Tumor necrosis factor-α: presynaptic sensitivity is modified after antidepressant drug administration
Presynaptic adrenergic functioning was coupled to cytokine sensitivity in order to further establish the mechanism of action of a tricyclic antidepressant drug. Antidepressant administration of desipramine to rats twice-daily for 2 weeks increased hippocampal TNF levels and transformed the presynapt...
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| Veröffentlicht in: | Brain research 1994-12, Vol.665 (2), p.293-299 |
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| creator | Ignatowski, Tracey A. Spengler, Robert N. |
| description | Presynaptic adrenergic functioning was coupled to cytokine sensitivity in order to further establish the mechanism of action of a tricyclic antidepressant drug. Antidepressant administration of desipramine to rats twice-daily for 2 weeks increased hippocampal TNF levels and transformed the presynaptic TNF response. One day of desipramine administration resulted in increased locus coeruleus TNF mRNA accumulation and, simultaneously, hippocampal TNF levels escalated. The fractional release of [
3H]norepinephrine during field stimulation of control hippocampal slices was decreased by the addition of TNF in a concentration-dependent manner, an effect which was potentiated by the
α
2-adrenergic
antagonist idazoxan. While no change in sensitivity to TNF was observed in the hippocampus after one day of desipramine administration, TNF enhanced, rather than inhibited [
3H]norepinephrine release after 14 days. In addition, TNF potentiation of [
3H]norepinephrine release after chronic desipramine administration was reversed in the presence of idazoxan to a greater inhibition than in control slices exposed to idazoxan. Therefore, TNF-induced regulation of [
3H]norepinephrine releaase appears to be associated with an alteration of
α
2-adrenergic
receptor responsiveness. The reversal in presynaptic TNF responsiveness after 14 days of tricyclic antidepressant drug administration describes a mechanism of action for their delayed clinical effect. |
| doi_str_mv | 10.1016/0006-8993(94)91350-1 |
| format | Article |
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3H]norepinephrine during field stimulation of control hippocampal slices was decreased by the addition of TNF in a concentration-dependent manner, an effect which was potentiated by the
α
2-adrenergic
antagonist idazoxan. While no change in sensitivity to TNF was observed in the hippocampus after one day of desipramine administration, TNF enhanced, rather than inhibited [
3H]norepinephrine release after 14 days. In addition, TNF potentiation of [
3H]norepinephrine release after chronic desipramine administration was reversed in the presence of idazoxan to a greater inhibition than in control slices exposed to idazoxan. Therefore, TNF-induced regulation of [
3H]norepinephrine releaase appears to be associated with an alteration of
α
2-adrenergic
receptor responsiveness. The reversal in presynaptic TNF responsiveness after 14 days of tricyclic antidepressant drug administration describes a mechanism of action for their delayed clinical effect.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/0006-8993(94)91350-1</identifier><identifier>PMID: 7895065</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Adrenergic ; Animals ; Antidepressant ; Antidepressive Agents - pharmacology ; Biological and medical sciences ; Brain ; Desipramine - pharmacology ; Dioxanes - pharmacology ; Drug Resistance ; Electric Stimulation ; Hippocampus ; Hippocampus - cytology ; Hippocampus - metabolism ; Idazoxan ; Locus coeruleus ; Male ; Medical sciences ; Neurons - metabolism ; Neuropharmacology ; Norepinephrine - metabolism ; Pharmacology. Drug treatments ; Presynaptic Terminals - drug effects ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopharmacology ; Rats ; Rats, Sprague-Dawley ; Sympathetic Nervous System - metabolism ; Time Factors ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>Brain research, 1994-12, Vol.665 (2), p.293-299</ispartof><rights>1994 Elsevier Science B.V. All rights reserved</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-6f4fec9179635d1513081bd423b5a313dbf294919242557a26367b807e2e46de3</citedby><cites>FETCH-LOGICAL-c417t-6f4fec9179635d1513081bd423b5a313dbf294919242557a26367b807e2e46de3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0006-8993(94)91350-1$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3323427$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7895065$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ignatowski, Tracey A.</creatorcontrib><creatorcontrib>Spengler, Robert N.</creatorcontrib><title>Tumor necrosis factor-α: presynaptic sensitivity is modified after antidepressant drug administration</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Presynaptic adrenergic functioning was coupled to cytokine sensitivity in order to further establish the mechanism of action of a tricyclic antidepressant drug. Antidepressant administration of desipramine to rats twice-daily for 2 weeks increased hippocampal TNF levels and transformed the presynaptic TNF response. One day of desipramine administration resulted in increased locus coeruleus TNF mRNA accumulation and, simultaneously, hippocampal TNF levels escalated. The fractional release of [
3H]norepinephrine during field stimulation of control hippocampal slices was decreased by the addition of TNF in a concentration-dependent manner, an effect which was potentiated by the
α
2-adrenergic
antagonist idazoxan. While no change in sensitivity to TNF was observed in the hippocampus after one day of desipramine administration, TNF enhanced, rather than inhibited [
3H]norepinephrine release after 14 days. In addition, TNF potentiation of [
3H]norepinephrine release after chronic desipramine administration was reversed in the presence of idazoxan to a greater inhibition than in control slices exposed to idazoxan. Therefore, TNF-induced regulation of [
3H]norepinephrine releaase appears to be associated with an alteration of
α
2-adrenergic
