Medial vestibular nucleus neurons develop a sustained increase in electrophysiological excitability after deafferentation, which may be an important component of 'vestibular compensation' (the behavioural recovery that follows peripheral vestibular lesions). We investigated the effects of gamma-aminobutyric acid, glutamate and glycine receptor blockade on the spontaneous activity of deafferented medial vestibular nucleus neurons in slices, to determine whether changes in synaptic inputs contribute to their increased excitability. Soon after deafferentation (4 h after labyrinthectomy) synaptic blockade had no effect on the elevated in-vitro firing of medial vestibular nucleus neurons, while later (48 h, 1 week), synaptic blockade reduced the elevated activity to normal. Intrinsic mechanisms therefore appear to mediate the elevated excitability of medial vestibular nucleus cells initially after deafferentation. Subsequently, changes in the efficacy of synaptic inputs are implicated, presumably involving intranuclear projections that are preserved in slices.
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Guilding et al. (2005) studied this question.
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