Two studies were conducted examining the role of afferent activity on synaptic connectivity in the cat's visual pathways. The first study investigated the effects of retinal inactivity on cell size in the lateral geniculate nucleus (LGN). A complete retinal blockade was produced in one eye of 7-week-old kittens by intravitreal injections of tetrodotoxin (TTX). Within one week, cell shrinkage of ~20% in laminae with input from the inactive eye was observed in the binocular and monocular segments of the LGN. Cell growth of 10% was observed in active laminae only in the binocular segment. Adult cats subjected to one week of monocular TTX treatment and kittens placed in the dark during the treatment period underwent uniform changes in cell size of ~20% throughout the binocular and monocular segments of the LGN. The cell size changes in the monocular segment of the kittens left in the light, and throughout the LGN of the kittens placed in the dark and of the adult cats were not indicative of a competitive response to differential activity from the two eyes. The results suggest a strong control of LGN cell size by afferent (retinal) activity.
In the second study, cats were reared in the dark from birth until adulthood, then subjected to various visual exposure paradigms to test their residual cortical plasticity. Animals allowed two weeks of binocular visual exposure after dark-rearing, then monocularly lid-sutured underwent changes in cortical ocular dominance in response to the monocular deprivation. Animals which were monocularly deprived immediately upon removal from the dark and 25 days later reverse-sutured for 4-6 months (closure of initially open eye, opening of previously sutured eye) underwent shifts in ocular dominance towards the experienced eye both after the initial monocular deprivation and again in response to reverse-suturing. The LGN of dark-reared/monocularly deprived animals did not exhibit any morphological abnormalities. Depletion of cortical norepinephrine reduced but did not abolish the sensitivity of the dark-reared cortex to monocular deprivation. Visual exposure for four weeks after birth, followed by extended dark-rearing did not halt the subsequent prolongation of cortical plasticity in the dark.
