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Journal of pain research
Por Ke D, Deng P, Hua J y 6 más.
Contenido en inglés
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Chemotherapy-induced peripheral neuropathy (CIPN) is a common dose-limiting adverse effect of anticancer therapy and is frequently accompanied by anxiety-related symptoms. Effective preventive treatments are lacking, and available pharmacological options provide limited relief, highlighting the need for adjunctive non-pharmacological strategies in cancer care. Emerging evidence suggests that astrocyte-neuron crosstalk within the anterior cingulate cortex (ACC) contributes to chronic pain and pain-associated emotional disorders. Electroacupuncture (EA) has shown beneficial effects in CIPN; however, the central mechanisms underlying its therapeutic actions remain unclear. This study investigated whether astrocyte-mediated neuronal activation in the ACC is associated with the analgesic and anxiolytic effects of EA in CIPN.
A mouse model of CIPN was established by repeated intraperitoneal administration of paclitaxel. Mice received EA or sham EA once daily for seven consecutive days. Mechanical allodynia, thermal hyperalgesia, and anxiety-like behaviors were assessed using the von Frey test, Hargreaves test, and open field test, respectively. Astrocytic and neuronal activation, GAT-1 expression, and GABA levels in the ACC were evaluated by immunofluorescence staining, Western blotting, and ELISA. Chemogenetic approaches were used to selectively activate or inhibit ACC astrocytes.
CIPN mice exhibited significant mechanical and thermal hypersensitivity and anxiety-like behaviors. EA significantly alleviated pain hypersensitivity and anxiety-like behaviors while suppressing astrocytic activation, downregulating GAT-1 expression, restoring GABA levels, and reducing neuronal activation. Chemogenetic inhibition of ACC astrocytes alleviated pain- and anxiety-like behaviors in CIPN mice, whereas astrocytic activation markedly attenuated the beneficial effects of EA.
EA alleviates CIPN-induced pain hypersensitivity and anxiety-like behaviors by suppressing astrocytic activation, normalizing GAT-1 expression and GABA levels, and attenuating neuronal activation in the ACC. These findings identify astrocyte-mediated neuronal activation as a novel mechanism involved in EA-induced analgesia and a potential therapeutic target for CIPN and its associated affective comorbidities. Overall, this study provides preclinical mechanistic evidence for further evaluating EA as an adjunctive non-pharmacological approach for the integrated management of neuropathic pain and affective symptoms in patients with CIPN.
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