Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex
The prefrontal cortex and brainstem modulate autonomic and arousal state control but the neurotransmitter mechanisms underlying communication between prefrontal cortex and brainstem remain poorly understood. This study examined the hypothesis that microdialysis delivery of carbachol to the pontine r...
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| creator | Demarco, G.J Baghdoyan, H.A Lydic, R |
| description | The prefrontal cortex and brainstem modulate autonomic and arousal state control but the neurotransmitter mechanisms underlying communication between prefrontal cortex and brainstem remain poorly understood. This study examined the hypothesis that microdialysis delivery of carbachol to the pontine reticular formation (PRF) of anesthetized C57BL/6J (B6) mouse modulates acetylcholine (ACh) release in the frontal association cortex. Microdialysis delivery of carbachol (8.8 mM) to the PRF caused a significant (
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| doi_str_mv | 10.1016/j.neuroscience.2003.08.045 |
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P<0.01) decrease (−28%) in ACh release in the frontal association cortex, a significant (
P<0.01) decrease (−23%) in respiratory rate, and a significant (
P<0.01) increase (223%) in time to righting after anesthesia. Additional
in vitro studies used the [
35S]guanylyl-5′-
O-(γ-thio)-triphosphate ([
35S]GTPγS) assay to test the hypothesis that muscarinic cholinergic receptors activate guanine nucleotide binding proteins (G proteins) in the frontal association cortex and basal forebrain.
In vitro treatment with carbachol (1 mM) caused a significant (
P<0.01) increase in [
35S]GTPγS binding in the frontal association cortex (62%) and basal forebrain nuclei including medial septum (227%), vertical (210%) and horizontal (165%) limbs of the diagonal band of Broca, and substantia innominata (127%). G protein activation by carbachol was concentration-dependent and blocked by atropine, indicating that the carbachol-stimulated [
35S]GTPγS binding was mediated by muscarinic cholinergic receptors. Together, the
in vitro and
in vivo data show for the first time in B6 mouse that cholinergic neurotransmission in the PRF can significantly alter ACh release in frontal association cortex, arousal from anesthesia, and respiratory rate.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/j.neuroscience.2003.08.045</identifier><identifier>PMID: 14667438</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Acetylcholine - antagonists & inhibitors ; Acetylcholine - metabolism ; Animals ; arousal ; basal forebrain ; Biological and medical sciences ; breathing ; Carbachol - pharmacology ; cortical excitability ; Fundamental and applied biological sciences. Psychology ; G proteins ; Guanosine 5'-O-(3-Thiotriphosphate) - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Pons - drug effects ; Pons - metabolism ; Prefrontal Cortex - drug effects ; Prefrontal Cortex - metabolism ; Protein Binding - drug effects ; Protein Binding - physiology ; REM sleep ; Reticular Formation - drug effects ; Reticular Formation - metabolism ; Sleep. Vigilance ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 2004, Vol.123 (1), p.17-29</ispartof><rights>2003 IBRO</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-8e0e381ec29efb783f452b89aa0cc036c651a875c1ff2900da87a6e97259452b3</citedby><cites>FETCH-LOGICAL-c437t-8e0e381ec29efb783f452b89aa0cc036c651a875c1ff2900da87a6e97259452b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0306452203006651$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15367625$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14667438$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Demarco, G.J</creatorcontrib><creatorcontrib>Baghdoyan, H.A</creatorcontrib><creatorcontrib>Lydic, R</creatorcontrib><title>Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>The prefrontal cortex and brainstem modulate autonomic and arousal state control but the neurotransmitter mechanisms underlying communication between prefrontal cortex and brainstem remain poorly understood. This study examined the hypothesis that microdialysis delivery of carbachol to the pontine reticular formation (PRF) of anesthetized C57BL/6J (B6) mouse modulates acetylcholine (ACh) release in the frontal association cortex. Microdialysis delivery of carbachol (8.8 mM) to the PRF caused a significant (
P<0.01) decrease (−28%) in ACh release in the frontal association cortex, a significant (
P<0.01) decrease (−23%) in respiratory rate, and a significant (
P<0.01) increase (223%) in time to righting after anesthesia. Additional
in vitro studies used the [
35S]guanylyl-5′-
O-(γ-thio)-triphosphate ([
35S]GTPγS) assay to test the hypothesis that muscarinic cholinergic receptors activate guanine nucleotide binding proteins (G proteins) in the frontal association cortex and basal forebrain.
