Sleep-dependent plasticity requires cortical activity

Sushil K Jha; Brian E Jones; Tammi Coleman; Nick Steinmetz; Chi-Tat Law; Gerald Griffin; Josh Hawk; Nooreen Dabbish; Valery A Kalatsky; Marcos G Frank

doi:10.1523/JNEUROSCI.2722-05.2005

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Sleep-dependent plasticity requires cortical activity

Journal article

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Peer reviewed

Sleep-dependent plasticity requires cortical activity

Sushil K Jha, Brian E Jones, Tammi Coleman, Nick Steinmetz, Chi-Tat Law, Gerald Griffin, Josh Hawk, Nooreen Dabbish, Valery A Kalatsky and Marcos G Frank

The Journal of neuroscience, Vol.25(40), pp.9266-9274

10/05/2005

DOI: https://doi.org/10.1523/JNEUROSCI.2722-05.2005

Handle:

https://hdl.handle.net/2376/114001

PMCID: PMC6725765

PMID: 16207886

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https://doi.org/10.1523/JNEUROSCI.2722-05.2005View

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Abstract

Lidocaine - pharmacology

Neuronal Plasticity - drug effects

Critical Period (Psychology)

Anesthetics, Local - pharmacology

Visual Cortex - physiology

Behavior, Animal

Diagnostic Imaging - methods

Visual Pathways - physiology

Neuronal Plasticity - physiology

Functional Laterality - physiology

Sleep - physiology

Action Potentials - drug effects

Animals, Newborn

Cats

Visual Cortex - cytology

Electroencephalography - methods

Action Potentials - physiology

Sensory Deprivation - physiology

Animals

Visual Pathways - drug effects

Analysis of Variance

Brain Mapping

Dominance, Ocular

Visual Cortex - drug effects

Electromyography - methods

In Vitro Techniques

Recent findings in humans and animals suggest that sleep promotes synaptic plasticity, but the underlying mechanisms have not been identified. We have demonstrated recently an important role for sleep in ocular dominance (OD) plasticity, a classic form of in vivo cortical remodeling triggered by monocular deprivation (MD) during a critical period of development. The mechanisms responsible for the effects of sleep on OD plasticity are unknown but may depend on neuronal activity in the sleeping brain. We investigated the role of cortical activity in sleep-dependent plasticity by reversibly inactivating the sleeping visual cortex (V1) after a period of MD. Critical period cats were bilaterally implanted with cannulas in V1 and standard EEG/EMG electrodes for polysomnographic recording. After a period of MD, visual cortices were infused with the sodium channel blocker lidocaine in vehicle or vehicle only during sleep. A third group of cats served as sham controls and were infused with lidocaine outside of V1 (into the CSF). Both optical imaging of intrinsic cortical signals and microelectrode recordings showed that OD plasticity was significantly reduced in cats whose visual cortices were reversibly silenced during sleep. These findings demonstrate that the mechanisms governing this form of sleep-dependent plasticity require cortical activity. They provide an important insight into how sleep modifies synaptic circuitry by narrowing the range of possible candidate mechanisms to those that are activity dependent.

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Title: Sleep-dependent plasticity requires cortical activity
Creators: Sushil K Jha - Department of Neuroscience, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6074, USA
Brian E Jones
Tammi Coleman
Nick Steinmetz
Chi-Tat Law
Gerald Griffin
Josh Hawk
Nooreen Dabbish
Valery A Kalatsky
Marcos G Frank
Publication Details: The Journal of neuroscience, Vol.25(40), pp.9266-9274
Academic Unit: Biomedical Sciences, Department of
Publisher: United States
Grant note: 5-R01-MH067568 / NIMH NIH HHS
Identifiers: 99900548304501842
Language: English
Resource Type: Journal article