The raphe neuronal system and serotonergic effects of LSD
Earlier work from this laboratory had shown that LSD caused significant increases in rat brain serotonin (5-HT). The increase was later localized to a subsynaptosomal fraction consisting largely of synaptic vesicles. However, the source of the increase and the mechanism by which LSD caused the enhan...
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Veröffentlicht in: | Neuropharmacology 1982-01, Vol.21 (8), p.811-816 |
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creator | Halaris, A.E. Rosenthal, M. DeMet, E.M. Freedman, D.X. |
description | Earlier work from this laboratory had shown that LSD caused significant increases in rat brain serotonin (5-HT). The increase was later localized to a subsynaptosomal fraction consisting largely of synaptic vesicles. However, the source of the increase and the mechanism by which LSD caused the enhanced 5-HT binding or retention had not been elucidated. The present study was undertaken to evaluate the serotonergic effects of LSD following destruction of raphe nuclei with radiofrequency lesions. When LSD was given to animals with large midbrain raphe lesions, it caused significant increases in forebrain or cortical 5-HT up to 48 hr, or 7 days post-lesion, respectively. It was concluded that an intact cell body is not necessary for the expression of the LSD-mediated increases in 5-HT occurring in the nerve-ending. The possible mechanisms by which LSD could act directly at the nerve-ending are discussed. |
doi_str_mv | 10.1016/0028-3908(82)90069-7 |
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The increase was later localized to a subsynaptosomal fraction consisting largely of synaptic vesicles. However, the source of the increase and the mechanism by which LSD caused the enhanced 5-HT binding or retention had not been elucidated. The present study was undertaken to evaluate the serotonergic effects of LSD following destruction of raphe nuclei with radiofrequency lesions. When LSD was given to animals with large midbrain raphe lesions, it caused significant increases in forebrain or cortical 5-HT up to 48 hr, or 7 days post-lesion, respectively. It was concluded that an intact cell body is not necessary for the expression of the LSD-mediated increases in 5-HT occurring in the nerve-ending. The possible mechanisms by which LSD could act directly at the nerve-ending are discussed.</description><identifier>ISSN: 0028-3908</identifier><identifier>EISSN: 1873-7064</identifier><identifier>DOI: 10.1016/0028-3908(82)90069-7</identifier><identifier>PMID: 6181428</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>5-hydroxytryptamine ; Animals ; Brain Stem - physiology ; d-LSD ; Dopamine - metabolism ; Hydroxyindoleacetic Acid - metabolism ; lesions ; LSD receptor ; Lysergic Acid Diethylamide - pharmacology ; Male ; Neurons - drug effects ; Radio Waves ; raphe neurons ; Raphe Nuclei - drug effects ; Raphe Nuclei - physiology ; Raphe Nuclei - radiation effects ; Rats ; Rats, Inbred Strains ; Serotonin - metabolism ; Serotonin - physiology</subject><ispartof>Neuropharmacology, 1982-01, Vol.21 (8), p.811-816</ispartof><rights>1982</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-4e096b92178d6dd62799eb1243d2f9f770681c4f815ee74b99ca1143afeb63a23</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0028-3908(82)90069-7$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6181428$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Halaris, A.E.</creatorcontrib><creatorcontrib>Rosenthal, M.</creatorcontrib><creatorcontrib>DeMet, E.M.</creatorcontrib><creatorcontrib>Freedman, D.X.</creatorcontrib><title>The raphe neuronal system and serotonergic effects of LSD</title><title>Neuropharmacology</title><addtitle>Neuropharmacology</addtitle><description>Earlier work from this laboratory had shown that LSD caused significant increases in rat brain serotonin (5-HT). The increase was later localized to a subsynaptosomal fraction consisting largely of synaptic vesicles. However, the source of the increase and the mechanism by which LSD caused the enhanced 5-HT binding or retention had not been elucidated. The present study was undertaken to evaluate the serotonergic effects of LSD following destruction of raphe nuclei with radiofrequency lesions. When LSD was given to animals with large midbrain raphe lesions, it caused significant increases in forebrain or cortical 5-HT up to 48 hr, or 7 days post-lesion, respectively. It was concluded that an intact cell body is not necessary for the expression of the LSD-mediated increases in 5-HT occurring in the nerve-ending. The possible mechanisms by which LSD could act directly at the nerve-ending are discussed.