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GW7647 shifted the concentration-response curve for proton downwards, with a decrease of 36.9 ± 2.3% in the maximal current response to proton. GW7647 inhibition of proton-gated currents can be blocked reebok pump by GW6471, a selective PPAR-± antagonist. Moreover, PPAR-± activation decreased the number of acidosis-evoked action potentials in rat DRG neurons. Finally, peripheral administration of GW7647 dose-dependently relieved nociceptive responses to injection of acetic acid in rats. These results indicated that activation of peripheral PPAR-± acutely inhibited functional activity of ASICs in a non-genomic manner, which revealed a novel mechanism underlying rapid analgesia through peripheral PPAR-±.

Acid-sensing ion channels (ASICs) are a family of proton-sensing channels. they are activated by lowering extracellular pH. So far, at least six different ASIC subunits derived from reebok shoes 4 genes have been found in mammals [ 14 ]. Most of the ASIC subunits (i.e. ASIC1a and b, ASIC2a and b, and ASIC3) are expressed in both DRG cell bodies and peripheral terminals, which contribute to proton-induced pain signaling [ 15 - 18 ]. It is known that pain can be produced by tissue acidosis. Protons depolarize DRG neurons and generate action potenials through activating ASICs. For instance, direct application of an acidic solution into the skin induces non-adapting pain [ 19 ].

GW7647 shifted the proton concentration response curve downward and decreased the maximum response without changing the IC 50 values, indicating that PPAR-± activation resulted in a decrease in the efficiency of ASICs and had no effect on the affinity of ASICs for protons. ASICs are mostly permeable to Na , activation of these channels can thus depolarize membrane potentials to the threshold of excitability and result in bursts of action potentials [ 37 ]. Data from current clamp experiments revealed that acidosis-triggered action potentials were also inhibited by reebok cross trainers GW7647. This decreased neuronal excitability may correlate with results that ASIC currents were attenuated by GW7647 in voltage clamp experiments.

In the behavior experiments, we found that intraplantar administration of GW7647 relieved the acidosis-evoked nociceptive responses in rats in a dose-dependent manner. The GW7647 exerted an analgesic effect on acidosis-evoked nociceptive responses through PPAR-±, since its effect was blocked by PPAR-± antagonist. Obviously, the behavioral data corroborated the electrophysiological data and vice versa. The combined data strongly demonstrated that PPAR-± activation indeed inhibited the activity of ASICs, not only at the cellular level but also at the behavioral level.