The Effects of Glutamate Agonists on Voltage-Clamped Motoneurons of the Lobster Cardiac Ganglion Available to Purchase

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 μmoll⁻¹. The rank order of potencies of the various agonists was quisqualate > L-glutamate= L-aspartate>kainate>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⁺.