NaHS modulates astrocytic EAAT2 expression to impact SNI-induced neuropathic pain and depressive-like behaviors.

Abstract

The potential role of hydrogen sulfide (HS) in the modulation of neuropathic pain is increasingly recognized. This study investigated the therapeutic effect of intraperitoneal injection of the HS donor sodium hydrosulfide (NaHS) on neuropathic pain. Utilizing the spared nerve injury (SNI) model in mice, the research investigates the role of astrocytes and the excitatory neurotransmitter glutamate in chronic pain. The findings reveal that sodium hydrosulfide (NaHS), an HS donor, effectively enhances the mechanical pain threshold and thermal pain escape latency in SNI mice. The study further demonstrates NaHS's potential in reducing glutamate levels in the spinal cord and the discharge frequency of neurons in the primary somatosensory cortex hindlimb region (S1HL) brain area, suggesting a novel therapeutic approach for neuropathic pain through the modulation of astrocyte function and EAAT2 expression.