The effect of glutamate on frog crista ampullaris was investigated in order to assess the potential role of this agent as an afferent transmitter in inner ear organs. Intracellular recordings from single afferent axons in the isolated labyrinth showed that, after blocking synaptic transmission with high concentrations of Mg2+, micro-injections of glutamate elicit a dose-dependent postsynaptic depolarization. The amplitude of depolarization was reduced dose-dependently by the competitive non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. When Na+ concentration in the bath was progressively reduced, depolarization decreased gradually and disappeared almost completely in Na(+)-free Ringer. On the contrary, complete substitution of Ca2+ ions in the bath was without apparent effects. These results indicate that the postsynaptic depolarization induced by glutamate in frog semicircular canals involves the activation of non-NMDA amino acid receptors.
Non-NMDA receptors mediate glutamate-induced depolarization in frog crista ampullaris
PRIGIONI, IVO;RUSSO, GIANCARLO;MASETTO, SERGIO
1994-01-01
Abstract
The effect of glutamate on frog crista ampullaris was investigated in order to assess the potential role of this agent as an afferent transmitter in inner ear organs. Intracellular recordings from single afferent axons in the isolated labyrinth showed that, after blocking synaptic transmission with high concentrations of Mg2+, micro-injections of glutamate elicit a dose-dependent postsynaptic depolarization. The amplitude of depolarization was reduced dose-dependently by the competitive non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. When Na+ concentration in the bath was progressively reduced, depolarization decreased gradually and disappeared almost completely in Na(+)-free Ringer. On the contrary, complete substitution of Ca2+ ions in the bath was without apparent effects. These results indicate that the postsynaptic depolarization induced by glutamate in frog semicircular canals involves the activation of non-NMDA amino acid receptors.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
