Evidence for GABA as the synaptic transmitter of the inhibitory vestibulo-ocular pathway.

Abstract

This paper gives an account of the action of two antagonists of GABA on the vestibulo-trochlear inhibitory pathway, and of neurochemical determinations of its suggested synaptic transmitter (GABA) within the trochlear nuclei. Extra- and intracellular potentials were recorded from the trochlear nucleus following stimulation of the ipsilateral vestibular nerve, contralateral vestibular nerve and the trochlear nerve. 1. The disynaptic inhibitory vestibulo-trochlear reflex was shown to be mediated solely through the medial longitudinal fasciculus as lesion of this pathway removed it entirely. 2. Picrotoxin blocked completely the IPSP, the extracellular positive potential and the inhibitory effect on the antidromic response. 3. Bicuculline had a similar effect on the inhibitory potentials, the action was reversible lasting less than one hour at a dose less than 1 mg/kg, and the sequence of block and recovery could be repeated several times in the same experiment with a similar dose. 4. Both bicuculline and picrotoxin selectively suppressed the postsynaptic, in contrast to the presynaptic, component of the field potential, and did not markedly affect the excitatory pathway (EPSP). 5. The normal concentration of GABA in the trochlear nucleus area was 3.6 μ mole/g. After lesions of the ipsilateral medial longitudinal fasciculus the GABA content was significantly decreased suggesting degeneration of GABA containing terminals. 6. These results corroborate the hypothesis that GABA is the inhibitory synaptic transmitter of the vestibular neurons projecting to trochlear and other ocular motoneurons.