Role of serotonin in the regulation of β-adrenoceptors by antidepressants
The role of serotonin (5-HT) in the regulation of the β-receptor density induced by long-term treatment with typical and atypical antidepressants was examined. Treatment with either mianserin (15 mg/kg, twice daily) or maprotiline (10 mg/kg, twice daily) for 7 days caused a significant decrease in t...
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Veröffentlicht in: | European journal of pharmacology 1987-09, Vol.141 (1), p.95-100 |
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description | The role of serotonin (5-HT) in the regulation of the β-receptor density induced by long-term treatment with typical and atypical antidepressants was examined. Treatment with either mianserin (15 mg/kg, twice daily) or maprotiline (10 mg/kg, twice daily) for 7 days caused a significant decrease in the β-receptor density, measured 6 h after the last dose, without a change in affinity. The reduction in β-receptors disappeared rapidly (within 24 h). However, treatment with mianserin or maprotiline combined with fluoxetine, a selective 5-HT uptake inhibitor, significantly decreased the β-receptor density even 24 h after the last dose. The combined administration of mianserin and 5-hydroxytryptophan (5-HTP) mimicked the effect of the combination with fluoxetine. Following pretreatment with p-chlorophenylalanine (PCPA) for 6 days, desipramine treatment for 3 days significantly decreased the β-receptors 6 h after the last dose but this desipramine-induced decrease in β-receptors was rapidly reversible (within 24 h). These results demonstrates that while intrasyneptic 5-HT levels are not a factor in the decrease in β-receptors they do play an important role in the preservation of the down-regulated state of the β-receptor caused by antidepressants from rapid reversibility. |
doi_str_mv | 10.1016/0014-2999(87)90414-6 |
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Treatment with either mianserin (15 mg/kg, twice daily) or maprotiline (10 mg/kg, twice daily) for 7 days caused a significant decrease in the β-receptor density, measured 6 h after the last dose, without a change in affinity. The reduction in β-receptors disappeared rapidly (within 24 h). However, treatment with mianserin or maprotiline combined with fluoxetine, a selective 5-HT uptake inhibitor, significantly decreased the β-receptor density even 24 h after the last dose. The combined administration of mianserin and 5-hydroxytryptophan (5-HTP) mimicked the effect of the combination with fluoxetine. Following pretreatment with p-chlorophenylalanine (PCPA) for 6 days, desipramine treatment for 3 days significantly decreased the β-receptors 6 h after the last dose but this desipramine-induced decrease in β-receptors was rapidly reversible (within 24 h). These results demonstrates that while intrasyneptic 5-HT levels are not a factor in the decrease in β-receptors they do play an important role in the preservation of the down-regulated state of the β-receptor caused by antidepressants from rapid reversibility.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/0014-2999(87)90414-6</identifier><identifier>PMID: 2822448</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>5-HT ; 5-Hydroxytryptophan - pharmacology ; Animals ; Antidepressants ; Antidepressive Agents - pharmacology ; beta -adrenergic ; Biological and medical sciences ; brain ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; Desipramine - pharmacology ; Down-regulation ; Fenclonine - pharmacology ; Fluoxetine - pharmacology ; In Vitro Techniques ; Male ; Maprotiline ; Maprotiline - pharmacology ; Medical sciences ; Membranes - drug effects ; Mianserin ; Mianserin - pharmacology ; Neuropharmacology ; Pharmacology. Drug treatments ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopharmacology ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, beta - drug effects ; serotonin ; Serotonin - physiology ; β-Receptors</subject><ispartof>European journal of pharmacology, 1987-09, Vol.141 (1), p.95-100</ispartof><rights>1987</rights><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-754a9324e64117405f666951d24ea8f52f518418066151a5b020fbc7dad1f47d3</citedby><cites>FETCH-LOGICAL-c417t-754a9324e64117405f666951d24ea8f52f518418066151a5b020fbc7dad1f47d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0014299987904146$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7778147$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2822448$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ASAKURA, M</creatorcontrib><creatorcontrib>TSUKAMOTO, T</creatorcontrib><creatorcontrib>KUBOTA, H</creatorcontrib><creatorcontrib>IMAFUKU, J</creatorcontrib><creatorcontrib>INO, M</creatorcontrib><creatorcontrib>NISHIZAKI, J</creatorcontrib><creatorcontrib>SATO, A</creatorcontrib><creatorcontrib>SHINBO, K</creatorcontrib><creatorcontrib>HASEGAWA, K</creatorcontrib><title>Role of serotonin in the regulation of β-adrenoceptors by antidepressants</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>The role of serotonin (5-HT) in the regulation of the β-receptor density induced by long-term treatment with typical and atypical antidepressants was examined. Treatment with either mianserin (15 mg/kg, twice daily) or maprotiline (10 mg/kg, twice daily) for 7 days caused a significant decrease in the β-receptor density, measured 6 h after the last dose, without a change in affinity. The reduction in β-receptors disappeared rapidly (within 24 h). However, treatment with mianserin or maprotiline combined with fluoxetine, a selective 5-HT uptake inhibitor, significantly decreased the β-receptor density even 24 h after the last dose. The combined administration of mianserin and 5-hydroxytryptophan (5-HTP) mimicked the effect of the combination with fluoxetine. Following pretreatment with p-chlorophenylalanine (PCPA) for 6 days, desipramine treatment for 3 days significantly decreased the β-receptors 6 h after the last dose but this desipramine-induced decrease in β-receptors was rapidly reversible (within 24 h). These results demonstrates that while intrasyneptic 5-HT levels are not a factor in the decrease in β-receptors they do play an important role in the preservation of the down-regulated state of the β-receptor caused by antidepressants from rapid reversibility.</description><subject>5-HT</subject><subject>5-Hydroxytryptophan - pharmacology</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Antidepressive Agents - pharmacology</subject><subject>beta -adrenergic</subject><subject>Biological and medical sciences</subject><subject>brain</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>Desipramine - pharmacology</subject><subject>Down-regulation</subject><subject>Fenclonine - pharmacology</subject><subject>Fluoxetine - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Maprotiline</subject><subject>Maprotiline - pharmacology</subject><subject>Medical sciences</subject><subject>Membranes - drug effects</subject><subject>Mianserin</subject><subject>Mianserin - pharmacology</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopharmacology</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Receptors, Adrenergic, beta - drug effects</subject><subject>serotonin</subject><subject>Serotonin - physiology</subject><subject>β-Receptors</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtqWzEQhkVoSZy0b5DAWZSSLk6rkXXdBIJJeiEQKO1ayNKoVTg-cqTjQl6rD5JnqlwbL1sQSKP_m2H4CDkH-h4oyA-UAu-ZMeZSq3eG8lbJIzIDrUxPFbAXZHZATshprQ-UUmGYOCbHTDPGuZ6RL1_zgF2OXcWSpzymsWtn-oldwR-bwU0pj9v4-XfvQsExe1xPudRu-dS5cUoB1wVrbc_6iryMbqj4en-fke-3N98Wn_q7-4-fF9d3veegpl4J7syccZQcQHEqopTSCAjty-koWBSgOWgqJQhwYkkZjUuvggsQuQrzM_J2N3dd8uMG62RXqXocBjdi3lSrgUqgWv0XBK7UHJhpIN-BvuRaC0a7LmnlypMFareu7Vak3Yq0Wtm_rq1sbRf7-ZvlCsOhaS-35W_2uaveDbG40ad6wJRSuq3QsKsdhk3ar4TFVp9w9BhSQT_ZkNO_9_gD0USZzg</recordid><startdate>19870902</startdate><enddate>19870902</enddate><creator>ASAKURA, M</creator><creator>TSUKAMOTO, T</creator><creator>KUBOTA, H</creator><creator>IMAFUKU, J</creator><creator>INO, M</creator><creator>NISHIZAKI, J</creator><creator>SATO, A</creator><creator>SHINBO, K</creator><creator>HASEGAWA, K</creator><general>Elsevier B.V</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>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19870902</creationdate><title>Role of serotonin in the regulation of β-adrenoceptors by antidepressants</title><author>ASAKURA, M ; TSUKAMOTO, T ; KUBOTA, H ; IMAFUKU, J ; INO, M ; NISHIZAKI, J ; SATO, A ; SHINBO, K ; HASEGAWA, K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-754a9324e64117405f666951d24ea8f52f518418066151a5b020fbc7dad1f47d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>5-HT</topic><topic>5-Hydroxytryptophan - pharmacology</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Antidepressive Agents - pharmacology</topic><topic>beta -adrenergic</topic><topic>Biological and medical sciences</topic><topic>brain</topic><topic>Cerebral Cortex - drug effects</topic><topic>Cerebral Cortex - metabolism</topic><topic>Desipramine - pharmacology</topic><topic>Down-regulation</topic><topic>Fenclonine - pharmacology</topic><topic>Fluoxetine - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Maprotiline</topic><topic>Maprotiline - pharmacology</topic><topic>Medical sciences</topic><topic>Membranes - drug effects</topic><topic>Mianserin</topic><topic>Mianserin - pharmacology</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Receptors, Adrenergic, beta - drug effects</topic><topic>serotonin</topic><topic>Serotonin - physiology</topic><topic>β-Receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ASAKURA, M</creatorcontrib><creatorcontrib>TSUKAMOTO, T</creatorcontrib><creatorcontrib>KUBOTA, H</creatorcontrib><creatorcontrib>IMAFUKU, J</creatorcontrib><creatorcontrib>INO, M</creatorcontrib><creatorcontrib>NISHIZAKI, J</creatorcontrib><creatorcontrib>SATO, A</creatorcontrib><creatorcontrib>SHINBO, K</creatorcontrib><creatorcontrib>HASEGAWA, K</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ASAKURA, M</au><au>TSUKAMOTO, T</au><au>KUBOTA, H</au><au>IMAFUKU, J</au><au>INO, M</au><au>NISHIZAKI, J</au><au>SATO, A</au><au>SHINBO, K</au><au>HASEGAWA, K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of serotonin in the regulation of β-adrenoceptors by antidepressants</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>1987-09-02</date><risdate>1987</risdate><volume>141</volume><issue>1</issue><spage>95</spage><epage>100</epage><pages>95-100</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>The role of serotonin (5-HT) in the regulation of the β-receptor density induced by long-term treatment with typical and atypical antidepressants was examined. Treatment with either mianserin (15 mg/kg, twice daily) or maprotiline (10 mg/kg, twice daily) for 7 days caused a significant decrease in the β-receptor density, measured 6 h after the last dose, without a change in affinity. The reduction in β-receptors disappeared rapidly (within 24 h). However, treatment with mianserin or maprotiline combined with fluoxetine, a selective 5-HT uptake inhibitor, significantly decreased the β-receptor density even 24 h after the last dose. The combined administration of mianserin and 5-hydroxytryptophan (5-HTP) mimicked the effect of the combination with fluoxetine. Following pretreatment with p-chlorophenylalanine (PCPA) for 6 days, desipramine treatment for 3 days significantly decreased the β-receptors 6 h after the last dose but this desipramine-induced decrease in β-receptors was rapidly reversible (within 24 h). These results demonstrates that while intrasyneptic 5-HT levels are not a factor in the decrease in β-receptors they do play an important role in the preservation of the down-regulated state of the β-receptor caused by antidepressants from rapid reversibility.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>2822448</pmid><doi>10.1016/0014-2999(87)90414-6</doi><tpages>6</tpages></addata></record> |
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subjects | 5-HT 5-Hydroxytryptophan - pharmacology Animals Antidepressants Antidepressive Agents - pharmacology beta -adrenergic Biological and medical sciences brain Cerebral Cortex - drug effects Cerebral Cortex - metabolism Desipramine - pharmacology Down-regulation Fenclonine - pharmacology Fluoxetine - pharmacology In Vitro Techniques Male Maprotiline Maprotiline - pharmacology Medical sciences Membranes - drug effects Mianserin Mianserin - pharmacology Neuropharmacology Pharmacology. Drug treatments Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopharmacology Rats Rats, Inbred Strains Receptors, Adrenergic, beta - drug effects serotonin Serotonin - physiology β-Receptors |
title | Role of serotonin in the regulation of β-adrenoceptors by antidepressants |
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