Objective To evaluate the relationship between hydrogen sulfide (H2S) and P2X3 receptors in dorsal root ganglions (DRGs) of rats with neuropathic pain (NP).Methods Thirty-six healthy male Sprague-Dawley rats,aged 4-6 weeks,weighing 180-200 g,in which IT catheters were successfully implanted,were divided into 3 groups (n=12 each) using a random number table method:sham operation group (group S),group NP and endogenous H2S synthase (cystathionine beta-syntheses [CBS]) inhibitor animooxyacetic acid (AOAA) group (group A).NP was induced by chronic constriction injury (CCI) to the sciatic nerve at 3 days after IT catheters were successfully implanted.AOAA (10 μg/kg) 10 μl and normal saline 10 μl were intrathecally injected once a day for 14 consecutive days starting from 1 day after CCI in group A,and normal saline 20 μl was intrathecally injected instead in S and NP groups.At 1 day before CCI and 1,3,7,10 and 14 days after CCI,the thermal paw withdrawal latency (TWL) and mechanical paw withdrawal threshold (MWT) were measured at 30 min after intrathecal injection.The animals were sacrificed at 7 and 14 days after CCI,and ipsilateral DRGs of the lumbar segment (L4-6) were removed for detection of the expression of CBS and P2X3 receptors by Western blot.Results Compared with group S,the TWL was significantly shortened,MWT was decreased,and the expression of CBS and P2X3 receptors in DRGs was up-regulated at each time point after CCI in group NP (P＜0.05).Compared with group NP,the TWL was significantly prolonged,the MWT was increased,and the expression of CBS and P2X3 receptors in DRG s was down-regulated at each time point after CCI in group A (P＜0.05).Conclusion H2S in DRG s can up-regulate the expression of P2X3 receptors,which may be involved in the pathophysiological mechanism of NP in rats.

The mammalian central nervous system (CNS) is considered an immune privileged system as it is separated from the periphery by the blood brain barrier (BBB). Yet, immune functions have been postulated to heavily influence the functional state of the CNS, especially after injury or during neurodegeneration. There is controversy regarding whether adaptive immune responses are beneficial or detrimental to CNS injury repair. In this study, we utilized immunocompromised SCID mice and subjected them to spinal cord injury (SCI). We analyzed motor function, electrophysiology, histochemistry, and performed unbiased RNA-sequencing. SCID mice displayed improved CNS functional recovery compared to WT mice after SCI. Weighted gene-coexpression network analysis (WGCNA) of spinal cord transcriptomes revealed that SCID mice had reduced expression of immune function-related genes and heightened expression of neural transmission-related genes after SCI, which was confirmed by immunohistochemical analysis and was consistent with better functional recovery. Transcriptomic analyses also indicated heightened expression of neurotransmission-related genes before injury in SCID mice, suggesting that a steady state of immune-deficiency potentially led to CNS hyper-connectivity. Consequently, SCID mice without injury demonstrated worse performance in Morris water maze test. Taken together, not only reduced inflammation after injury but also dampened steady-state immune function without injury heightened the neurotransmission program, resulting in better or worse behavioral outcomes respectively. This study revealed the intricate relationship between immune and nervous systems, raising the possibility for therapeutic manipulation of neural function via immune modulation.