Catecholamine/Serotonin Interactions: Systems Thinking for Brain Function and Disease
Identifieur interne : 000265 ( Pmc/Corpus ); précédent : 000264; suivant : 000266Catecholamine/Serotonin Interactions: Systems Thinking for Brain Function and Disease
Auteurs : Julie G. Hensler ; Francesc Artigas ; Analía Bortolozzi ; Lynette C. Daws ; Philippe De Deurwaerdère ; Léa Milan ; Sylvia Navailles ; Wouter KoekSource :
- Advances in pharmacology (San Diego, Calif.) [ 1054-3589 ] ; 2013.
Abstract
This chapter brings together the work of several leading laboratories, each an outstanding example of integrative approaches to complex diseases of the central nervous system. Cognitive dysfunction and negative symptoms associated with schizophrenia are believed to result from hypofunction of the mesocortical dopaminergic projections to prefrontal cortex (PFC). Noradrenergic targets for the augmentation of dopaminergic function in PFC show promise to improve cognitive deficits as well as negative symptoms. Serotonergic targets for the modulation of mesocortical dopaminergic neurotransmission include 5-HT2A and 5-HT1A receptors. The hallmark of Parkinson’s disease is the destruction of nigrostriatal dopaminergic neurons.
Url:
DOI: 10.1016/B978-0-12-411512-5.00009-9
PubMed: 24054145
PubMed Central: 3902978
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PMC:3902978Le document en format XML
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<affiliation><nlm:aff id="A1">Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA</nlm:aff>
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<affiliation><nlm:aff id="A7">Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA</nlm:aff>
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<affiliation><nlm:aff id="A1">Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA</nlm:aff>
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<author><name sortKey="Artigas, Francesc" sort="Artigas, Francesc" uniqKey="Artigas F" first="Francesc" last="Artigas">Francesc Artigas</name>
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<affiliation><nlm:aff id="A3">Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), ISCIII, Madrid, Spain</nlm:aff>
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<author><name sortKey="Bortolozzi, Analia" sort="Bortolozzi, Analia" uniqKey="Bortolozzi A" first="Analía" last="Bortolozzi">Analía Bortolozzi</name>
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<affiliation><nlm:aff id="A3">Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), ISCIII, Madrid, Spain</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="A4">Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain</nlm:aff>
</affiliation>
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<author><name sortKey="Daws, Lynette C" sort="Daws, Lynette C" uniqKey="Daws L" first="Lynette C." last="Daws">Lynette C. Daws</name>
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<affiliation><nlm:aff id="A5">Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA</nlm:aff>
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<author><name sortKey="Milan, Lea" sort="Milan, Lea" uniqKey="Milan L" first="Léa" last="Milan">Léa Milan</name>
<affiliation><nlm:aff id="A6">Institute of Neurodegenerative diseases, CNRS UMR 5293, University of Bordeaux, Bordeaux, France</nlm:aff>
</affiliation>
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<affiliation><nlm:aff id="A7">Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA</nlm:aff>
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<front><div type="abstract" xml:lang="en"><p id="P1">This chapter brings together the work of several leading laboratories, each an outstanding example of integrative approaches to complex diseases of the central nervous system. Cognitive dysfunction and negative symptoms associated with schizophrenia are believed to result from hypofunction of the mesocortical dopaminergic projections to prefrontal cortex (PFC). Noradrenergic targets for the augmentation of dopaminergic function in PFC show promise to improve cognitive deficits as well as negative symptoms. Serotonergic targets for the modulation of mesocortical dopaminergic neurotransmission include 5-HT<sub>2A</sub>
and 5-HT<sub>1A</sub>
receptors. The hallmark of Parkinson’s disease is the destruction of nigrostriatal dopaminergic neurons. <sc>L</sc>
-DOPA, a metabolic precursor of dopamine, is the standard of treatment. However, the ectopic release of dopamine (DA) from serotonin neurons and the clearance of extracellular DA by the norepinephrine transporter in areas enriched with noradrenergic terminals contribute to extracellular DA produced by <sc>L</sc>
-DOPA and offer opportunities to improve <sc>L</sc>
-DOPA therapy. The high-affinity transporters for monoamines are the primary targets for antidepressant drugs. However, many patients experience suboptimal therapeutic benefit or fail to respond to treatment. Organic cation transporters and plasma membrane monoamine transporter serve an important function in regulating monoamine neurotransmission and hold potential utility as targets for the development of therapeutic drugs. Improved therapeutic approaches will arise from not only understanding how monoamines influence one another within the central nervous system as an integrated whole but also addressing the pathophysiology of specific core symptoms or distinct syndromal dimensions (cognitive impairment, motor slowing, and negative affect) regardless of disease classification, for example, psychotic, affective, and neurodegenerative.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9015397</journal-id>
<journal-id journal-id-type="pubmed-jr-id">1826</journal-id>
<journal-id journal-id-type="nlm-ta">Adv Pharmacol</journal-id>
<journal-id journal-id-type="iso-abbrev">Adv. Pharmacol.</journal-id>
