Programming of brainstem serotonin transporter development by prenatal glucocorticoids
Prenatal stress or exposure to excess glucocorticoids are known to alter central nervous system function and to result in lasting changes in reactions to stress. The potential involvement of specific elements of brainstem serotonergic neurons was examined in the current study. Pregnant rats were giv...
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Veröffentlicht in: | Brain research. Developmental brain research 1996-05, Vol.93 (1), p.155-161 |
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description | Prenatal stress or exposure to excess glucocorticoids are known to alter central nervous system function and to result in lasting changes in reactions to stress. The potential involvement of specific elements of brainstem serotonergic neurons was examined in the current study. Pregnant rats were given 0.05, 0.2 or 0.8 mg/kg of dexamethasone on gestational days 17, 18 and 19, and the effects on development of the serotonin presynaptic transporter were assessed from birth to young adulthood by measurement of [
3H]paroxetine binding to membrane preparations. Dexamethasone produced a dose-dependent retardation of body and brainstem growth but evoked a significant elevation of [
3H]paroxetine binding that persisted into adulthood. Effects on [
3H]paroxetine binding were robust even at the lowest dose, which did not suppress growth, indicating that the programming of this transporter is more sensitive to glucocorticoids than is general development. At the highest dose, promotional effects on serotonin transporter expression were offset by impaired growth, so that the peak effect was seen at the intermediate dose of dexamethasone. There were no comparable effects on serotonin transmitter levels, indicating selectivity toward promotion of transporter expression as distinct from simply increasing the number of serotonergic persistent than those on other monoamine transporters, and is not shared by postnatal treatment or by treatment in adulthood, it likely represents specific programming by glucocorticoids during the prenatal period. Aberrant serotonergic transporter expression may contribute to alterations of synaptic function that ultimately produce the physiological abnormalities seen after prenatal stress or glucocorticoid treatment. |
doi_str_mv | 10.1016/0165-3806(96)00027-2 |
format | Article |
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3H]paroxetine binding to membrane preparations. Dexamethasone produced a dose-dependent retardation of body and brainstem growth but evoked a significant elevation of [
3H]paroxetine binding that persisted into adulthood. Effects on [
3H]paroxetine binding were robust even at the lowest dose, which did not suppress growth, indicating that the programming of this transporter is more sensitive to glucocorticoids than is general development. At the highest dose, promotional effects on serotonin transporter expression were offset by impaired growth, so that the peak effect was seen at the intermediate dose of dexamethasone. There were no comparable effects on serotonin transmitter levels, indicating selectivity toward promotion of transporter expression as distinct from simply increasing the number of serotonergic persistent than those on other monoamine transporters, and is not shared by postnatal treatment or by treatment in adulthood, it likely represents specific programming by glucocorticoids during the prenatal period. Aberrant serotonergic transporter expression may contribute to alterations of synaptic function that ultimately produce the physiological abnormalities seen after prenatal stress or glucocorticoid treatment.</description><identifier>ISSN: 0165-3806</identifier><identifier>DOI: 10.1016/0165-3806(96)00027-2</identifier><identifier>PMID: 8804702</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Binding Sites - physiology ; Body Weight - drug effects ; Brain Stem - chemistry ; Brain Stem - cytology ; Brain Stem - embryology ; Carrier Proteins - drug effects ; Carrier Proteins - metabolism ; Cell Differentiation - drug effects ; Cell Division - drug effects ; Dexamethasone - pharmacology ; Dexamethasone, effects on serotonin transporter ; Female ; Glucocorticoids - pharmacology ; Glucocorticoids, effects on serotonin transporter ; Membrane Glycoproteins - drug effects ; Membrane Glycoproteins - metabolism ; Membrane Transport Proteins ; Nerve Tissue Proteins - drug effects ; Nerve Tissue Proteins - physiology ; Neurons - cytology ; Neurons - drug effects ; Paroxetine - metabolism ; Paroxetine - pharmacology ; Paroxetine, binding to serotonin transporter ; Pregnancy ; Prenatal Exposure Delayed Effects ; Rats ; Rats, Sprague-Dawley ; Serotonin - analysis ; Serotonin Plasma Membrane Transport Proteins ; Serotonin transporter, development ; Serotonin Uptake Inhibitors - metabolism ; Serotonin Uptake Inhibitors - pharmacology ; Tritium</subject><ispartof>Brain research. Developmental brain research, 1996-05, Vol.93 (1), p.155-161</ispartof><rights>1996</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-c6736b4ecc95dd0795fe9c383aedc5a54f974c49f3b61e2744759210b53681be3</citedby><cites>FETCH-LOGICAL-c423t-c6736b4ecc95dd0795fe9c383aedc5a54f974c49f3b61e2744759210b53681be3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8804702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Slotkin, T.A.