Neuroscience 2005 Abstract
| Presentation Number: | 291.19 |
|---|---|
| Abstract Title: | Mechanical allodynia induced by P2Y2 receptor activation. |
| Authors: |
Koizumi, S.*1
; Tsuda, M.2
; Inoue, K.2
1Div. of Pharmacol., Natl Inst. Health Sci, Tokyo, Japan 2Japan, 1-18-1 Kamiyoga, Setagaya, 158-8501, |
| Primary Theme and Topics |
Sensory and Motor Systems - Pain -- Pain transduction molecules and channels |
| Secondary Theme and Topics | Neural Excitability, Synapses, and Glia: Cellular Mechanisms<br />- G-Protein Linked Receptors<br />-- Purine receptors |
| Session: |
291. Nocieptive Processing: Modulation Poster |
| Presentation Time: | Sunday, November 13, 2005 3:00 PM-4:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # CC15 |
| Keywords: | PURINERGIC, ATP, PAIN |
ATP has been implicated in the initial algogenic signal via ionotropic P2X receptors in sensory neurons. However, possible roles for metabotropic P2Y receptors in nociceptive signaling have received limited attention in spite of the fact that they are expressed in dorsal root ganglion (DRG) neurons. In the 34th SFN meeting 2004, we showed that epidermal keratinocytes release ATP that propagates Ca2+ wave from keratinocytes to sensory neurons via P2Y2 receptors. The aim of this study is to characterize functional P2Y receptors in DRG neurons in relation to pain behavior. Injection of the P2Y2 and P2Y4 receptor agonist uridine 5'-triphosphate (UTP) into plantar surface in rats produced the mechanical allodynia. The UTP-induced mechanical allodynia was inhibited by suramin or antisense oligonucleotide for P2Y2 receptors. The UTP-evoked pain behavior was different from the P2X receptor agonist alpha-beta-meATP-evoked one in that the former induced only mechanical allodynia whereas the latter induced thermal hyperalgesia as well as mechanical allodynia. Mechanism underlying P2X receptor-mediated mechanical allodynia was different from the P2Y2 receptor-mediated one. The P2X receptor-mediated mechanical allodynia was independent of capsaicin-sensitive neurons, whereas the P2Y2 receptor-mediated one was almost abolished when capsaicin-sensitive neurons were destroyed by neonatal capsaicin-treatment. The mechanical allodynia however was unaffected by capsazepine, an antagonist to capsaicin receptor TRPV1. UTP produced elevations in [Ca2+]i in over 90 % of small-sized and capsaicin-sensitive DRG neurons, which was independent of extracellular Ca2+ but inhibited by suramin, a P2 receptor antagonist. UTP acting on P2Y2 receptors in small-sized and capsaicin-sensitive DRG neurons, produces hypersensitivity to innocuous mechanical stimulation, i.e., mechanical allodynia. Activation of capsaicin receptors seems to be independent of the event.
Supported by The Naito Foundation
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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