Argiotoxin-636 blocks effects of N-methyl-D-aspartate on lateral line of Xenopus laevis at concentrations which do not alter spontaneous or evoked neural activity.

Activity of primary afferent neurons in acousticolateralis organs can be modulated by excitatory amino acids (EAA) and their antagonists, and EAA are among the better candidates for the transmitter(s) between hair cells and afferent neurons. Argiotoxin-636 (ATX) is a spider venom toxin that is a selective antagonist of the N-methyl-D-aspartate (NMDA) subtype of excitatory amino acid receptors in vertebrates. In the present study, the effects of NMDA alone and in combination with ATX on resting firing rate (spontaneous activity) and mechanically stimulated activity of lateral line afferent neurons of post-metamorphic Xenopus laevis were compared. Perfusion of NMDA (100 or 200 microM) typically produced a biphasic effect on spontaneous activity consisting of a transient increase followed by a decrease in firing rate. Mechanical stimulation applied after the initial response to NMDA produced an increase in firing activity that was not significantly different from the increase in firing activity evoked in the absence of NMDA. ATX at 1-2 microM did not alter either spontaneous or evoked activity, but blocked in a reversible manner both the excitatory and inhibitory actions of NMDA on spontaneous activity. These results suggest the presence of an NMDA receptor in the lateral line but do not support the hypothesis that the generation of action potentials by the afferent transmitter is solely dependent on activation of postsynaptic NMDA receptor-ion channels.