Emerging roles of miRNAs in neuropathic pain: From new findings to novel mechanisms.

Neuropathic pain, which results from damage to the somatosensory nervous system, is a global clinical condition that affects many people. Neuropathic pain imposes significant economic and public health burdens and is often difficult to manage because the underlying mechanisms remain unclear. However, mounting evidence indicates a role for neurogenic inflammation and neuroinflammation in pain pattern development.

Effect of Stellate Ganglion Block Combined with Lidocaine at Different Concentrations for Preemptive Analgesia on Postoperative Pain Relief and Adverse Reactions of Patients Undergoing Laparoscopic Cholecystectomy.

Objective: To explore the effect of stellate ganglion block (SGB) combined with lidocaine at different concentrations for preemptive analgesia on postoperative pain relief and adverse reactions of patients undergoing laparoscopic cholecystectomy (LC).

Methods: Ninety patients undergoing LC in our hospital from June 2019 to June 2020 were selected as the subjects and were randomly divided into group A (30 cases), group B (30 cases), and group C (30 cases), all patients received SGB, and 10 mL of lidocaine at concentrations of 0.25%, 0.

P2Y1 purinergic receptor inhibition attenuated remifentanil-induced postoperative hyperalgesia via decreasing NMDA receptor phosphorylation in dorsal root ganglion.

Background: Remifentanil-induced postoperative hyperalgesia is an intractable side effect of the clinical use of remifentanil, the mechanism of which remains obscure, especially in the peripheral nervous system. N-methyl-D-aspartate receptor (NMDAR) phosphorylation in dorsal root ganglion (DRG) plays a pronociceptive role in neuropathic pain. The contribution of the P2Y1 purinergic receptor (P2Y1R) in DRG to pain hypersensitivity derived from various origins and P2Y1R upregulation-induced NMDAR activation in neurons have also been uncovered.

P2Y1 Purinergic Receptor Contributes to Remifentanil-Induced Cold Hyperalgesia via Transient Receptor Potential Melastatin 8-Dependent Regulation of N-methyl-d-aspartate Receptor Phosphorylation in Dorsal Root Ganglion.

Background: Remifentanil can induce postinfusion cold hyperalgesia. N-methyl-d-aspartate receptor (NMDAR) activation and upregulation of transient receptor potential melastatin 8 (TRPM8) membrane trafficking in dorsal root ganglion (DRG) are critical to cold hyperalgesia derived from neuropathic pain, and TRPM8 activation causes NMDAR-dependent cold response. Contribution of P2Y1 purinergic receptor (P2Y1R) activation in DRG to cold pain hypersensitivity and NMDAR activation induced by P2Y1R upregulation in neurons are also unraveled.