Observations made by Wiesel and Hubel in kittens during the critical period have shown that monocular visual deprivation (MD) produces hypotrophic changes in the deprived layers of the LGN. Since, in addition to retinal inputs, the LGN also receives extraretinal inputs which are particularly active during REM sleep (a phase which is highly represented at birth), we performed experiments to find out whether total sleep deprivation (SD) interferes with the neuronal maturation in the LGN, thus modifying the susceptibility of LGN neurons to MD. 2. Ten groups of twin kittens were submitted to eyelid suture of one side at the age of 12 to 42 days after birth, and maintained into MD for periods of time which produced only slight or negligible changes in the deprived LGN layers. However, one of the twins in each group was allowed to sleep, while the other was submitted to 2 to 6 days of SD obtained by gentle handling during the last period of MD. At the end of the experiments cross-sectional areas of cell bodies were measured in the binocular segment of different layers of the LGN of both sides, at comparable levels. 3. MD, started 25 to 42 days after birth and continued for 11 to 23 days produced a slight but significant reduction of the mean cell area in the visual-deprived magnocellular ventral (C) and/or dorsal (A) layers of the contralateral LGN, but not in the middle (A1) layer of the ipsilateral LGN. This shrinkage, however, was most severe and involved also the layer A1 if kittens were also submitted to 5-6 days of SD during the last period of MD. There was also a tendency towards increased size in the nondeprived geniculate layers, probably due to an increased monocular visual experience resulting from an increased wake time in the light. However, the slight increase in cell size seen in these layers contrasted with the prominent increase in shrinkage of the visual-deprived layers after SD, indicating that this finding might have resulted from removing an influence of sleep. The effects of SD appeared to depend on the age of kittens (critical period) and the duration of MD. 4. In conclusion, shortly after birth, SD enhanced the structural abnormalities produced by monocular eyelid closure in the visual-deprived LGN layers. Since rhythmic discharges of pontine structures impinge on the LGN neurons during REM sleep, it is postulated that they could represent an endogenous source of stimulation leading to periodic read out of the synaptic connections between primary optic fibers and LGN neurons. This extraretinal input may thus collaborate with the retinal input to facilitate neuronal maturation of the LGN. The possibility that specific noradrenergic and cholinergic neurons, normally acting on the visual system during the sleep-waking cycle, intervene in the postnatal development of the LGN neurons has been discussed.
