Abstract
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 (2min). 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.
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