Somatostatin directly inhibits substantia gelatinosa neurons in adult rat spinal dorsal horn in vitro.

Effects of somatostatin (SST) on the synaptic transmission to substantia gelatinosa (SG) neurons of adult spinal cord slices were investigated using intracellular recording and blind whole-cell patch-clamp technique. Bath application of SST (1 microM) induced the membrane hyperpolarization that was accompanied by a decrease in input resistance and had the reversal potential of -92 +/- 3 mV (n=5) in the intracellular recording experiment. In patch-clamp experiment, SST (1 microM) induced an outward current with amplitude of 14 +/- 2 pA (n=60) at the holding potential of -60 mV, and was not affected by TTX (n=3). The effect was dose-dependent with EC50 value of 0.82 microM (Hill coefficient: 0.89). The outward current was suppressed when the patch-pipette solution containing potassium channel blockers, Cs+ and tetraethylammonium (TEA), and was inhibited by Ba2+ (200 microM) to 15 +/- 6% of the control (n=3). In addition, the SST current reversed its polarity at potential close to the equilibrium potential of K+ channel calculated by the Nernst equation. No significant changes were found in amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs) and dorsal root evoked EPSC (eEPSC) by SST. Also, SST did not affect both of the miniature inhibitory postsynaptic currents (mIPSCs) and evoked inhibitory postsynaptic currents (eIPSCs), mediated by either the GABA or glycine receptor. We conclude that SST activates the K+ channel resulting in postsynaptic hyperpolarization in adult rat SG neurons without affecting presynaptic component of the transmission, which are considered to account, at least a part, for the analgesic effects of SST reported previously.