In vitro treatment with carbachol (1 mM) caused a significant (
P<0.01) increase in [
35S]GTPγS binding in the frontal association cortex (62%) and basal forebrain nuclei including medial septum (227%), vertical (210%) and horizontal (165%) limbs of the diagonal band of Broca, and substantia innominata (127%). G protein activation by carbachol was concentration-dependent and blocked by atropine, indicating that the carbachol-stimulated [
35S]GTPγS binding was mediated by muscarinic cholinergic receptors. Together, the
in vitro and
in vivo data show for the first time in B6 mouse that cholinergic neurotransmission in the PRF can significantly alter ACh release in frontal association cortex, arousal from anesthesia, and respiratory rate.</description><subject>Acetylcholine - antagonists & inhibitors</subject><subject>Acetylcholine - metabolism</subject><subject>Animals</subject><subject>arousal</subject><subject>basal forebrain</subject><subject>Biological and medical sciences</subject><subject>breathing</subject><subject>Carbachol - pharmacology</subject><subject>cortical excitability</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>G proteins</subject><subject>Guanosine 5'-O-(3-Thiotriphosphate) - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Pons - drug effects</subject><subject>Pons - metabolism</subject><subject>Prefrontal Cortex - drug effects</subject><subject>Prefrontal Cortex - metabolism</subject><subject>Protein Binding - drug effects</subject><subject>Protein Binding - physiology</subject><subject>REM sleep</subject><subject>Reticular Formation - drug effects</subject><subject>Reticular Formation - metabolism</subject><subject>Sleep. Vigilance</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUuPFCEUhYnROO3oXzDERHdVA0XxKHdO-04nbnRNaOqSoUMVLVDG-fdS6UrGnbIhkO-ee-85CL2ipKWEiptTO8OSYrYeZgttRwhriWpJzx-hHVWSNZL3_WO0I4yIpuddd4We5Xwi9fCePUVXtBdC9kztUN6bdDT2LgbsZ1zuAJ_jXPwMOEHxdgkmYRfTZIqPM44O77m8PdyIr3iKSwY8gk1gMmRsLJT7sCpdqsP6vYqeE7hURU3ANqYCv5-jJ86EDC-2-xr9-Pjh-_5zc_j26cv-3aGxPZOlUUCAKQq2G8AdpWKurnJUgzHEWsKEFZwaJbmlznUDIWN9GAGD7PiwkuwavbnonlP8uUAuevLZQghmhjq8lpSL6p34J0iHrhqvaAXfXkBb7c91L31OfjLpXlOi12z0Sf-djV6z0UTpmk0tfrl1WY4TjA-lWxgVeL0BJlsTXDKz9fmB40xI0a1C7y8cVPN-eUh6azf6BLboMfr_mecPQpW05Q</recordid><startdate>2004</startdate><enddate>2004</enddate><creator>Demarco, G.J</creator><creator>Baghdoyan, H.A</creator><creator>Lydic, R</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>2004</creationdate><title>Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex</title><author>Demarco, G.J ; Baghdoyan, H.A ; Lydic, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-8e0e381ec29efb783f452b89aa0cc036c651a875c1ff2900da87a6e97259452b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acetylcholine - antagonists & inhibitors</topic><topic>Acetylcholine - metabolism</topic><topic>Animals</topic><topic>arousal</topic><topic>basal forebrain</topic><topic>Biological and medical sciences</topic><topic>breathing</topic><topic>Carbachol - pharmacology</topic><topic>cortical excitability</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>G proteins</topic><topic>Guanosine 5'-O-(3-Thiotriphosphate) - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Pons - drug effects</topic><topic>Pons - metabolism</topic><topic>Prefrontal Cortex - drug effects</topic><topic>Prefrontal Cortex - metabolism</topic><topic>Protein Binding - drug effects</topic><topic>Protein Binding - physiology</topic><topic>REM sleep</topic><topic>Reticular Formation - drug effects</topic><topic>Reticular Formation - metabolism</topic><topic>Sleep. Vigilance</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Demarco, G.J</creatorcontrib><creatorcontrib>Baghdoyan, H.A</creatorcontrib><creatorcontrib>Lydic, R</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Demarco, G.J</au><au>Baghdoyan, H.A</au><au>Lydic, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>2004</date><risdate>2004</risdate><volume>123</volume><issue>1</issue><spage>17</spage><epage>29</epage><pages>17-29</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>The prefrontal cortex and brainstem modulate autonomic and arousal state control but the neurotransmitter mechanisms underlying communication between prefrontal cortex and brainstem remain poorly understood. This study examined the hypothesis that microdialysis delivery of carbachol to the pontine reticular formation (PRF) of anesthetized C57BL/6J (B6) mouse modulates acetylcholine (ACh) release in the frontal association cortex. Microdialysis delivery of carbachol (8.8 mM) to the PRF caused a significant (
P<0.01) decrease (−28%) in ACh release in the frontal association cortex, a significant (
P<0.01) decrease (−23%) in respiratory rate, and a significant (
P<0.01) increase (223%) in time to righting after anesthesia. Additional
in vitro studies used the [
35S]guanylyl-5′-
O-(γ-thio)-triphosphate ([
35S]GTPγS) assay to test the hypothesis that muscarinic cholinergic receptors activate guanine nucleotide binding proteins (G proteins) in the frontal association cortex and basal forebrain.
In vitro treatment with carbachol (1 mM) caused a significant (
P<0.01) increase in [
35S]GTPγS binding in the frontal association cortex (62%) and basal forebrain nuclei including medial septum (227%), vertical (210%) and horizontal (165%) limbs of the diagonal band of Broca, and substantia innominata (127%). G protein activation by carbachol was concentration-dependent and blocked by atropine, indicating that the carbachol-stimulated [
35S]GTPγS binding was mediated by muscarinic cholinergic receptors. Together, the
in vitro and
in vivo data show for the first time in B6 mouse that cholinergic neurotransmission in the PRF can significantly alter ACh release in frontal association cortex, arousal from anesthesia, and respiratory rate.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>14667438</pmid><doi>10.1016/j.neuroscience.2003.08.045</doi><tpages>13</tpages></addata></record> |
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| subjects | Acetylcholine - antagonists & inhibitors Acetylcholine - metabolism Animals arousal basal forebrain Biological and medical sciences breathing Carbachol - pharmacology cortical excitability Fundamental and applied biological sciences. Psychology G proteins Guanosine 5'-O-(3-Thiotriphosphate) - metabolism Male Mice Mice, Inbred C57BL Pons - drug effects Pons - metabolism Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism Protein Binding - drug effects Protein Binding - physiology REM sleep Reticular Formation - drug effects Reticular Formation - metabolism Sleep. Vigilance Vertebrates: nervous system and sense organs |
| title | Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex |
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