Sleeping brain is still hard at work: Mechanisms for consolidation of cortical plasticity

February 11, 2009

New research provides strong support for the idea that one of the key functions of sleep is the consolidation of memories. The study, published by Cell Press in the February 12th issue of the journal Neuron, provides fascinating insight into the cellular mechanisms that govern the sleep-dependent consolidation of experiences that occur while we are awake.

Although sleep is thought to facilitate memory and learning, the molecular links between sleep and synaptic plasticity are not well understood. Ocular dominance plasticity (ODP) is a classic model of experience-dependent cortical plasticity that allows scientists to follow specific changes in the visual cortex in response to the occlusion of one eye.

"We have shown that ODP is consolidated by sleep," says senior study author Dr. Marcos G. Frank from the Department of Neuroscience at the University of Pennsylvania School of Medicine. "Our previous studies indicate that the underlying mechanisms, though still unknown, may involve N-methyl D-aspartate receptors (NMDARs) and intracellular kinases." Dr. Frank and colleagues performed a series of experiments designed to test this hypothesis.

The researchers found that sleep consolidates ODP primarily by strengthening cortical responses to stimulation of the nondeprived eye. NMDAR- and protein kinase A-mediated intracellular cascades were critical components of the cellular machinery required for sleep-dependent consolidation of ODP, and their activation during sleep promoted synaptic strengthening.

Further, sleep-specific elevations in cortical activity were observed in remodeling cortical neurons. The remodeling visual cortex exhibited a sleep-dependent activation of several kinases that are downstream of NMDARs, which also had been previously linked to learning and memory processes.

Interestingly, both blockade of NMDARs and sleep deprivation interfered with ODP consolidation. This suggests that aberrant NMDAR signaling may mediate the negative effects of sleep loss on cognitive function.

"These findings demonstrate that when the cortex is triggered to remodel in wakefulness, synaptic changes are further modified and consolidated by cortical reactivation and a secondary series of NMDAR and kinase-mediated signaling cascades during sleep," offers Dr. Frank.
The researcher is Sara J. Aton, University of Pennsylvania School of Medicine, Philadelphia, PA; Julie Seibt, University of Pennsylvania School of Medicine, Philadelphia, PA; Michelle Dumoulin, University of Pennsylvania School of Medicine, Philadelphia, PA; Sushil K. Jha, University of Pennsylvania School of Medicine, Philadelphia, PA; Jawaharlal Nehru University, New Delhi, India; Nicholas Steinmetz, University of Pennsylvania School of Medicine, Philadelphia, PA; Tammi Coleman, Nirinjini Naidoo, University of Pennsylvania School of Medicine, Philadelphia, PA; and Marcos G. Frank, University of Pennsylvania School of Medicine, Philadelphia, PA.

Cell Press

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