5-HT potentiates GABA- and glycine-activated chloride currents on the same neurons in rat spinal cord.

The electrophysiological and pharmacological properties of GABA- and glycine (Gly)-induced responses were investigated in neurons acutely dissociated from the rat sacral dorsal commissural nucleus (SDCN) using the nystatin perforated patch recording configuration under voltage-clamp conditions. At a holding potential of -40 mV, the currents evoked by GABA and Gly increased in a sigmoidal fashion with increasing agonist concentration. The reversal potentials of I(GABA)and I(Gly) were close to the Cl- equilibrium potential. Bicuculline (BIC) and strychnine (STR) suppressed I(GABA) and I(Gly) in a concentration-dependent manner, although they have different affinities for GABA and Gly. 5-HT potentiated both I(GABA) and I(Gly) via intracellular protein kinase C on the same neurons. The results indicated that the acutely dissociated SDCN neurons responded to both exogenous GABA and Gly, which activated GABA(A) and STR-sensitive Gly receptors, respectively, and 5-HT may produce spinal antinociception through postsynaptic potentiation of I(GABA) and I(Gly) when they are coreleased; GABA and Gly may act as cotransmitters implicated in the control of spinal nociceptive signal processing in the mammalian spinal cord.