Abstract
To elucidate the role of TRPA1, a member of the TRP family of mediating membrane depolarization by opening cation channels, on noxious transmission in the spinal dorsal horn, we investigated the effects of TRPA1 agonists cinnamaldehyde (CA) and allyl isothiocynate (AI) on synaptic transmission in substantia gelatinosa (SG) neurons of adult spinal dorsal horn. Whole-cell patch-clamp recordings were performed from SG neurons of spinal cord slice preparations. Under current-clamp conditions, CA increased the frequency of excitatory postsynaptic potentials (EPSPs) in SG neurons tested, some of which elicited a burst of action potentials. Under voltage-clamp conditions, CA dose-dependently (300 μM- 1 mM) increased the frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) while it increased only the frequency of miniature EPSCs (mEPSCs) observed in presence of 1 μM of TTX. At higher doses, CA gave a desensitizing effect. On the other hand, they had no effects on the frequency and amplitude of both glycinergic and GABAergic mIPSCs. The effects of CA and AI on mEPSCs were blocked by application of a TRP antagonist ruthenium red (30 μM). These findings suggest that TRPA1 receptors are expressed at the presynaptic terminals but not postsynaptic membranes in the SG and their activation by CA or AI enhances the excitatory but not glycinergic and GABAergic synaptic transmission. Such presynaptic activation of TRPA1 receptors may increase the gain of cold noxious transmission. [J Physiol Sci. 2007;57 Suppl:S102]
