<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hulse BK</submitter><funding>NIMH NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>1549-55</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3134628</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>122(8)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>It has been hypothesized that slow wave activity, a well established measure of sleep homeostasis that increases after waking and decreases after sleep, may reflect changes in cortical synaptic strength. If so, the amplitude of sensory evoked responses should also vary as a function of time awake and asleep in a way that reflects sleep homeostasis.&lt;h4>Methods&lt;/h4>Using 256-channel, high-density electroencephalography (EEG) in 12 subjects, auditory evoked potentials (AEP) and spontaneous waking data were collected during wakefulness before and after sleep.&lt;h4>Results&lt;/h4>The amplitudes of the N1 and P2 waves of the AEP were reduced after a night of sleep. In addition, the decline in N1 amplitude correlated with low-frequency EEG power during non-rapid eye movement sleep and spontaneous wakefulness, both homeostatically regulated measures of sleep need.&lt;h4>Conclusions&lt;/h4>The decline in AEP amplitude after a night of sleep may reflect a homeostatic reduction in synaptic strength.&lt;h4>Significance&lt;/h4>These findings provide further evidence for a connection between synaptic plasticity and sleep homeostasis.</pubmed_abstract><journal>Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology</journal><pubmed_title>A postsleep decline in auditory evoked potential amplitude reflects sleep homeostasis.</pubmed_title><pmcid>PMC3134628</pmcid><funding_grant_id>T32 GM008692</funding_grant_id><funding_grant_id>5T20MH077967</funding_grant_id><funding_grant_id>P20 MH077967</funding_grant_id><funding_grant_id>F30 MH082601</funding_grant_id><funding_grant_id>F30MH082601</funding_grant_id><funding_grant_id>P20 MH077967-03</funding_grant_id><funding_grant_id>P20 MH077967-02</funding_grant_id><funding_grant_id>P20 MH077967-04</funding_grant_id><funding_grant_id>F30 MH082601-04</funding_grant_id><funding_grant_id>F30 MH082601-02</funding_grant_id><funding_grant_id>F30 MH082601-03</funding_grant_id><pubmed_authors>Hulse BK</pubmed_authors><pubmed_authors>Tononi G</pubmed_authors><pubmed_authors>Wanger T</pubmed_authors><pubmed_authors>Landsness EC</pubmed_authors><pubmed_authors>Ferrarelli F</pubmed_authors><pubmed_authors>Sarasso S</pubmed_authors><pubmed_authors>Guokas JJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>A postsleep decline in auditory evoked potential amplitude reflects sleep homeostasis.</name><description>&lt;h4>Objective&lt;/h4>It has been hypothesized that slow wave activity, a well established measure of sleep homeostasis that increases after waking and decreases after sleep, may reflect changes in cortical synaptic strength. If so, the amplitude of sensory evoked responses should also vary as a function of time awake and asleep in a way that reflects sleep homeostasis.&lt;h4>Methods&lt;/h4>Using 256-channel, high-density electroencephalography (EEG) in 12 subjects, auditory evoked potentials (AEP) and spontaneous waking data were collected during wakefulness before and after sleep.&lt;h4>Results&lt;/h4>The amplitudes of the N1 and P2 waves of the AEP were reduced after a night of sleep. In addition, the decline in N1 amplitude correlated with low-frequency EEG power during non-rapid eye movement sleep and spontaneous wakefulness, both homeostatically regulated measures of sleep need.&lt;h4>Conclusions&lt;/h4>The decline in AEP amplitude after a night of sleep may reflect a homeostatic reduction in synaptic strength.&lt;h4>Significance&lt;/h4>These findings provide further evidence for a connection between synaptic plasticity and sleep homeostasis.</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Aug</publication><modification>2025-04-27T02:19:53.552Z</modification><creation>2019-03-27T03:07:00Z</creation></dates><accession>S-EPMC3134628</accession><cross_references><pubmed>21420904</pubmed><doi>10.1016/j.clinph.2011.01.041</doi></cross_references></HashMap>