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1 ensory neurons express messenger RNA for the P2X3 receptor.
2 latability of potential analgesics targeting P2X3 receptors.
3 responsible for the potency drop in primate P2X3 receptors.
4 express TRPV1, bradykinin B2, and purinergic P2X3 receptors.
5 ors, and enhanced the expression of P2X2 and P2X3 receptors.
6 ochemically stained with an antibody against P2X3 receptors.
7 p, 11, was also very potent at both P2X1 and P2X3 receptors.
8 e, 10, was 28-fold selective for P2X1 versus P2X3 receptors.
9 with activation of the rapidly desensitising P2X3 receptors.
10 tivation of nociceptive fibres which possess P2X3 receptors.
11 phenomena are normalized by the blockade of P2X3 receptors.
12 .03) but was significantly higher (0.07) for P2X3 receptors.
15 ndogenously active CaMKII up-regulates basal P2X3 receptor activity in dorsal root ganglion neurons.
17 s of 5 mM at the P2X2 receptor, 89 mM at the P2X3 receptor and 15 mM at both the P2X2/3 heteromeric r
18 s probably due to co-expression of homomeric P2X3 receptors and heteromeric receptors comprising P2X3
22 agonist, A-317491, all indicate that ATP and P2X3 receptors are more likely to be involved in chronic
24 These data support the identification of the P2X3 receptor as a potential new target for the control
32 al assays at recombinant rat P2X1, P2X2, and P2X3 receptors expressed in Xenopus oocytes (ion flux st
35 ckout mice lacking expression of P2X2 and/or P2X3 receptors failed to show increases in apical surfac
38 showed weak antagonistic activity at the rat P2X3 receptor (IC50 58.3 +/- 0.1 microM), while at recom
39 report X-ray crystal structures of the human P2X3 receptor in apo/resting, agonist-bound/open-pore, a
40 ATP currents that are mediated by homomeric P2X3 receptors in dorsal root ganglion (DRG) neurons iso
42 we studied the presence and distribution of P2X3 receptors in human dental pulp, and their co-locali
44 rical stimulation enhances the expression of P2X3 receptors in the membrane and that the enhancement
46 substitutions at equivalent positions in the P2X3 receptor (Lys63 and Lys299) also prevented channel
50 We therefore studied the effects of PGE2 on P2X3 receptor-mediated ATP currents in DRG neurons disso
52 sis, unbinding of [32P]ATP from desensitized P2X3 receptors mirrored the rate of recovery from desens
53 n the supposed ATP binding site of the human P2X3 receptor on the agonistic effect of nucleotide anal
54 studies demonstrate increased expression of P2X3 receptors on CGRP-ir ENFs during tumor growth and s
55 identify whether changes in the labeling of P2X3 receptors on epidermal nerve fibers (ENFs) occurred
58 ssumption has been that eliminating P2X2 and P2X3 receptors only removes postsynaptic targets but tha
59 e largely abolished in mice lacking P2X2 and P2X3 receptors [P2X2 and P2X3 double knock-out (DKO) mic
61 rgic, placodal in origin, expresses P2X2 and P2X3 receptors, responds to alpha,beta-methylene ATP, an
65 nusual subtype of ATP-gated ion channel, the P2X3 receptor, that rapidly desensitizes (<100 msec) and
67 l evidence showed that immunostaining of the P2X3 receptors was more intense in both IB4-positive (C-
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