Amphiregulin contributes to neuropathic pain by enhancing glycolysis that stimulates histone lactylation in sensory neurons.

The genesis of neuropathic pain after peripheral nerve injury is associated with changes in gene expression and cell metabolism in sensory neurons and the release of inflammatory cytokines. Here, we connected glycolytic metabolism induced by the epidermal growth factor receptor (EGFR) ligand amphiregulin (AREG) to histone lactylation and changes in gene expression that promote chronic neuropathic pain. In both male and female mice subjected to peripheral nerve injury, the mRNA and protein abundance of AREG and its receptor EGFR was increased in dorsal root ganglia (DRGs).

From sensation to regulation: the diverse functions of peripheral sensory nervous system.

The peripheral sensory nervous system (PNS) has been widely recognized for its role in the collection, processing, and transmission of sensory information, including thermal, mechanical, chemical, and proprioceptive stimuli. In recent years, there has been a growing scholarly interest in the PNS attributable to its multiple physiological and pathophysiological non-sensory roles in the organs it innervates. The PNS exerts regulatory functions within the organs it innervates through direct interactions with local cells or through microbe-nerve-cell interactions that differ from the traditional feedback regulatory modes used by the hormonal and sensory brain-sympathetic/parasympathetic systems.

An atlas of neuropathic pain-associated molecular pathological characteristics in the mouse spinal cord.

Peripheral nerve injury (PNI)-induced neuropathic pain (NP) is a severe disease with high prevalence in clinics. Gene reprogramming and tissue remodeling in the dorsal root ganglia (DRG) and spinal cord (SC) drive the development and maintenance of neuropathic pain (NP). However, our understanding of the NP-associated spatial molecular processing landscape of SC and the non-synaptic interactions between DRG neurons and SC cells remains limited.