TY - JOUR
T1 - Rapid eye movement sleep deprivation in kittens amplifies LGN cell-size disparity induced by monoclonal deprivation
AU - Oksenberg, Arie
AU - Shaffery, James P.
AU - Marks, Gerald A.
AU - Speciale, Samuel G.
AU - Mihailoff, Gregory
AU - Roffwarg, Howard P.
N1 - Funding Information:
The authors wish to express their appreciation to Glenda Connick, Joie Stouffer Shelton, Bonnie Claussen, Doris Burton, Denise Jones, and Jenny Spence for their secretarial support, and to Drew Hoelscher, B.A., Kari Ann Eamma, B.A., and Ken W. Bourell, M.Sc. for their technical assistance. This research was supported in part by NINDS Grant R01-NS31720.
PY - 1996/11/22
Y1 - 1996/11/22
N2 - The abundance of rapid eye movement (REM) sleep in the neonatal mammal and its subsequent decline in the course of development, as well as the dramatic and widespread enhancement of CNS activity during REM sleep, led us to propose that this state plays a functional role in the normative physiological and structural maturation of the brain. When, after 1 week of monocular deprivation (MD), a second week of MD was coupled with behavioral deprivation of REM sleep, the structural alteration in the visual system provoked by MD alone (interlaminar relay cell-size disparity in the lateral geniculate nucleus (LGN)) was amplified. With the addition of REM deprivation during MD, the LGN cells connected to the surgically patched eye, which are smaller than normal after MD, became even smaller, whereas the LGN cells receiving input from the seeing eye, which display compensatory hypertrophy after MD, grew even larger. We believe that the interlaminar disparity effect widened because during REM deprivation, the already vision-compromised LGN cells associated with the patched eye also lose the ascending brainstem 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 synaptic connections in cortex, which is reflected in the relative soma sizes of the LGN relay cells. It is likely that the relatively abundant REM state in early maturation provides symmetric stimulation to all LGN relay cells, irrespective of eye of innervation. The symmetric activation propagated from brainstem to LGN acts to 'buffer' abnormal, asymmetric 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 has the effect of 'protecting' the CNS against excessive plasticity changes. This is consistent with the possibility that REM sleep plays a role in the genetically programmed processes that direct normative brain development.
AB - The abundance of rapid eye movement (REM) sleep in the neonatal mammal and its subsequent decline in the course of development, as well as the dramatic and widespread enhancement of CNS activity during REM sleep, led us to propose that this state plays a functional role in the normative physiological and structural maturation of the brain. When, after 1 week of monocular deprivation (MD), a second week of MD was coupled with behavioral deprivation of REM sleep, the structural alteration in the visual system provoked by MD alone (interlaminar relay cell-size disparity in the lateral geniculate nucleus (LGN)) was amplified. With the addition of REM deprivation during MD, the LGN cells connected to the surgically patched eye, which are smaller than normal after MD, became even smaller, whereas the LGN cells receiving input from the seeing eye, which display compensatory hypertrophy after MD, grew even larger. We believe that the interlaminar disparity effect widened because during REM deprivation, the already vision-compromised LGN cells associated with the patched eye also lose the ascending brainstem 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 synaptic connections in cortex, which is reflected in the relative soma sizes of the LGN relay cells. It is likely that the relatively abundant REM state in early maturation provides symmetric stimulation to all LGN relay cells, irrespective of eye of innervation. The symmetric activation propagated from brainstem to LGN acts to 'buffer' abnormal, asymmetric 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 has the effect of 'protecting' the CNS against excessive plasticity changes. This is consistent with the possibility that REM sleep plays a role in the genetically programmed processes that direct normative brain development.
KW - Activity dependence
KW - Development
KW - Lateral geniculate nucleus
KW - Monocular occlusion
KW - Plasticity
KW - Ponto-geniculo-occipital wave
KW - Visual system
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U2 - 10.1016/S0165-3806(96)00131-9
DO - 10.1016/S0165-3806(96)00131-9
M3 - Article
C2 - 8946054
AN - SCOPUS:0038709929
SN - 0165-3806
VL - 97
SP - 51
EP - 61
JO - Developmental Brain Research
JF - Developmental Brain Research
IS - 1
ER -