Abstract
In frogs, the horizontal monocular optokinetic nystagmus (OKN) is asymmetrical, with only the temporal-nasal (T-N) stimulation being efficient to evoke the reflex. Coil recordings showed that, in adult animals, prolonged monocular visual deprivation by unilateral eyelid suture provoked the appearance of the N-T component. A unique microinjection of GABA A agonist THIP or of muscarinic antagonist atropine into the nucleus lentiformis mesencephali (nLM), the pretectal mesencephalic structure involved in OKN, transiently abolished the presence of the N-T component. Daily microinjections of the NMDA antagonist APV into the nLM, during the week of monocular deprivation, prevented the appearance of the N-T component. The results suggest that this phenomenon of visual plasticity can be due to reduction in pretectal GABAergic inhibition, and to concomitant activation of both cholinergic muscarinic and NMDA receptors.
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