EYE-MOVEMENT SLEEP-DEPRIVATION IN KITTENS AMPLIFIES LGN CELL-SIZE DISPARITY INDUCED BY MONOCULAR DEPRIVATION

The abundance of rapid eye movement (REM) sleep in the neonatal mammal and its subsequent decline in the course of development, as well as t he dramatic and widespread enhancement of CNS activity during REM slee p, led us to propose that this state plays a functional role in the no rmative physiological and structural maturation of the brain [54]. Whe n, after 1 week of monocular deprivation (MD), a second week of MD was coupled with behavioral deprivation of REM sleep, the structural alte ration in the visual system provoked by MD alone (interlaminar relay c ell-size disparity in the lateral geniculate nucleus (LGN)) was amplif ied. With the addition of REM deprivation during MD, the LGN cells con nected to the surgically patched eye, which are smaller than normal af ter MD, became even smaller, whereas the LGN cells receiving input fro m the seeing eye, which display compensatory hypertrophy after MD, gre w even larger. We believe that the interlaminar disparity effect widen ed because during REM deprivation, the already vision-compromised LGN cells associated with the patched eye also lose the ascending brainste m activation reaching them during the REM state. Loss of the two main sources of 'afference' by these LGN cells permits their seeing-eye LGN counterparts to gain even greater advantage in the competition for sy naptic connections in cortex, which is reflected in the relative soma sizes of the LGN relay cells. It is likely that the relatively abundan t REM state in early maturation provides symmetric stimulation to all LGN relay cells, irrespective of eye of innervation. The symmetric act ivation propagated from brainstem to LGN acts to 'buffer' abnormal, as ymmetric visual input and, thereby diminishes the extreme, asymmetric structural alteration that results from MD in the absence of REM sleep . We conclude that REM sleep-generated CNS discharge in development ha s the effect of 'protecting' the CNS against excessive plasticity chan ges. This is consistent with the possibility that REM sleep plays a ro le in the genetically programmed processes that direct normative brain development.