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This study demonstrated that the P2X3-immunoreactive nerve endings in the rat tracheal mucosa have unique morphological characteristics, and these endings may be rapidly adapting receptors and/or irritant receptors that are activated by mucosal irritant stimuli.
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Data suggest that the negative inhibition of P2X3R activity by the BNP/NPR-A pathway results in a decreased P2X3R-mediated excitability of trigeminal neurons in wildetype cultures. In familial hemiplegic migraine type-1 model cultures, however, lack of efficient P2X3Rs downregulation contributes to the neuronal hyperexcitability phenotype.
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P2X3 receptors on mouse trigeminal ganglion neurons are subjected to contrasting modulation by inhibitory brain natriuretic peptide and facilitatory calcitonin gene-related peptide that both operate via complex intracellular signaling.
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mouse trigeminal neurons endogenous BNP acts on NPR-A receptors to determine constitutive depression of P2X3 receptor function. Tonic inhibition of P2X3 receptor activity by BNP/NPR-A/PKG pathways occurs via two distinct mechanisms: P2X3 serine phosphorylation and receptor redistribution to non-raft membrane compartments
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may be involved in skeletal pain due to high bone turnover
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This study observed maltodextrin and fat preference deficits in "taste-blind" P2X2/P2X3 knockout mice.
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a slow modulatory action by BNP on TRPV1 and P2X3 receptors outlining the role of this peptide as a negative regulator of trigeminal sensory neuron excitability to nociceptive stimuli
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P2X(3)R overexpression may underlie ectopic mechanical allodynia in the whisker pad skin
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genetic manipulation of TRPV1 and P2X3 leads to reduction in colorectal mechanosensation peripherally and compensatory changes and/or disinhibition of other channels centrally.
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up-regulation of P2X3 receptors probably is already maximal and is apparently contributed by basal CGRP and BDNF levels
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Structure and function of P2RX3 is reviewed, and its role in treatment of pain is discussed. [Review Article]
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interaction between P2X3/TRPV1 and ERs expression in sensory neurons may represent a novel mechanism that can explain the sex differences in nociception observed in clinical practice.
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An interaction between P2X3 and membrane-associated ERalpha in primary sensory neurones that may represent a novel mechanism to explain sex differences observed in the clinical presentation of visceral nociceptive syndromes.
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Transcripts for P2X3 were present in nearly all colon neurons examined. About half of the cells only containing P2X3 transcripts, and zymosan did not change this. The fast current triggered by ATP and alpha,beta-meATP is dependent on P2X3 receptors.
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CACNA1A mutation conferred a novel molecular phenotype to P2X3 receptors of trigeminal ganglion neurons via CaMKII-dependent activation of calcineurin.
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chronic esophagitis results in upregulation of P2X(3) and its co-localization with TRPV1 receptor in vagal and spinal afferents.
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Data suggest that double P2X2/P2X3 purinergic receptor knockout mice are unable to respond to NaCl or the artificial sweetener SC45647 as taste stimuli, mirroring the lack of gustatory nerve responses to these substances.
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In brief access tests, double P2X2/P2X3 purinergic receptor null mice avoided citric acid and hydrochloric acid at the same concentrations as their wild-type counterparts, indicating that these weak acids activate oropharyngeal chemoreceptors.
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P2X3-/- DRG neurons lacked rapidly desensitizing response to ATP, and both DRG and nodose neurons from P2X3-null mutant mice no longer responded to alpha,beta-methylene ATP (alphabetameATP).
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P2X3-mediated responses in dorsal root ganglion neurons were changed in the A/J inbred mouse strain, suggesting that the downregulation of sensory P2X3 might cause low sensitivity to tissue injury pain.
