antagonist group and VNS group, 42 rats in each group. The latter three groups were established TBI model with impact, and the rats in coma at least 30 minutes were included. VNS group accepted VNS, the antagonist group were injected intralateroventricularly Orexin A receptor 1 (OXR1) antagonist SB334867, and TBI group accepted sham VNS. Their behaviors were observed to determine the level of con-sciousness six, twelve and 24 hours after intervention, while the expression ofγ-aminobutyric acid b1 receptor (GABAb1R) in prefrontal cortex was detected with immunohistochemistry and Western blotting. Results There were 42 rats in the blank group, 11 rats in TBI group, 13 rats in the antagonist group, and 28 rats in VNS group awakened finally. The expression of GABAb1R in prefrontal cortex ranged as TBI group, antagonist group, blank group and VNS group from more to less twelve and 24 hours after intervention under Western blotting (F>60.412, P<0.001), and it ranged as TBI group, antagonist group, VNS group and blank group under immunohistochemistry (H=15.121, P=0.002), with no significant difference among time points (H=3.028, P=0.220). Conclusion VNS can promote waking from coma in rats after TBI, which may relate with the decrease of GABAb1R in prefrontal cortex that induced by Orexin A.