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Opioid modulates voltage - insensitive K+current in substantia gelatinosa neurons of rat


, : Opioid modulates voltage - insensitive K+current in substantia gelatinosa neurons of rat. Society for Neuroscience Abstract Viewer & Itinerary Planner : Abstract No 899 10

In this study, we investigated the effect of opioid on leak K+ current (IK(L)) in rat substantia gelatinosa (SG) neurons, receiving the synaptic inputs from pain-transmitting primary afferent neurons and integrate the noxious information. The analgesic mechanism of opioid has been known to decrease the excitability of SG neurons by increasing inward rectifying K+ current (IKir). Here we observed that DAMGO increased voltage-insensitive K+ current (IK(L)), using the whole-cell tight seal recording in the transverse slice of rat spinal cord. DAMGO caused a repeatable hyperpolarization in current clamp or outward current in voltage-clamp in SG neurons lacking Ih (n=25). The current induced by DAMGO developed instantaneously and did not show any time-dependent inactivation. However, the I-V relationship of the DAMGO-sensitive current was diverse. Half of neurons (n=13) exhibited a linear relationship, suggesting that DAMGO opens IK(L). Three neurons were almost exhibiting pure IKir. In rest of neurons DAMGO-sensitive current was mixture of IK(L) and IKir. A low concentration of extracellular Ba2+ (100 muM) decreased the effect of DAMGO on IKir leaving IK(L) component, whereas a high concentration of Ba2+ (1 mM) completely blocked the effect on IK(L). The hyperpolarization by DAMGO of SG neurons appears to be carried by IK(L) in addition to IKir. Taken together, DAMGO-induced hyperpolarization of SG neurons is associated with the enhancement of IK(L) as well as IKir. It is suggested that IK(L) plays an important role in the regulation of excitability in SG neurons.

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