Neuronal plasticity induced by neonatal monocular (and binocular) enucleation

Monocular (ME) and binocular enucleation has become a useful experimental tool for analyzing the mechanisms of neural plasticity. ME when performed during an early postnatal period (up to 15 days after birth) initiates a series of adaptive reactions in the visual (and other sensory) system(s) which tend to compensate for the lost sensory capacity. Extirpation of one eye (usually the right) destroys afferents to both lateral geniculate bodies dorsal nucleus (CGLd) and superior colliculi (CS), being severely impaired by the degeneration of retino-geniculate and collicular synapses. The sprouting of retinogeniculate fibers coming from the remaining eye replaces these synapses in both CGLds. Ipsilateral representation of the remaining eye (usually of minor significance) becomes extended in the left CGLd and consequently in the left visual area, just as in the superior colliculi. A similar but somewhat smaller extension takes place in the contralateral CGLd and visual cortex. The strengthening of commissural connections results in a remarkable extension of callosally connected stripes and patches in both hemispheres. After ME in the critical period, the control over behavior is taken over by the remaining eye. Its power of resolution is improved because of the higher survival of (mainly ipsilaterally projecting) ganglion cells. Therefore, both hemispheres are still available for storing visual information. In ME rats the learning of visual tasks requires both hemispheres, but relearning is still possible after extirpation of the contralateral one. The possible two main mechanisms of adaptive plastic changes are: (i) replacement of degenerated synapses by sprouting collaterals of ingrowing foreign fibers, and (ii) neurons having morphologically intact but inactive synapses establishing connections with afferent fibers other than the usual. The same mechanism is seen operating in cross-modal adaptive reactions as well.