Rapid eye movement sleep deprivation revives a form of developmentally regulated synaptic plasticity in the visual cortex of post-critical period rats

• Published in: Neuroscience letters 2006-01, Vol.391 (3), p.96-101
• Main Authors: Shaffery, James P., Lopez, Jorge, Bissette, Garth, Roffwarg, Howard P.
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Brain maturation; Corticosterone; Corticosterone - blood; Critical Period (Psychology); Homeostasis; In vitro; Long-Term Potentiation; Male; Neuronal Plasticity; Rats; Rats, Long-Evans; Sleep Deprivation - embryology; Sleep Deprivation - physiopathology; Small-pedestals-over-water; Synapses; Visual Cortex - embryology; Visual Cortex - physiopathology
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2005.08.044

The critical period for observing a developmentally regulated form of synaptic plasticity in the visual cortex of young rats normally ends at about postnatal day 30. This developmentally regulated form of in vitro long-term potentiation (LTP) can be reliably induced in layers II–III by aiming high frequency, theta burst stimulation (TBS) at the white matter situated directly below visual cortex (LTPWM-III). Previous work has demonstrated that suppression of sensory activation of visual cortex, achieved by rearing young rats in total darkness from birth, delays termination of the critical period for inducing LTPWM-III. Subsequent data also demonstrated that when rapid eye movement sleep (REMS) is suppressed, thereby reducing REMS cortical activation, just prior to the end of the critical period, termination of this developmental phase is delayed, and LTPWM-III can still be reliably produced in the usual post-critical period. Here, we report that for approximately 3 weeks immediately following the usual end of the critical period, suppression of REMS disrupts the maturational processes that close the critical period, and LTPWM-III is readily induced in brain slices taken from these somewhat older animals. Insofar as in vitro LTP is a model for the cellular and molecular changes that underlie developmental synaptic plasticity, these results suggest that mechanisms of synaptic plasticity, which participate in brain development and perhaps also in learning and memory processes, remain susceptible to the effects of REMS deprivation during the general period of adolescence in the rat.