| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6264612 | Brain Research | 2011 | 7 Pages |
We investigated the mechanism underlying inhibition of spinal dorsal horn GABAergic neurotransmission to elucidate the role of protease-activated receptor-2 (PAR2). Initially, we confirmed that PAR2 agonist SL-NH2 applied intrathecally produced mechanical hyperalgesia. Then we performed patch-clamp experiments in substantia gelatinosa neurons of spinal cord slice, and found that spontaneous inhibitory post-synaptic currents (sIPSCs) were significantly decreased in both frequency and amplitude when neurons were incubated with PAR2 agonist SL-NH2 for a brief time period (2Â min). The GABA-mediated currents were significantly reduced, and there was no impact on glycine-mediated currents during this SL-NH2 treatment. These results suggest that PAR2 activation enhanced the pain response, potentially via inhibition of dorsal horn GABAergic neurotransmission.
⺠PAR2 agonist applied intrathecally produced mechanical hyperalgesia. ⺠Acute PAR2 activation decreased spontaneous IPSCs in substantia gelatinosa. ⺠Acute PAR2 activation reduced GABA-induced currents in substantia gelatinosa. ⺠PAR2 agonist had no effect on glycine-induced currents in substantia gelatinosa.
