Recent studies have revealed a critical role for sleep in learning, memory, and cortical plasticity. We have previously shown that sleep enhances ocular dominance plasticity (OOP), a form of in vivo synaptic remodeling triggered by monocular deprivation (MD) during a critical period of development. Postsynaptic activity in the primary visual cortex during post-MD sleep is critical for this process. However, the relative contributions of rapid eye movement (REM) and non-REM (NREM) sleep to OOP are unknown, as are the precise intracellular mechanisms underlying sleep-mediated ODP. The early stages of ODP share key features with long-term depression (LTD) and long-term potentiation (LTP) in the visual cortex during the critical period. It is possible that sleep enhances ODP through mechanisms similar to LTD, LTP, or both. The goals of the proposed studies are first, to clarify the roles of REM and NREM sleep in this process, and second, to investigate the contribution of LTP-like and LTD-like plasticity mechanisms to sleep-dependent ODP. To test the roles of REM and NREM sleep in ODP, we will selectively manipulate these sleep stages following a period of MD. To determine whether sleep enhances ODP via LTD-like or LTP-like mechanisms, we will test the effects of blocking protein phosphatase or kinase pathways - critical for LTD or LTP, respectively - in the visual cortex during post-MD sleep. While the primary function of sleep is still unknown, its role in learning and memory has become an area of increasing interest. It is likely that the mechanisms underlying sleep enhancement of ODP also underlie sleep effects on other types of learning and memory;understanding the role of sleep in ODP will further our understanding of its role in cognitive function. Our findings may have important implications for patients taking medications that affect sleep architecture, and those affected by insomnia and other increasingly prevalent sleep disorders.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32EY017766-02
Application #
7623036
Study Section
Special Emphasis Panel (ZRG1-F02A-A (20))
Program Officer
Steinmetz, Michael A
Project Start
2008-07-01
Project End
2011-06-30
Budget Start
2009-07-01
Budget End
2010-06-30
Support Year
2
Fiscal Year
2009
Total Cost
$51,710
Indirect Cost
Name
University of Pennsylvania
Department
Neurosciences
Type
Schools of Medicine
DUNS #
042250712
City
Philadelphia
State
PA
Country
United States
Zip Code
19104
Dumoulin, Michelle C; Aton, Sara J; Watson, Adam J et al. (2015) Extracellular signal-regulated kinase (ERK) activity during sleep consolidates cortical plasticity in vivo. Cereb Cortex 25:507-15
Dumoulin Bridi, Michelle C; Aton, Sara J; Seibt, Julie et al. (2015) Rapid eye movement sleep promotes cortical plasticity in the developing brain. Sci Adv 1:e1500105
Aton, Sara J; Broussard, Christopher; Dumoulin, Michelle et al. (2013) Visual experience and subsequent sleep induce sequential plastic changes in putative inhibitory and excitatory cortical neurons. Proc Natl Acad Sci U S A 110:3101-6
Frank, Marcos G; Waldrop, Robert H; Dumoulin, Michelle et al. (2012) A preliminary analysis of sleep-like states in the cuttlefish Sepia officinalis. PLoS One 7:e38125
Seibt, Julie; Dumoulin, Michelle C; Aton, Sara J et al. (2012) Protein synthesis during sleep consolidates cortical plasticity in vivo. Curr Biol 22:676-82
Aton, Sara J; Seibt, Julie; Dumoulin, Michelle et al. (2009) Mechanisms of sleep-dependent consolidation of cortical plasticity. Neuron 61:454-66
Aton, Sara J; Seibt, Julie; Dumoulin, Michelle C et al. (2009) The sedating antidepressant trazodone impairs sleep-dependent cortical plasticity. PLoS One 4:e6078
Uebele, Victor N; Nuss, Cindy E; Santarelli, Vincent P et al. (2009) T-type calcium channels regulate cortical plasticity in-vivo. [corrected]. Neuroreport 20:257-62