Abstract
BackgroundPain is a subjective experience derived from complex interactions among biological, environmental, and psychosocial pathways. Sex differences in pain sensitivity and chronic pain prevalence are well established. However, the molecular basis underlying these sex dimorphisms are poorly understood particularly with regard to the role of the peripheral nervous system. Here we sought to identify shared and distinct gene networks functioning in the peripheral nervous systems that may contribute to sex differences of pain in rats after nerve injury.ResultsWe performed RNA-seq on dorsal root ganglia following chronic constriction injury of the sciatic nerve in male and female rats. Analysis from paired naive and injured tissues showed that 1513 genes were differentially expressed between sexes. Genes which facilitated synaptic transmission in naïve and injured females did not show increased expression in males.ConclusionsAppreciating sex-related gene expression differences and similarities in neuropathic pain models may help to improve the translational relevance to clinical populations and efficacy of clinical trials of this major health issue.
Highlights
Pain is a subjective experience derived from complex interactions among biological, environmental, and psychosocial pathways
Ribonucleic Acid (RNA)-seq transcriptome profiles of Dorsal Root Ganglion (DRG) from gonadally intact, adult male and female rats were measured from naïve animals and animals at 14 days after sciatic chronic constriction injury (CCI) (Fig. 1)
Regulated genes in DRGs of naïve male and female rats To identify sex-specific differences of gene expression in DRG under physiological conditions, we performed RNA-seq and measured all poly(A)-containing transcripts expressed in the L4-L6 DRG of naïve rats (Fig. 2a)
Summary
Pain is a subjective experience derived from complex interactions among biological, environmental, and psychosocial pathways. Sex differences in pain sensitivity and chronic pain prevalence are well established. Sex differences in the susceptibility to most chronic pain conditions are well established [5] and experimental pain studies consistently demonstrate greater pain sensitivity, increased pain ratings, and decreased tolerance to a variety of pain modalities in women versus men [5,6,7,8,9]. The few studies that have used rodent models of chronic pain to examine sex-specific differences have primarily focused on the hormonal and neuroimmune effects on pain modulation in the central nervous system (CNS) [12]. The role of microglia-neuronal signaling pathways in pain pathophysiology had been characterized using predominantly male mice, recent evidence demonstrated that female and male mice use distinct immune cell types to modulate pain behaviors [14, 15]
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