Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats.
During rapid eye movement (REM) sleep, activity of non-retinal origin is propagated into central visual-system pathways in a manner similar, in pattern and intensity, to central visual-system activity that is exogenously generated in waking. It has been hypothesized that REM sleep, which is more abundantly represented early in life than later, functions to provide adjunct 'afferent' input for shaping synaptic connectivity during brain maturation. Here we present data that support this proposal. Recent studies have described a developmentally regulated form of in vitro long-term potentiation (LTP) in the visual cortex that is experience- and age-dependent. In immature rats, suppression of retinal activation of the visual system by removal of visual experience (dark rearing) extends the age when the developmentally regulated form of LTP can be produced. This study tests whether suppression of REM-state activation of the visual system also lengthens the developmental period in which this specific form of LTP can be elicited. Young rats were deprived of REM sleep by the multiple-small-platforms-over-water method during the typically latest week for induction of such LTP in slices of visual cortex. After this week, we could still induce LTP in slices from nearly all the REM-sleep-deprived rats (8/9) but not from age-matched rats that had not lost REM sleep (0/5). The control rats had been housed on large platforms that allow the animals to obtain REM sleep. Only body weights and the concentration of thyrotrophin-releasing hormone in the hypothalamus distinguished home-caged, normal-sleeping controls from both groups of platform animals. On all measures, stress levels were not dissimilar in the two platforms groups. After 7 days of behavioral suppression of REM sleep in immature rats, and consequent reduction of the intense, extra-retinal activity endogenously generated during this sleep state, we found that the period was extended in which developmentally regulated synaptic plasticity (LTP) could be elicited in slices of visual neocortex. These studies support the role of REM sleep and its associated neuronal activity in brain maturation.
Shaffery
J P
JP
Department of Psychiatry and Human Behavior, Division of Neurobiology and Behavior Research, University of Mississipi Medical Center, Jackson 39216-4505, USA. jshaffery@psychiatry.umsmed.edu
Sinton
C M
CM
Bissette
G
G
Roffwarg
H P
HP
Marks
G A
GA
D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D001522:Behavior, Animal / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology*; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D004558:Electric Stimulation; D005260:Female; D017774:Long-Term Potentiation / Q000502:physiology*; D009434:Neural Pathways / Q000166:cytology / Q000254:growth & development* / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000502:physiology*; D011247:Pregnancy; D051381:Rats; D020318:Rats, Long-Evans; D012892:Sleep Deprivation / Q000503:physiopathology*; D013004:Somatostatin / Q000378:metabolism; D009435:Synaptic Transmission / Q000502:physiology*; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism; D014793:Visual Cortex / Q000166:cytology / Q000254:growth & development* / Q000502:physiology
D013004:Somatostatin; D013973:Thyrotropin-Releasing Hormone; D003346:Corticotropin-Releasing Hormone