The action of glutamate on frog ampullar receptors was investigated to
assess the potential role of this excitatory amino acid as an afferen
t transmitter in the hair cell system. Intracellular recordings from s
ingle afferent units in the isolated labyrinth revealed that glutamate
and the glutamate receptor agonists, N-methyl-D-aspartic acid, quisqu
alic acid and kainic acid increase dose-dependently the frequency of t
he resting afferent discharge of EPSPs and spikes and produce long las
ting depolarizations. After blocking synaptic transmission by using 5
mM Co2+, the same compounds elicited only depolarizations of amplitude
comparable to those observed in normal saline. Quisqualic acid and ka
inic acid were much more potent than N-methyl-D-aspartic acid in incre
asing the frequency of afferent discharge and in causing axonal depola
rizations. The depolarization caused by glutamate was reduced dose-dep
endently by the competitive non-NMDA receptor antagonist 6-cyano-7-nit
roquinaxoline-2,3 dione and disappeared almost completely in Na+-free
Ringer solution. These results are consistent with the hypothesis that
glutamate is the afferent transmitter in vestibular organs and indica
te that receptors mainly of the non-NMDA type are present not only at
postsynaptic level but also in hair cells. Presynaptic glutamate recep
tors may function as autoreceptors controlling by a positive feed-back
mechanism the release of the afferent transmitter.