抄録
G-protein gated potassium channels contribute to the modulation of synaptic transmission in the CNS. Recent studies have implicated that an inactivation of spinal G-protein gated potassium channels elicits thermal hyperalgesia. In this study, we have shown that G-protein gated potassium channels are activated by an endogenous neurotrasmitter in the spinal dorsal horn using whole-cell patch-clamp recordings from substantia gelatinosa (SG) neurons of adult rat spinal cord slices. Although repetitive stimuli applied to the dorsal root did not induce any slow responses, repetitive stimuli focally-applied to the deep spinal dorsal horn produced slow inhibitory postsynaptic currents (IPSCs) at a holding potential of –50 mV in 32 of 101 SG neurons recorded. The slow IPSCs increased in amplitude and duration with increasing number of stimuli and significantly decreased by the removal of Ca2+ from external Krebs solution. The slow IPSC was associated with an increase in membrane conductance and reversed its polarity at a potential close to the equilibrium potential for K+, calculated from the Nernst equation. The slow IPSC was blocked by the addition of GDP-β-S into patch-pipette solution, and was reduced in amplitude in the presence of Ba2+. These results indicate that an endogenous neurotrasmitter released from interneurons or descending fibers induces slow IPSCs through the activation of G-protein gated potassium channels in SG neurons. This finding may serve to understand pathological pain sensations such as thermal hyperalgesia. [Jpn J Physiol 55 Suppl:S158 (2005)]
