By means of microiontophoretic techniques, effects of excitant amino acids, aspartate, glutamate, N-methy1-D-aspartic acid (NMDA), quisqualic acid and kainic acid, as well as their antagonists, glutamic acid diethyl ester (GDEE) and D-a-amino adipic acid (DAA) and cholinergic antagonist atropine were tested on spontaneously firing vestibular neurons, evoked field potentials in the vestibular complex following electric stimulation of vestibular nerve and on evoked excitation of spike potentials of single vestibular neurone of anaesthetized albino rats. Stimulation of vestibular nerve produced characteristic field potential sequence consisted of P, N1 and N2 waves, denoted incoming volley, monosynaptic and polysynaptic excitation respectively. DAA and GDEE preferentially and reversible reduced N1 and N2 potentials, while P wave was unaffected. By contrast, atropine was ineffective in antagonizing the occurrence of the evoked field potentials. Following intravenous application, none of the three antagonists tested produced any effects on the field potentials. All excitant amino acid agonists produced marked excitation of all spontaneously firing vestibular neurons tested. Quisqualic acid and kainic acid seemed to be more effective in producing this induced excitation since these two agonists required less current to produced equipotential excitation as compared to those required by the other agonists. Both antagonists, DAA and GDEE, produced inhibition of spontaneous firing of the vestibular neurons, with GDEE being more effective since it required approximately half of the intophoretic current of the that of DAA to produce the same degree (50%) of firing depression. Both monosynaptically and polysynaptically evoked potentials were completely antagonized by GDEE following a brief period of application (55-60 nA, 5-6 sec for monosyaptic excitation and 40-80 nA, 4-6 sec for polysynaptic excitation). By contrast, it was observed that supplication of 140-150 nA DAA for 15-20 sec depressed both monosynaptically and polysynaptically evoked spikes by 20%. Atropine did not show any discernable effects on the evoked excitations. These results support the proporsal that excitant amino acid related to ‘glutamate receptor’ may involve as a neurotransmitter of the vestibular primary afferents.
