A mechanism of central compensation of vestibular function following hemilabyrinthectomy.

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Abstract
Following unilateral destruction of the labyrinth in the cat, postural abnormalities and postrotatory nystagmus were observed in the acute stage (3-4 days after operation) and in the compensated stage (30-45 days after operation). After these observations, extracellular microelectrode recording of vestibular type I and type II neuron activities was performed under decerebrate and decerebellate condition without anesthesia. Spontaneous discharges of type I neurons and their frequency responses to horizontal angular acceleration were more easily found in the chronically deaff erented vestibular nuclei, as compared with tose in the acutely deafferented nuclei. The thresholds of electric stimulation of the contralateral intact vestibular nerve for producing inhibition of type I neurons in the chronically deafferented vestibular nuclei were significantly lower than those observed in the animal with bilaterally intact labyrinths. The recovery of fairly symmetric control of ocular movements induced by rotation was explained by reappearance of spontaneous activity of type I neurons on the destroyed side and by the highly developed inhibitory influence from the intact labyrinth.

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