receptor responsiveness. The reversal in presynaptic TNF responsiveness after 14 days of tricyclic antidepressant drug administration describes a mechanism of action for their delayed clinical effect.</description><subject>Adrenergic</subject><subject>Animals</subject><subject>Antidepressant</subject><subject>Antidepressive Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Desipramine - pharmacology</subject><subject>Dioxanes - pharmacology</subject><subject>Drug Resistance</subject><subject>Electric Stimulation</subject><subject>Hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - metabolism</subject><subject>Idazoxan</subject><subject>Locus coeruleus</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurons - metabolism</subject><subject>Neuropharmacology</subject><subject>Norepinephrine - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Presynaptic Terminals - drug effects</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, Sprague-Dawley</subject><subject>Sympathetic Nervous System - metabolism</subject><subject>Time Factors</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2KFDEQgIMo67j6Bgo5iOih1_z_eBBk2dWFBS_rOaSTikSmu8ckvTCP5YvsM223M8xRT1VFfVUUXyH0mpILSqj6SAhRnbGWv7fig6Vcko4-QRtqNOsUE-Qp2pyQ5-hFrb-WknNLztCZNlYSJTco3c3DVPAIoUw1V5x8aFPpHv58wrsCdT_6XcsBVxhrbvk-tz1eqGGKOWWI2KcGBfux5QgrX5cUxzL_xD4Oecy1Fd_yNL5Ez5LfVnh1jOfox_XV3eW37vb715vLL7ddEFS3TiWRIFiqreIyUkk5MbSPgvFeek557BOzwlLLBJNSe6a40r0hGhgIFYGfo3eHvbsy_Z6hNjfkGmC79SNMc3Vaa2MUkf8FqVLGSLOC4gCugmqB5HYlD77sHSVu_YNbJbtVsrPC_f2Do8vYm-P-uR8gnoaO4pf-22Pf1-C3qfgx5HrCOGdcML1gnw8YLNLuMxRXQ4YxQMwFQnNxyv--4xF8o6Ve</recordid><startdate>19941205</startdate><enddate>19941205</enddate><creator>Ignatowski, Tracey A.</creator><creator>Spengler, Robert N.</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>7X8</scope></search><sort><creationdate>19941205</creationdate><title>Tumor necrosis factor-α: presynaptic sensitivity is modified after antidepressant drug administration</title><author>Ignatowski, Tracey A. ; Spengler, Robert N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-6f4fec9179635d1513081bd423b5a313dbf294919242557a26367b807e2e46de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Adrenergic</topic><topic>Animals</topic><topic>Antidepressant</topic><topic>Antidepressive Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Desipramine - pharmacology</topic><topic>Dioxanes - pharmacology</topic><topic>Drug Resistance</topic><topic>Electric Stimulation</topic><topic>Hippocampus</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - metabolism</topic><topic>Idazoxan</topic><topic>Locus coeruleus</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurons - metabolism</topic><topic>Neuropharmacology</topic><topic>Norepinephrine - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Presynaptic Terminals - drug effects</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, Sprague-Dawley</topic><topic>Sympathetic Nervous System - metabolism</topic><topic>Time Factors</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ignatowski, Tracey A.</creatorcontrib><creatorcontrib>Spengler, Robert N.</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>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ignatowski, Tracey A.</au><au>Spengler, Robert N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor necrosis factor-α: presynaptic sensitivity is modified after antidepressant drug administration</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1994-12-05</date><risdate>1994</risdate><volume>665</volume><issue>2</issue><spage>293</spage><epage>299</epage><pages>293-299</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Presynaptic adrenergic functioning was coupled to cytokine sensitivity in order to further establish the mechanism of action of a tricyclic antidepressant drug. Antidepressant administration of desipramine to rats twice-daily for 2 weeks increased hippocampal TNF levels and transformed the presynaptic TNF response. One day of desipramine administration resulted in increased locus coeruleus TNF mRNA accumulation and, simultaneously, hippocampal TNF levels escalated. The fractional release of [
3H]norepinephrine during field stimulation of control hippocampal slices was decreased by the addition of TNF in a concentration-dependent manner, an effect which was potentiated by the
α
2-adrenergic
antagonist idazoxan. While no change in sensitivity to TNF was observed in the hippocampus after one day of desipramine administration, TNF enhanced, rather than inhibited [
3H]norepinephrine release after 14 days. In addition, TNF potentiation of [
3H]norepinephrine release after chronic desipramine administration was reversed in the presence of idazoxan to a greater inhibition than in control slices exposed to idazoxan. Therefore, TNF-induced regulation of [
3H]norepinephrine releaase appears to be associated with an alteration of
α
2-adrenergic
receptor responsiveness. The reversal in presynaptic TNF responsiveness after 14 days of tricyclic antidepressant drug administration describes a mechanism of action for their delayed clinical effect.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>7895065</pmid><doi>10.1016/0006-8993(94)91350-1</doi><tpages>7</tpages></addata></record> |
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| subjects | Adrenergic Animals Antidepressant Antidepressive Agents - pharmacology Biological and medical sciences Brain Desipramine - pharmacology Dioxanes - pharmacology Drug Resistance Electric Stimulation Hippocampus Hippocampus - cytology Hippocampus - metabolism Idazoxan Locus coeruleus Male Medical sciences Neurons - metabolism Neuropharmacology Norepinephrine - metabolism Pharmacology. Drug treatments Presynaptic Terminals - drug effects Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopharmacology Rats Rats, Sprague-Dawley Sympathetic Nervous System - metabolism Time Factors Tumor necrosis factor Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - pharmacology |
| title | Tumor necrosis factor-α: presynaptic sensitivity is modified after antidepressant drug administration |
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