Abstract
The distributions of P2X subtypes during peripheral neuropathic pain conditions and their differential roles are not fully understood. To explore these characteristics, the lumbosacral dorsal root ganglion (DRG) in the chronic constriction injury (CCI) sciatic nerve rat model was studied. Retrograde trace labeling combined with immunofluorescence technology was applied to analyze the distribution of neuropathic nociceptive P2X1-6 receptors. Our results suggest that Fluoro-Gold (FG) retrograde trace labeling is an efficient method for studying lumbosacral DRG neurons in the CCI rat model, especially when the DRG neurons are divided into small, medium, and large subgroups. We found that neuropathic nociceptive lumbosacral DRG neurons (i.e., FG-positive cells) were significantly increased in medium DRG neurons, while they declined in the large DRG neurons in the CCI group. P2X3 receptors were markedly upregulated in medium while P2X2 receptors were significantly decreased in small FG-positive DRG neurons. There were no significant changes in other P2X receptors (including P2X1, P2X4, P2X5, and P2X6). We anticipate that P2X receptors modulate nociceptive sensitivity primarily through P2X3 subtypes that are upregulated in medium neuropathic nociceptive DRG neurons and/or via the downregulation of P2X2 cells in neuropathic nociceptive small DRG neurons.
Highlights
Pain is an annoying sensory or experience initiated by a primary lesion or dysfunction in the nervous system [1]
FG retrograde labeling combined with an immunofluorescence method was utilized to explore the P2XR expression profile in neuropathic nociceptive lumbosacral dorsal root ganglion (DRG) neurons in the constriction injury (CCI) rat model
Our results suggest that FG retrograde trace labeling is an efficient method to obtain more details about neuropathic nociceptive lumbosacral DRG neurons in the CCI rat model, especially when the DRG neurons are divided into three subgroups
Summary
Pain is an annoying sensory or experience initiated by a primary lesion or dysfunction in the nervous system [1]. The underlying reason is partly due to the plasticity of nociceptive receptors, making it difficult to understand the development of peripheral neuropathic pain. Dissecting the nociceptive receptor plasticity characteristics in sensory neurons allows the design of appropriate receptor-targeted approaches for its treatment [2]. Ion channel activity is considerable during the process of neuropathic pain pathophysiology. ATP, a powerful mediator that activates ligand-gated ion channels (P2X receptors), has been reported to be involved in migraine [4] and to participate in pain signaling in the spinal cord [5]. Some researchers have shown that P2X3 expression during neuropathic pain remains unchanged [10] or decreases after peripheral nerve injury [11].
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