Psychosis pathways converge via D2High dopamine receptors
Identifieur interne : 002757 ( Istex/Curation ); précédent : 002756; suivant : 002758Psychosis pathways converge via D2High dopamine receptors
Auteurs : Philip Seeman [Canada] ; Johannes Schwarz [Allemagne] ; Jiang-Fan Chen [États-Unis] ; Henry Szechtman [Canada] ; Melissa Perreault [Canada] ; G. Stanley Mcknight [États-Unis] ; John C. Roder [Canada] ; Rémi Quirion [Canada] ; Patricia Boksa [Canada] ; Lalit K. Srivastava [Canada] ; Kazuhiko Yanai [Japon] ; David Weinshenker [États-Unis] ; Tomiki Sumiyoshi [Japon]Source :
- Synapse [ 0887-4476 ] ; 2006-09-15.
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Abstract
The objective of this review is to identify a target or biomarker of altered neurochemical sensitivity that is common to the many animal models of human psychoses associated with street drugs, brain injury, steroid use, birth injury, and gene alterations. Psychosis in humans can be caused by amphetamine, phencyclidine, steroids, ethanol, and brain lesions such as hippocampal, cortical, and entorhinal lesions. Strikingly, all of these drugs and lesions in rats lead to dopamine supersensitivity and increase the high‐affinity states of dopamine D2 receptors, or D2High, by 200–400% in striata. Similar supersensitivity and D2High elevations occur in rats born by Caesarian section and in rats treated with corticosterone or antipsychotics such as reserpine, risperidone, haloperidol, olanzapine, quetiapine, and clozapine, with the latter two inducing elevated D2High states less than that caused by haloperidol or olanzapine. Mice born with gene knockouts of some possible schizophrenia susceptibility genes are dopamine supersensitive, and their striata reveal markedly elevated D2High states; suchgenes include dopamine‐β‐hydroxylase, dopamine D4 receptors, G protein receptor kinase 6, tyrosine hydroxylase, catechol‐O‐methyltransferase, the trace amine‐1 receptor, regulator of G protein signaling RGS9, and the RIIβ form of cAMP‐dependent protein kinase (PKA). Striata from mice that are not dopamine supersensitive did not reveal elevated D2High states; these include mice with knockouts of adenosine A2A receptors, glycogen synthase kinase GSK3β, metabotropic glutamate receptor 5, dopamine D1 or D3 receptors, histamine H1, H2, or H3 receptors, and rats treated with ketanserin or aD1 antagonist. The evidence suggests that there are multiple pathways that convergetoelevate the D2High state in brain regions and that this elevation may elicit psychosis. This proposition is supported by the dopamine supersensitivity that is a common feature of schizophrenia and that also occurs in many types of genetically altered, drug‐altered, and lesion‐altered animals. Dopamine supersensitivity, in turn, correlates with D2High states. The finding that all antipsychotics, traditional and recent ones, act on D2High dopamine receptors further supports the proposition. Synapse 60: 319–346, 2006. © 2006 Wiley‐Liss, Inc.
