The role of muscarinic acetylcholine receptors in ocular dominance plasticity

Summary

During a critical period of postnatal development neuronal connections in the visual cortex are susceptible to experience-dependent modifications. In normally reared kittens the majority of neurons respond to visual stimulation of either eye. A few days of monocular deprivation, however, are sufficient to render most cortical neurons unresponsive to visual stimuli presented to the deprived eye. Among other factors the cholinergic projection to striate cortex has been identified as having a permissive role in this use-dependent modification of synaptic transmission. In order to analyze further the influence of acetylcholine in cortical plasticity, we tested whether the blockade of muscarinic or nicotinic receptors interfered with ocular dominance plasticity. At four weeks of age kittens had one eyelid sutured closed and osmotic minipumps implanted, which delivered scopolamine (1 nmol/h) or hexamethonium (1 or 10 nmol/h) into the striate cortex of one hemisphere and vehicle solution (saline) into the other. After one week, ocular dominance distributions were determined in area 17 with single unit recording. In the control hemispheres, most neurons became unresponsive to the deprived eye, while in the scopolamine-treated hemispheres most neurons remained binocular. In contrast to the effects of scopolamine, the intracortical infusion of hexamethonium had no effect on ocular dominance plasticity. These results demonstrate that blockade of muscarinic, but not nicotinic receptors renders kitten striate cortex resistent to the effects of monocular deprivation.