<journal-title-group><journal-title>Advances in pharmacology (San Diego, Calif.)</journal-title>
</journal-title-group>
<issn pub-type="ppub">1054-3589</issn>
<issn pub-type="epub">1557-8925</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">24054145</article-id>
<article-id pub-id-type="pmc">3902978</article-id>
<article-id pub-id-type="doi">10.1016/B978-0-12-411512-5.00009-9</article-id>
<article-id pub-id-type="manuscript">NIHMS537012</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Catecholamine/Serotonin Interactions: Systems Thinking for Brain Function and Disease</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Hensler</surname>
<given-names>Julie G.</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
<xref ref-type="corresp" rid="CR1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Artigas</surname>
<given-names>Francesc</given-names>
</name>
<xref ref-type="aff" rid="A2">†</xref>
<xref ref-type="aff" rid="A3">‡</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bortolozzi</surname>
<given-names>Analía</given-names>
</name>
<xref ref-type="aff" rid="A2">†</xref>
<xref ref-type="aff" rid="A3">‡</xref>
<xref ref-type="aff" rid="A4">§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Daws</surname>
<given-names>Lynette C.</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
<xref ref-type="aff" rid="A5">¶</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Deurwaerdère</surname>
<given-names>Philippe De</given-names>
</name>
<xref ref-type="aff" rid="A6">||</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Milan</surname>
<given-names>Léa</given-names>
</name>
<xref ref-type="aff" rid="A6">||</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Navailles</surname>
<given-names>Sylvia</given-names>
</name>
<xref ref-type="aff" rid="A6">||</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Koek</surname>
<given-names>Wouter</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
<xref ref-type="aff" rid="A7">#</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>*</label>
Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA</aff>
<aff id="A2"><label>†</label>
Department of Neurochemistry and Neuropharmacology, IIBB-CSIC-IDIBAPS, Barcelona, Spain</aff>
<aff id="A3"><label>‡</label>
Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), ISCIII, Madrid, Spain</aff>
<aff id="A4"><label>§</label>
Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain</aff>
<aff id="A5"><label>¶</label>
Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA</aff>
<aff id="A6"><label>||</label>
Institute of Neurodegenerative diseases, CNRS UMR 5293, University of Bordeaux, Bordeaux, France</aff>
<aff id="A7"><label>#</label>
Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA</aff>
<author-notes><corresp id="CR1"><sup>1</sup>
Corresponding author: <email>hensler@uthscsa.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>12</day>
<month>12</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub"><year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>27</day>
<month>1</month>
<year>2014</year>
</pub-date>
<volume>68</volume>
<fpage>167</fpage>
<lpage>197</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/B978-0-12-411512-5.00009-9</pmc-comment>
<permissions><copyright-statement>© 2013 Elsevier Inc.</copyright-statement>
<copyright-year>2013</copyright-year>
</permissions>
<abstract><p id="P1">This chapter brings together the work of several leading laboratories, each an outstanding example of integrative approaches to complex diseases of the central nervous system. Cognitive dysfunction and negative symptoms associated with schizophrenia are believed to result from hypofunction of the mesocortical dopaminergic projections to prefrontal cortex (PFC). Noradrenergic targets for the augmentation of dopaminergic function in PFC show promise to improve cognitive deficits as well as negative symptoms. Serotonergic targets for the modulation of mesocortical dopaminergic neurotransmission include 5-HT<sub>2A</sub>
and 5-HT<sub>1A</sub>
receptors. The hallmark of Parkinson’s disease is the destruction of nigrostriatal dopaminergic neurons. <sc>L</sc>
-DOPA, a metabolic precursor of dopamine, is the standard of treatment. However, the ectopic release of dopamine (DA) from serotonin neurons and the clearance of extracellular DA by the norepinephrine transporter in areas enriched with noradrenergic terminals contribute to extracellular DA produced by <sc>L</sc>
-DOPA and offer opportunities to improve <sc>L</sc>
-DOPA therapy. The high-affinity transporters for monoamines are the primary targets for antidepressant drugs. However, many patients experience suboptimal therapeutic benefit or fail to respond to treatment. Organic cation transporters and plasma membrane monoamine transporter serve an important function in regulating monoamine neurotransmission and hold potential utility as targets for the development of therapeutic drugs. Improved therapeutic approaches will arise from not only understanding how monoamines influence one another within the central nervous system as an integrated whole but also addressing the pathophysiology of specific core symptoms or distinct syndromal dimensions (cognitive impairment, motor slowing, and negative affect) regardless of disease classification, for example, psychotic, affective, and neurodegenerative.</p>
</abstract>
<funding-group><award-group><funding-source country="United States">National Institute of Mental Health : NIMH</funding-source>
<award-id>R01 MH093320 || MH</award-id>
</award-group>
<award-group><funding-source country="United States">National Institute of Mental Health : NIMH</funding-source>
<award-id>R01 MH064489 || MH</award-id>
</award-group>
</funding-group>
</article-meta>
</front>
</pmc>
</record>
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