</creatorcontrib><creatorcontrib>Barnes, G.A.</creatorcontrib><creatorcontrib>McCook, E.C.</creatorcontrib><creatorcontrib>Seidler, F.J.</creatorcontrib><title>Programming of brainstem serotonin transporter development by prenatal glucocorticoids</title><title>Brain research. Developmental brain research</title><addtitle>Brain Res Dev Brain Res</addtitle><description>Prenatal stress or exposure to excess glucocorticoids are known to alter central nervous system function and to result in lasting changes in reactions to stress. The potential involvement of specific elements of brainstem serotonergic neurons was examined in the current study. Pregnant rats were given 0.05, 0.2 or 0.8 mg/kg of dexamethasone on gestational days 17, 18 and 19, and the effects on development of the serotonin presynaptic transporter were assessed from birth to young adulthood by measurement of [
3H]paroxetine binding to membrane preparations. Dexamethasone produced a dose-dependent retardation of body and brainstem growth but evoked a significant elevation of [
3H]paroxetine binding that persisted into adulthood. Effects on [
3H]paroxetine binding were robust even at the lowest dose, which did not suppress growth, indicating that the programming of this transporter is more sensitive to glucocorticoids than is general development. At the highest dose, promotional effects on serotonin transporter expression were offset by impaired growth, so that the peak effect was seen at the intermediate dose of dexamethasone. There were no comparable effects on serotonin transmitter levels, indicating selectivity toward promotion of transporter expression as distinct from simply increasing the number of serotonergic persistent than those on other monoamine transporters, and is not shared by postnatal treatment or by treatment in adulthood, it likely represents specific programming by glucocorticoids during the prenatal period. Aberrant serotonergic transporter expression may contribute to alterations of synaptic function that ultimately produce the physiological abnormalities seen after prenatal stress or glucocorticoid treatment.</description><subject>Animals</subject><subject>Binding Sites - physiology</subject><subject>Body Weight - drug effects</subject><subject>Brain Stem - chemistry</subject><subject>Brain Stem - cytology</subject><subject>Brain Stem - embryology</subject><subject>Carrier Proteins - drug effects</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Division - drug effects</subject><subject>Dexamethasone - pharmacology</subject><subject>Dexamethasone, effects on serotonin transporter</subject><subject>Female</subject><subject>Glucocorticoids - pharmacology</subject><subject>Glucocorticoids, effects on serotonin transporter</subject><subject>Membrane Glycoproteins - drug effects</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Membrane Transport Proteins</subject><subject>Nerve Tissue Proteins - drug effects</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>Neurons - cytology</subject><subject>Neurons - drug effects</subject><subject>Paroxetine - metabolism</subject><subject>Paroxetine - pharmacology</subject><subject>Paroxetine, binding to serotonin transporter</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Serotonin - analysis</subject><subject>Serotonin Plasma Membrane Transport Proteins</subject><subject>Serotonin transporter, development</subject><subject>Serotonin Uptake Inhibitors - metabolism</subject><subject>Serotonin Uptake Inhibitors - pharmacology</subject><subject>Tritium</subject><issn>0165-3806</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LAzEQhnNQqlb_gUJOoofVfO1HLoIUv6CgB_UastnZEtlN1iQt9N-7S0uPHoZh5n1nhnkQuqTkjhJa3I-RZ7wixY0sbgkhrMzYETo9tE_QWYw_o0B5RWdoVlVElISdou-P4FdB9711K-xbXAdtXUzQ4wjBJ--swyloFwcfEgTcwAY6P_TgEq63eAjgdNIdXnVr483oscbbJp6j41Z3ES72eY6-np8-F6_Z8v3lbfG4zIxgPGWmKHlRCzBG5k1DSpm3IA2vuIbG5DoXrSyFEbLldUGBlUKUuWSU1DkvKloDn6Pr3d4h-N81xKR6Gw10nXbg11GVFaeUCToaxc5ogo8xQKuGYHsdtooSNSFUEys1sVJyLCaEio1jV_v967qH5jC05zfqDzsdxic3FoKKxoIz0NgAJqnG2_8P_AGKSoPg</recordid><startdate>19960531</startdate><enddate>19960531</enddate><creator>Slotkin, T.A.</creator><creator>Barnes, G.A.</creator><creator>McCook, E.C.</creator><creator>Seidler, F.J.