Electroacupuncture-induced cannabinoid receptor expression in repair of abducens nerve.

Objective: Through the development of beagle abducens nerve injury model, taking electroacupuncture as the core and microglia as the starting point, the author investigated whether electroacupuncture can promote the repair of injured abducens nerve by cannabinoid receptor-mediated regulation of microglia activation. Methods: Healthy beagle dogs were randomly divided into five groups: sham operation group (A), injury group (B), electroacupuncture pretreatment group (C), antagonist group (D) and solvent group (E). After stimulation with electroacupuncture, the expression of cannabinoid 1 receptor (CB1R) and cannabinoid 2 receptor (CB2R) in A, B and C microglia cells was detected by Western Bolt analysis, and further the expression of CB2R in five groups was further analyzed by immunofluorescence, thereby statistical differences were analyzed. Results: Among group A, group B and group C, Western Blot analysis showed that there were no significant changes in the expression of CB1R protein after electroacupuncture [F (2, 12)=1.75, p = 0.215]. After electroacupuncture preconditioning for 15 min for 2 weeks, group C was compared with group A and group B, which showed CB2 was affected. The expression of CB2R protein was significantly increased among groups A, B and C [F (2, 12)=5189.57, p < 0.001], but there was no significant difference in the expression of CB2R protein between group A and group B (p > 0.05). The results of immunofluorescence showed that Arginse/CD11b was significantly increased in group C comparing to group A (*p < 0.001), while there was a significant increase in group E comparing to group A about Arginse/CD11b [F (4, 20)=4345.44, p < 0.001]. Conclusions: The CB2R in the cannabinoid receptor is mainly involved in the electro-acupuncture-induced neuroprotection. Electroacupuncture can promote the repair of injured abducens nerve by CB2R-mediated activation of microglia.

Activation of c-Jun and ATF-2 in primate motor cranial nerve nuclei is not associated with apoptosis following axotomy.

Nerve transection induces complex changes in gene regulation and expression that can have profound phenotypic effects on the fate of axotomized neurons. The transcription factors c-Jun and ATF-2 (activating transcription factor-2) are components of a regulatory network that mediates survival, regeneration, and apoptosis following axotomy in rodents. The activation and function of c-Jun and ATF-2 after nerve injury have not been examined in primates. Using a novel model of cranial nerve injury in baboons, we have examined the temporality of c-Jun activation (phosphorylation) in cranial nerve (CN) III and CN VI neurons and ATF-2 activation in CN VI neurons at 2, 4, and 9 days post-injury by immunohistochemistry. Furthermore, we have addressed whether the activation of these factors is associated with apoptosis by the TUNEL assay. We report that activated c-Jun is present in CN III and CN VI neurons ipsilateral to axotomy at 2, 4, and 9 days post-injury, but not in neurons contralateral to injury. Additionally, CN VI neurons ipsilateral to injury at 4 and 9 days contain activated ATF-2. Furthermore, no evidence of TUNEL reactivity was observed in either nucleus, regardless of laterality, at any of the examined time points. These findings suggest that activation of both c-Jun and ATF-2 does not mediate apoptosis in axotomized primate CN III and CN VI neurons at time points up to 9 days. This report serves as a basic inquiry into the neuronal response to cranial nerve injury in primates.