Overexpression of P2X3 and P2X7 Receptors and TRPV1 Channels in Adrenomedullary Chromaffin Cells in a Rat Model of Neuropathic Pain

We have tested the hypothesis that neuropathic pain acting as a stressor drives functional plasticity in the sympathoadrenal system. The relation between neuropathic pain and adrenal medulla function was studied with behavioral, immunohistochemical and electrophysiological techniques in rats subject...

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Bibliographic Details
Authors: Arribas Blázquez, Marina, Olivos Ore, Luis Alcides, Barahona Gomáriz, María Victoria, Sánchez de la Muela, Mercedes, Solar, Virginia, Jiménez, Esperanza, Gualix Sánchez, Francisco Javier, McIntosh, J. Michael, Ferrer-Montiel, Antonio, Miras Portugal, María Teresa, Rodríguez Artalejo, Antonio
Format: article
Publication Date:2019
Country:España
Institution:Universidad Complutense de Madrid (UCM)
Repository:Docta Complutense
Language:English
OAI Identifier:oai:docta.ucm.es:20.500.14352/12515
Online Access:https://hdl.handle.net/20.500.14352/12515
Access Level:Open access
Keyword:P2X3 receptors
P2X7 receptors
TRPV1 channels
α9 nicotinic acetylcholine receptors
neuropathic pain
chromaffin cells
adrenal medulla
stress
Microbiología (Veterinaria)
Patología veterinaria
3109.05 Microbiología
3109.07 Patología
Description
Summary:We have tested the hypothesis that neuropathic pain acting as a stressor drives functional plasticity in the sympathoadrenal system. The relation between neuropathic pain and adrenal medulla function was studied with behavioral, immunohistochemical and electrophysiological techniques in rats subjected to chronic constriction injury of the sciatic nerve. In slices of the adrenal gland from neuropathic animals, we have evidenced increased cholinergic innervation and spontaneous synaptic activity at the splanchnic nerve–chromaffin cell junction. Likewise, adrenomedullary chromaffin cells displayed enlarged acetylcholine-evoked currents with greater sensitivity to α-conotoxin RgIA, a selective blocker of α9 subunit-containing nicotinic acetylcholine receptors, as well as increased exocytosis triggered by voltage-activated Ca2+ entry. Altogether, these adaptations are expected to facilitate catecholamine output into the bloodstream. Last, but most intriguing, functional and immunohistochemical data indicate that P2X3 and P2X7 purinergic receptors and transient receptor potential vanilloid-1 (TRPV1) channels are overexpressed in chromaffin cells from neuropathic animals. These latter observations are reminiscent of molecular changes characteristic of peripheral sensitization of nociceptors following the lesion of a peripheral nerve, and suggest that similar phenomena can occur in other tissues, potentially contributing to behavioral manifestations of neuropathic pain.