Electroacupuncture suppresses glucose metabolism and GLUT-3 expression in medial prefrontal cortical in rats with neuropathic pain

Abstract

Background Accumulating evidence has demonstrated that the electroacupuncture (EA) stimulation could effectively alleviate neuropathic pain. The medial prefrontal cortex (mPFC) is a vital part of the cortical representation of pain in the brain, and its glucose metabolism is mostly affected in the progression of pain. However, the central mechanism of EA analgesia remains unclear. Methods Fifty-four male SD rats were equally randomized into sham surgery (Sham) group, chronic constriction injury (CCI) group and EA stimulation (EA) group. The CCI model, involving ligature of the right sciatic nerve, was established in all animals except the Sham group. EA stimulation was applied on the right side acupoints of Huantiao (GB30) and Yanglingquan (GB34) in the EA group. Paw withdrawal threshold (PWT) and paw thermal withdrawal latency (PWL) were measured. The 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET) was used to evaluate glucose metabolism changes in the mPFC. The expression of glucose transporter 3 (GLUT-3) in the mPFC was determined by immune histochemistry and ELISA. Results Comparing with CCI groups, EA treatment was obviously reversed CCI-induced mechanical allodynia (P < 0.01), thermal hyperalgesia (P < 0.01) and the increase of glucose metabolism in the left mPFC (P < 0.05). Furthermore, EA treatment significantly decreased the protein expression of GLUT-3 in the left mPFC (P < 0.01). Conclusions Our results indicate that EA analgesia effect may be related to suppressing the glucose metabolism and GLUT-3 expression in the mPFC. This study could provide a potential insight into the central mechanisms involved in the analgesic effect of EA.

Baihui (DU20), Shenmen (HT7) and Sanyinjiao (SP6) target the cAMP/CREB/BDNF and PI3K/Akt pathways to reduce central nervous system apoptosis in rats with insomnia

“…In the PCPA+7,8-DHF group (n = 10), the TrkB agonist 7,8-DHF was injected intraperitoneally at a concentration of 10 mg/ml on day 2 after the model was established. In the PCPA + DHS+7,8-DHF group (n = 10), the TrkB agonist 7,8-DHF was injected intraperitoneally at a concentration of 10 mg/ml on day 2 after the model was established, and needling was performed 6 h later (same procedure as in the PCPA + DHS group) once per day for 5 days [ 18 ].…”

Role of nerve signal transduction and neuroimmune crosstalk in mediating the analgesic effects of acupuncture for neuropathic pain

“…Recently it has been revealed that the analgesic effect of acupuncture for NP may be related to metabolic regulation. EA at GB30 and GB34 significantly reversed increase in glucose metabolism induced by CCI and decreased the protein expression of glucose transporter 3 (GLUT-3) in the left medial Prefrontal Cortex (mPFC), suggesting that the analgesic effect of EA may be related to the inhibition of glucose metabolism and GLUT-3 expression in the mPFC ( 12 ). In a study involving the BPAI model, the brain metabolic connections between the bilateral hemisphere: somatosensory cortex (SC), the motor cortex (MC), caudate putamen (Cpu), and dorsolateral thalamus (DLT) were decreased compared with the normal animals.…”

Potential mechanisms of acupuncture for neuropathic pain based on somatosensory system

“…A variety of neuropathic pain animal models which induced by central or peripheral nerve injury have been used to study the acupuncture mechanism ( Table 3 ; Zhang Y. et al, 2018 ; Li et al, 2019b ; Huo B.B. et al, 2020 ; Du et al, 2021 ; Jang et al, 2021 ; Jiang et al, 2021 ; Wei et al, 2021 ; Xu et al, 2021 ; Zou et al, 2021 ). In addition to animal models of nerve ligation, there are injectable chemotherapy drug-induced neuropathy, post-herpetic neuralgia, and diabetes-induced peripheral nerve injury ( Colleoni and Sacerdote, 2010 ).…”