</creator><general>Elsevier B.V</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>7X8</scope></search><sort><creationdate>19960531</creationdate><title>Programming of brainstem serotonin transporter development by prenatal glucocorticoids</title><author>Slotkin, T.A. ; Barnes, G.A. ; McCook, E.C. ; Seidler, F.J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-c6736b4ecc95dd0795fe9c383aedc5a54f974c49f3b61e2744759210b53681be3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Binding Sites - physiology</topic><topic>Body Weight - drug effects</topic><topic>Brain Stem - chemistry</topic><topic>Brain Stem - cytology</topic><topic>Brain Stem - embryology</topic><topic>Carrier Proteins - drug effects</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Division - drug effects</topic><topic>Dexamethasone - pharmacology</topic><topic>Dexamethasone, effects on serotonin transporter</topic><topic>Female</topic><topic>Glucocorticoids - pharmacology</topic><topic>Glucocorticoids, effects on serotonin transporter</topic><topic>Membrane Glycoproteins - drug effects</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Membrane Transport Proteins</topic><topic>Nerve Tissue Proteins - drug effects</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Neurons - cytology</topic><topic>Neurons - drug effects</topic><topic>Paroxetine - metabolism</topic><topic>Paroxetine - pharmacology</topic><topic>Paroxetine, binding to serotonin transporter</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Serotonin - analysis</topic><topic>Serotonin Plasma Membrane Transport Proteins</topic><topic>Serotonin transporter, development</topic><topic>Serotonin Uptake Inhibitors - metabolism</topic><topic>Serotonin Uptake Inhibitors - pharmacology</topic><topic>Tritium</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Slotkin, T.A.</creatorcontrib><creatorcontrib>Barnes, G.A.</creatorcontrib><creatorcontrib>McCook, E.C.</creatorcontrib><creatorcontrib>Seidler, F.J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research. Developmental brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Slotkin, T.A.</au><au>Barnes, G.A.</au><au>McCook, E.C.</au><au>Seidler, F.J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Programming of brainstem serotonin transporter development by prenatal glucocorticoids</atitle><jtitle>Brain research. Developmental brain research</jtitle><addtitle>Brain Res Dev Brain Res</addtitle><date>1996-05-31</date><risdate>1996</risdate><volume>93</volume><issue>1</issue><spage>155</spage><epage>161</epage><pages>155-161</pages><issn>0165-3806</issn><abstract>Prenatal stress or exposure to excess glucocorticoids are known to alter central nervous system function and to result in lasting changes in reactions to stress. The potential involvement of specific elements of brainstem serotonergic neurons was examined in the current study. Pregnant rats were given 0.05, 0.2 or 0.8 mg/kg of dexamethasone on gestational days 17, 18 and 19, and the effects on development of the serotonin presynaptic transporter were assessed from birth to young adulthood by measurement of [
3H]paroxetine binding to membrane preparations. Dexamethasone produced a dose-dependent retardation of body and brainstem growth but evoked a significant elevation of [
3H]paroxetine binding that persisted into adulthood. Effects on [
3H]paroxetine binding were robust even at the lowest dose, which did not suppress growth, indicating that the programming of this transporter is more sensitive to glucocorticoids than is general development. At the highest dose, promotional effects on serotonin transporter expression were offset by impaired growth, so that the peak effect was seen at the intermediate dose of dexamethasone. There were no comparable effects on serotonin transmitter levels, indicating selectivity toward promotion of transporter expression as distinct from simply increasing the number of serotonergic persistent than those on other monoamine transporters, and is not shared by postnatal treatment or by treatment in adulthood, it likely represents specific programming by glucocorticoids during the prenatal period. Aberrant serotonergic transporter expression may contribute to alterations of synaptic function that ultimately produce the physiological abnormalities seen after prenatal stress or glucocorticoid treatment.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>8804702</pmid><doi>10.1016/0165-3806(96)00027-2</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Binding Sites - physiology Body Weight - drug effects Brain Stem - chemistry Brain Stem - cytology Brain Stem - embryology Carrier Proteins - drug effects Carrier Proteins - metabolism Cell Differentiation - drug effects Cell Division - drug effects Dexamethasone - pharmacology Dexamethasone, effects on serotonin transporter Female Glucocorticoids - pharmacology Glucocorticoids, effects on serotonin transporter Membrane Glycoproteins - drug effects Membrane Glycoproteins - metabolism Membrane Transport Proteins Nerve Tissue Proteins - drug effects Nerve Tissue Proteins - physiology Neurons - cytology Neurons - drug effects Paroxetine - metabolism Paroxetine - pharmacology Paroxetine, binding to serotonin transporter Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Sprague-Dawley Serotonin - analysis Serotonin Plasma Membrane Transport Proteins Serotonin transporter, development Serotonin Uptake Inhibitors - metabolism Serotonin Uptake Inhibitors - pharmacology Tritium |
title | Programming of brainstem serotonin transporter development by prenatal glucocorticoids |
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