Synaptic excitation in cultures of mouse spinal cord neurones: receptor pharmacology and behaviour of synaptic currents.

Fast monosynaptic excitatory post‐synaptic potentials between spinal cord neurones in cell culture (s.c.‐s.c. e.p.s.p.s) were studied with current‐clamp and two‐electrode voltage‐clamp methods. The reversal potential, response to acidic amino acid antagonists, and behaviour of the synaptic current were examined. The amplitude of the e.p.s.p. increased with membrane potential hyperpolarization and decreased with depolarization. The reversal potential of the e.p.s.p. was +3.8 +/‐ 2.5 mV (mean +/‐ S.E. of mean). The reversal potential for responses to ionophoretically applied L‐glutamate and L‐aspartate was also near 0 mV. The acidic amino acid antagonist, cis‐2,3‐piperidine dicarboxylic acid (PDA, 0.25‐1.0 mM) reversibly antagonized the monosynaptic e.p.s.p.s as well as responses to kainate (KA) or quisqualate (QA). The selective N‐methyl‐D‐aspartate antagonist, (+/‐) 2‐amino‐5‐phosphonovaleric acid (APV), had little effect on either the monosynaptic e.p.s.p.s or responses to QA or KA at concentrations that abolished responses to L‐aspartate. Under voltage clamp, the peak synaptic current (e.p.s.c.) was linearly related to the membrane potential, increasing in amplitude with hyperpolarization and decreasing with depolarization from the resting potential. The decay of a somatic e.p.s.c. was well fitted by a single exponential function with a time constant of 0.6 ms at 25 degrees C. E.p.s.c.s which had proximal dendritic locations had decay time constants of 1‐2 ms. The decay time constant was voltage‐insensitive between ‐80 and +10 mV. We suggest that an acidic amino acid receptor other than that for NMDA mediates excitatory transmission at the s.c.‐s.c. synapse; and that the underlying conductance mechanism is voltage insensitive with an estimated mean channel lifetime of less than 1 ms.