Suppression of preoptic sleep-regulatory neuronal activity during corticotropin-releasing factor-induced sleep disturbance
Corticotropin releasing factor (CRF) is implicated in sleep and arousal regulation. Exogenous CRF causes sleep suppression that is associated with activation of at least two important arousal systems: pontine noradrenergic and hypothalamic orexin/hypocretin neurons. It is not known whether CRF also...
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Veröffentlicht in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2015-11, Vol.309 (9), p.R1092-R1100 |
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creator | Gvilia, Irma Suntsova, Natalia Kumar, Sunil McGinty, Dennis Szymusiak, Ronald |
description | Corticotropin releasing factor (CRF) is implicated in sleep and arousal regulation. Exogenous CRF causes sleep suppression that is associated with activation of at least two important arousal systems: pontine noradrenergic and hypothalamic orexin/hypocretin neurons. It is not known whether CRF also impacts sleep-promoting neuronal systems. We hypothesized that CRF-mediated changes in wake and sleep involve decreased activity of hypothalamic sleep-regulatory neurons localized in the preoptic area. To test this hypothesis, we examined the effects of intracerebroventricular administration of CRF on sleep-wake measures and c-Fos expression in GABAergic neurons in the median preoptic nucleus (MnPN) and ventrolateral preoptic area (VLPO) in different experimental conditions. Administration of CRF (0.1 nmol) during baseline rest phase led to delayed sleep onset and decreases in total amount and mean duration of non-rapid eye movement (NREM) sleep. Administration of CRF during acute sleep deprivation (SD) resulted in suppression of recovery sleep and decreased c-Fos expression in MnPN/VLPO GABAergic neurons. Compared with vehicle controls, intracerebroventricular CRF potentiated disturbances of both NREM and REM sleep in rats exposed to a species-specific psychological stressor, the dirty cage of a male conspecific. The number of MnPN/VLPO GABAergic neurons expressing c-Fos was reduced in the CRF-treated group of dirty cage-exposed rats. These findings confirm the involvement of CRF in wake-sleep cycle regulation and suggest that increased CRF signaling in the brain 1) negatively affects homeostatic responses to sleep loss, 2) exacerbates stress-induced disturbances of sleep, and 3) suppresses the activity of sleep-regulatory neurons of the MnPN and VLPO. |
doi_str_mv | 10.1152/ajpregu.00176.2015 |
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Exogenous CRF causes sleep suppression that is associated with activation of at least two important arousal systems: pontine noradrenergic and hypothalamic orexin/hypocretin neurons. It is not known whether CRF also impacts sleep-promoting neuronal systems. We hypothesized that CRF-mediated changes in wake and sleep involve decreased activity of hypothalamic sleep-regulatory neurons localized in the preoptic area. To test this hypothesis, we examined the effects of intracerebroventricular administration of CRF on sleep-wake measures and c-Fos expression in GABAergic neurons in the median preoptic nucleus (MnPN) and ventrolateral preoptic area (VLPO) in different experimental conditions. Administration of CRF (0.1 nmol) during baseline rest phase led to delayed sleep onset and decreases in total amount and mean duration of non-rapid eye movement (NREM) sleep. Administration of CRF during acute sleep deprivation (SD) resulted in suppression of recovery sleep and decreased c-Fos expression in MnPN/VLPO GABAergic neurons. Compared with vehicle controls, intracerebroventricular CRF potentiated disturbances of both NREM and REM sleep in rats exposed to a species-specific psychological stressor, the dirty cage of a male conspecific. The number of MnPN/VLPO GABAergic neurons expressing c-Fos was reduced in the CRF-treated group of dirty cage-exposed rats. These findings confirm the involvement of CRF in wake-sleep cycle regulation and suggest that increased CRF signaling in the brain 1) negatively affects homeostatic responses to sleep loss, 2) exacerbates stress-induced disturbances of sleep, and 3) suppresses the activity of sleep-regulatory neurons of the MnPN and VLPO.