The effects of glutamate agonists on voltage-clamped motoneurons of the lobster cardiac ganglion.

The effects of L-glutamate and its analogues were studied in voltage-clamped motoneurons of the lobster cardiac ganglion. These excitatory amino acids caused a dose-dependent increase in membrane conductance and an inward current at the resting membrane potential. The EC50 for L-glutamate was 150 mumol 1(-1). The rank order of potencies of the various agonists was quisqualate greater than L-glutamate = L-aspartate greater than kainate greater than cysteine. Kainate, unlike the other agonists, showed no desensitization. Of various antagonists studied, only the quinoxalinediones inhibited the response to glutamate. These antagonists also reduced the amplitude and duration of the pacemaker-driven burst potential, suggesting that glutamate may be released by some of the endogenous synapses within the ganglion. The reversal potential of the glutamate-induced current was -15 mV. When Na+ was replaced with K+, the glutamate-induced current still reversed between 0 and -20 mV. When Na+ was replaced with the impermeant ion N-methyl-D-glucamine, the current was inhibited. The amplitude of responses evoked by glutamate and its analogues was reduced in salines containing either high or low concentrations of Ca2+. These results of pharmacological and of reversal potential and ion substitution experiments indicate that glutamate acts on receptors of the non-NMDA (N-methyl-D-aspartate), quisqualate/kainate type to open a channel permeable to both Na+ and K+.