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Abstract:
Physiologic and anatomic evidence has suggested an anatomic disconnection between the deprived eye and visual cortical neurons in cats made amblyopic by monocular deprivation. Clinical and visual-evoked response data suggest, however, that inhibition may play a major role in amblyopia. Accordingly, we intravenously administered anti-inhibitory compounds (bicuculline, ammonium ion, naloxone) to amblyopic cats and demonstrated a substantial restoration of binocular input to the visual cortex. Such pharmacologic reversal suggests that amblyopia is not an anatomically fixed lesion.