</description><identifier>ISSN: 0363-6119</identifier><identifier>EISSN: 1522-1490</identifier><identifier>DOI: 10.1152/ajpregu.00176.2015</identifier><identifier>PMID: 26333784</identifier><identifier>CODEN: AJPRDO</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Brain ; Corticotropin-Releasing Hormone - administration & dosage ; Corticotropin-Releasing Hormone - pharmacokinetics ; Eye movements ; GABAergic Neurons - drug effects ; GABAergic Neurons - metabolism ; Male ; Neural Inhibition - drug effects ; Neurons ; Preoptic Area - drug effects ; Preoptic Area - metabolism ; Rats ; Rats, Sprague-Dawley ; Sleep ; Sleep Stages - drug effects ; Sleep Wake Disorders - chemically induced ; Sleep Wake Disorders - metabolism ; Wakefulness - drug effects</subject><ispartof>American journal of physiology. 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Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><description>Corticotropin releasing factor (CRF) is implicated in sleep and arousal regulation. Exogenous CRF causes sleep suppression that is associated with activation of at least two important arousal systems: pontine noradrenergic and hypothalamic orexin/hypocretin neurons. It is not known whether CRF also impacts sleep-promoting neuronal systems. We hypothesized that CRF-mediated changes in wake and sleep involve decreased activity of hypothalamic sleep-regulatory neurons localized in the preoptic area. To test this hypothesis, we examined the effects of intracerebroventricular administration of CRF on sleep-wake measures and c-Fos expression in GABAergic neurons in the median preoptic nucleus (MnPN) and ventrolateral preoptic area (VLPO) in different experimental conditions. Administration of CRF (0.1 nmol) during baseline rest phase led to delayed sleep onset and decreases in total amount and mean duration of non-rapid eye movement (NREM) sleep. Administration of CRF during acute sleep deprivation (SD) resulted in suppression of recovery sleep and decreased c-Fos expression in MnPN/VLPO GABAergic neurons. Compared with vehicle controls, intracerebroventricular CRF potentiated disturbances of both NREM and REM sleep in rats exposed to a species-specific psychological stressor, the dirty cage of a male conspecific. The number of MnPN/VLPO GABAergic neurons expressing c-Fos was reduced in the CRF-treated group of dirty cage-exposed rats. These findings confirm the involvement of CRF in wake-sleep cycle regulation and suggest that increased CRF signaling in the brain 1) negatively affects homeostatic responses to sleep loss, 2) exacerbates stress-induced disturbances of sleep, and 3) suppresses the activity of sleep-regulatory neurons of the MnPN and VLPO.</description><subject>Animals</subject><subject>Brain</subject><subject>Corticotropin-Releasing Hormone - administration & dosage</subject><subject>Corticotropin-Releasing Hormone - pharmacokinetics</subject><subject>Eye movements</subject><subject>GABAergic Neurons - drug effects</subject><subject>GABAergic Neurons - metabolism</subject><subject>Male</subject><subject>Neural Inhibition - drug effects</subject><subject>Neurons</subject><subject>Preoptic Area - drug effects</subject><subject>Preoptic Area - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sleep</subject><subject>Sleep Stages - drug effects</subject><subject>Sleep Wake Disorders - chemically induced</subject><subject>Sleep Wake Disorders - metabolism</subject><subject>Wakefulness - drug effects</subject><issn>0363-6119</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctKxDAUhoMoznh5ARdScOOmY5KT3pYi3mDAhe5LmpwOGTpNTRphfHpTZ3ThxlVC8v0fnPMTcsHogrGM38j14HAVFpSyIl9wyrIDMo8fPGWioodkTiGHNGesmpET79eUUgECjsmM5wBQlGJOPl_DEC3eG9sntk3i3Q6jUYnvEId08ndytG6b9Bic7WWXSDWaDzNuEx2c6VeJsi4G7OjsYPqY6FD66b2NoHWp6XVQqHfCRBs_BtfIXuEZOWpl5_F8f56St4f7t7undPny-Hx3u0yVKMSYtropq0bkoLFokEGlQWKhy0I1QjSUQgsll7KRnOUVBdRtBlWcX7eKS63glFzvtIOz7wH9WG-MV9h1skcbfM1KKEBwqLL_0YJXkHGa5RG9-oOubXBxPRMFrIybZpOQ7yjlrPcO23pwZiPdtma0njqs9x3W3x3WU4cxdLlXh2aD-jfyUxp8AbcLnPY</recordid><startdate>20151101</startdate><enddate>20151101</enddate><creator>Gvilia, Irma</creator><creator>Suntsova, Natalia</creator><creator>Kumar, Sunil</creator><creator>McGinty, Dennis</creator><creator>Szymusiak, Ronald</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20151101</creationdate><title>Suppression of preoptic sleep-regulatory neuronal activity during corticotropin-releasing factor-induced sleep disturbance</title><author>Gvilia, Irma ; Suntsova, Natalia ; Kumar, Sunil ; McGinty, Dennis ; Szymusiak, Ronald</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-fdb89b463de7be139d3ae7d87cb44b003f382aaba216903edf539490dfc2adc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Brain</topic><topic>Corticotropin-Releasing Hormone - administration & dosage</topic><topic>Corticotropin-Releasing Hormone - pharmacokinetics</topic><topic>Eye movements</topic><topic>GABAergic Neurons - drug effects</topic><topic>GABAergic Neurons - metabolism</topic><topic>Male</topic><topic>Neural Inhibition - drug effects</topic><topic>Neurons</topic><topic>Preoptic Area - drug effects</topic><topic>Preoptic Area - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sleep</topic><topic>Sleep Stages - drug effects</topic><topic>Sleep Wake Disorders - chemically induced</topic><topic>Sleep Wake Disorders - metabolism</topic><topic>Wakefulness - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gvilia, Irma</creatorcontrib><creatorcontrib>Suntsova, Natalia</creatorcontrib><creatorcontrib>Kumar, Sunil</creatorcontrib><creatorcontrib>McGinty, Dennis</creatorcontrib><creatorcontrib>Szymusiak, Ronald</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gvilia, Irma</au><au>Suntsova, Natalia</au><au>Kumar, Sunil</au><au>McGinty, Dennis</au><au>Szymusiak, Ronald</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of preoptic sleep-regulatory neuronal activity during corticotropin-releasing factor-induced sleep disturbance</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><date>2015-11-01</date><risdate>2015</risdate><volume>309</volume><issue>9</issue><spage>R1092</spage><epage>R1100</epage><pages>R1092-R1100</pages><issn>0363-6119</issn><eissn>1522-1490</eissn><coden>AJPRDO</coden><abstract>Corticotropin releasing factor (CRF) is implicated in sleep and arousal regulation. Exogenous CRF causes sleep suppression that is associated with activation of at least two important arousal systems: pontine noradrenergic and hypothalamic orexin/hypocretin neurons. It is not known whether CRF also impacts sleep-promoting neuronal systems. We hypothesized that CRF-mediated changes in wake and sleep involve decreased activity of hypothalamic sleep-regulatory neurons localized in the preoptic area. To test this hypothesis, we examined the effects of intracerebroventricular administration of CRF on sleep-wake measures and c-Fos expression in GABAergic neurons in the median preoptic nucleus (MnPN) and ventrolateral preoptic area (VLPO) in different experimental conditions. Administration of CRF (0.1 nmol) during baseline rest phase led to delayed sleep onset and decreases in total amount and mean duration of non-rapid eye movement (NREM) sleep. Administration of CRF during acute sleep deprivation (SD) resulted in suppression of recovery sleep and decreased c-Fos expression in MnPN/VLPO GABAergic neurons. Compared with vehicle controls, intracerebroventricular CRF potentiated disturbances of both NREM and REM sleep in rats exposed to a species-specific psychological stressor, the dirty cage of a male conspecific. The number of MnPN/VLPO GABAergic neurons expressing c-Fos was reduced in the CRF-treated group of dirty cage-exposed rats. These findings confirm the involvement of CRF in wake-sleep cycle regulation and suggest that increased CRF signaling in the brain 1) negatively affects homeostatic responses to sleep loss, 2) exacerbates stress-induced disturbances of sleep, and 3) suppresses the activity of sleep-regulatory neurons of the MnPN and VLPO.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>26333784</pmid><doi>10.1152/ajpregu.00176.2015</doi><oa>free_for_read</oa></addata></record> |
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subjects | Animals Brain Corticotropin-Releasing Hormone - administration & dosage Corticotropin-Releasing Hormone - pharmacokinetics Eye movements GABAergic Neurons - drug effects GABAergic Neurons - metabolism Male Neural Inhibition - drug effects Neurons Preoptic Area - drug effects Preoptic Area - metabolism Rats Rats, Sprague-Dawley Sleep Sleep Stages - drug effects Sleep Wake Disorders - chemically induced Sleep Wake Disorders - metabolism Wakefulness - drug effects |
title | Suppression of preoptic sleep-regulatory neuronal activity during corticotropin-releasing factor-induced sleep disturbance |
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