Effects of transection of cervical sympathetic trunk on cognitive function of traumatic brain injury rats

Objective: To observe the effects of transection of cervical sympathetic trunk (TCST) on the cognitive function of traumatic brain injury (TBI) rats and the potential mechanisms. Methods: A total of 288 adult male SD rats were divided into 3 groups using a random number table: TBI group (n=96), TBI + TCST group (n=96) and Sham group (n=96). The water maze test was performed before TBI (T0) and at day 1 (T-1), day 2 (T-2), day 3 (T-3), 1 week (T-4), 2 weeks (T-5), 6 weeks (T-6) and 12 weeks (T-7) after TBI. The levels of alpha 1-adrenergic receptors (alpha 1-ARs), alpha 2-adrenergic receptors (alpha 2-ARs), toll-like receptor 4 (TLR-4) and P38 in hippocampi were detected by real-time PCR. Hippocampal P38 expression was assayed by Western blot. The expressions of interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha) and brain-derived neurotrophic factor (BDNF) were examined by immunohistochemistry. Noradrenaline (NE) expression in plasma was evaluated by ELISA. The respiratory control ratio (RCR) of brain mitochondria was detected using a Clark oxygen electrode. Results: TCST effectively improved the cognitive function of TBI rats. TCST significantly inhibited sympathetic activity in the rats and effectively inhibited inflammatory responses. The expression of BDNF at T-1-T-6 in TBI+TCST group was higher than that in TBI group (P<0.05). Furthermore, P38 expression was inhibited more effectively in TBI+TCST group (P<0.05), than in TBI group (P<0.05), and the RCR of the brain was significantly higher in TBI+TCST group than in TBI group (P<0.05). Conclusions: TCST can enhance cognitive function in TBI rats by inhibiting sympathetic activity, reducing inflammatory responses and brain edema, upregulating BDNF and improving brain mitochondrial function.