</description><subject>5-hydroxytryptamine</subject><subject>Animals</subject><subject>Brain Stem - physiology</subject><subject>d-LSD</subject><subject>Dopamine - metabolism</subject><subject>Hydroxyindoleacetic Acid - metabolism</subject><subject>lesions</subject><subject>LSD receptor</subject><subject>Lysergic Acid Diethylamide - pharmacology</subject><subject>Male</subject><subject>Neurons - drug effects</subject><subject>Radio Waves</subject><subject>raphe neurons</subject><subject>Raphe Nuclei - drug effects</subject><subject>Raphe Nuclei - physiology</subject><subject>Raphe Nuclei - radiation effects</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Serotonin - metabolism</subject><subject>Serotonin - physiology</subject><issn>0028-3908</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1982</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkDtPwzAQxy0EKqXwDUDKhGAI2I7jx4KEylOqxECZLcc5Q1ASFztB6rcnoVVHWO6G_-NOP4ROCb4imPBrjKlMM4XlhaSXCmOuUrGHpkSKLBWYs3003VkO0VGMnxhjJomcoAknkjAqp0gtPyAJZjXMFvrgW1MncR07aBLTlkmE4DvfQnivbALOge1i4l2yeL07RgfO1BFOtnuG3h7ul_OndPHy-Dy_XaQ2k7JLGWDFC0WJkCUvS06FUlAQyrKSOuXE8KkkljlJcgDBCqWsIYRlxkHBM0OzGTrf9K6C_-ohdrqpooW6Ni34PmrBKJO5yv41kjynmPKxkW2MNvgYAzi9ClVjwloTrEe0euSmR25aUv2LVoshdrbt74sGyl1oy3LQbzY6DDS-Kwg62gpaC2UVBm669NXfB34AFRWGOw</recordid><startdate>19820101</startdate><enddate>19820101</enddate><creator>Halaris, A.E.</creator><creator>Rosenthal, M.</creator><creator>DeMet, E.M.</creator><creator>Freedman, D.X.</creator><general>Elsevier Ltd</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>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>19820101</creationdate><title>The raphe neuronal system and serotonergic effects of LSD</title><author>Halaris, A.E. ; Rosenthal, M. ; DeMet, E.M. ; Freedman, D.X.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-4e096b92178d6dd62799eb1243d2f9f770681c4f815ee74b99ca1143afeb63a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1982</creationdate><topic>5-hydroxytryptamine</topic><topic>Animals</topic><topic>Brain Stem - physiology</topic><topic>d-LSD</topic><topic>Dopamine - metabolism</topic><topic>Hydroxyindoleacetic Acid - metabolism</topic><topic>lesions</topic><topic>LSD receptor</topic><topic>Lysergic Acid Diethylamide - pharmacology</topic><topic>Male</topic><topic>Neurons - drug effects</topic><topic>Radio Waves</topic><topic>raphe neurons</topic><topic>Raphe Nuclei - drug effects</topic><topic>Raphe Nuclei - physiology</topic><topic>Raphe Nuclei - radiation effects</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Serotonin - metabolism</topic><topic>Serotonin - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Halaris, A.E.</creatorcontrib><creatorcontrib>Rosenthal, M.</creatorcontrib><creatorcontrib>DeMet, E.M.</creatorcontrib><creatorcontrib>Freedman, D.X.</creatorcontrib><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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Halaris, A.E.</au><au>Rosenthal, M.</au><au>DeMet, E.M.</au><au>Freedman, D.X.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The raphe neuronal system and serotonergic effects of LSD</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>1982-01-01</date><risdate>1982</risdate><volume>21</volume><issue>8</issue><spage>811</spage><epage>816</epage><pages>811-816</pages><issn>0028-3908</issn><eissn>1873-7064</eissn><abstract>Earlier work from this laboratory had shown that LSD caused significant increases in rat brain serotonin (5-HT). The increase was later localized to a subsynaptosomal fraction consisting largely of synaptic vesicles. However, the source of the increase and the mechanism by which LSD caused the enhanced 5-HT binding or retention had not been elucidated. The present study was undertaken to evaluate the serotonergic effects of LSD following destruction of raphe nuclei with radiofrequency lesions. When LSD was given to animals with large midbrain raphe lesions, it caused significant increases in forebrain or cortical 5-HT up to 48 hr, or 7 days post-lesion, respectively. It was concluded that an intact cell body is not necessary for the expression of the LSD-mediated increases in 5-HT occurring in the nerve-ending. The possible mechanisms by which LSD could act directly at the nerve-ending are discussed.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>6181428</pmid><doi>10.1016/0028-3908(82)90069-7</doi><tpages>6</tpages></addata></record> |
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subjects | 5-hydroxytryptamine Animals Brain Stem - physiology d-LSD Dopamine - metabolism Hydroxyindoleacetic Acid - metabolism lesions LSD receptor Lysergic Acid Diethylamide - pharmacology Male Neurons - drug effects Radio Waves raphe neurons Raphe Nuclei - drug effects Raphe Nuclei - physiology Raphe Nuclei - radiation effects Rats Rats, Inbred Strains Serotonin - metabolism Serotonin - physiology |
title | The raphe neuronal system and serotonergic effects of LSD |
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