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DOI: 10.1002/syn.20303
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Neurology, University of Leipzig, Leipzig 04103</wicri:regionArea></affiliation></author><author><name sortKey="Chen, Jiang An" sort="Chen, Jiang An" uniqKey="Chen J" first="Jiang-Fan" last="Chen">Jiang-Fan Chen</name><affiliation wicri:level="2"><mods:affiliation>Molecular Neuropharmacology Laboratory, Department of Neurology, Boston University School of Medicine, Boston, Massachusetts 02118</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Molecular Neuropharmacology Laboratory, Department of Neurology, Boston University School of Medicine, Boston</wicri:cityArea></affiliation></author><author><name sortKey="Szechtman, Henry" sort="Szechtman, Henry" uniqKey="Szechtman H" first="Henry" last="Szechtman">Henry Szechtman</name><affiliation wicri:level="1"><mods:affiliation>Department of Psychiatry and Behavioural Neuroscience, McMaster University, Hamilton, Ontario, Canada L8N 3Z5</mods:affiliation><country>Canada</country><wicri:regionArea>Department of Psychiatry and Behavioural Neuroscience, McMaster University, Hamilton, Ontario</wicri:regionArea></affiliation></author><author><name sortKey="Perreault, Melissa" sort="Perreault, Melissa" uniqKey="Perreault M" first="Melissa" last="Perreault">Melissa Perreault</name><affiliation wicri:level="1"><mods:affiliation>Department of Psychiatry and Behavioural Neuroscience, McMaster University, Hamilton, Ontario, Canada L8N 3Z5</mods:affiliation><country>Canada</country><wicri:regionArea>Department of Psychiatry and Behavioural Neuroscience, McMaster University, Hamilton, Ontario</wicri:regionArea></affiliation></author><author><name sortKey="Mcknight, G Stanley" sort="Mcknight, G Stanley" uniqKey="Mcknight G" first="G. Stanley" last="Mcknight">G. Stanley Mcknight</name><affiliation wicri:level="2"><mods:affiliation>Department of Pharmacology, University of Washington, Seattle, Washington 98195</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Pharmacology, University of Washington, Seattle</wicri:cityArea></affiliation></author><author><name sortKey="Roder, John C" sort="Roder, John C" uniqKey="Roder J" first="John C." last="Roder">John C. Roder</name><affiliation wicri:level="1"><mods:affiliation>Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada M5G 1X5</mods:affiliation><country>Canada</country><wicri:regionArea>Research Institute, Mount Sinai Hospital, Toronto, Ontario</wicri:regionArea></affiliation></author><author><name sortKey="Quirion, Remi" sort="Quirion, Remi" uniqKey="Quirion R" first="Rémi" last="Quirion">Rémi Quirion</name><affiliation wicri:level="1"><mods:affiliation>Douglas Hospital Research Center, Verdun, Quebec, Canada H4H 1R3</mods:affiliation><country>Canada</country><wicri:regionArea>Douglas Hospital Research Center, Verdun, Quebec</wicri:regionArea></affiliation></author><author><name sortKey="Boksa, Patricia" sort="Boksa, Patricia" uniqKey="Boksa P" first="Patricia" last="Boksa">Patricia Boksa</name><affiliation wicri:level="1"><mods:affiliation>Douglas Hospital Research Center, Verdun, Quebec, Canada H4H 1R3</mods:affiliation><country>Canada</country><wicri:regionArea>Douglas Hospital Research Center, Verdun, Quebec</wicri:regionArea></affiliation></author><author><name sortKey="Srivastava, Lalit K" sort="Srivastava, Lalit K" uniqKey="Srivastava L" first="Lalit K." last="Srivastava">Lalit K. Srivastava</name><affiliation wicri:level="1"><mods:affiliation>Douglas Hospital Research Center, Verdun, Quebec, Canada H4H 1R3</mods:affiliation><country>Canada</country><wicri:regionArea>Douglas Hospital Research Center, Verdun, Quebec</wicri:regionArea></affiliation></author><author><name sortKey="Yanai, Kazuhiko" sort="Yanai, Kazuhiko" uniqKey="Yanai K" first="Kazuhiko" last="Yanai">Kazuhiko Yanai</name><affiliation wicri:level="1"><mods:affiliation>Department of Pharmacology, Tohoku University School of Medicine, Sendai 980‐8575, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pharmacology, Tohoku University School of Medicine, Sendai 980‐8575</wicri:regionArea></affiliation></author><author><name sortKey="Weinshenker, David" sort="Weinshenker, David" uniqKey="Weinshenker D" first="David" last="Weinshenker">David Weinshenker</name><affiliation wicri:level="2"><mods:affiliation>Department of Human Genetics, Emory University School of Medicine, Atlanta, Georgia 30322</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Géorgie (États-Unis)</region></placeName><wicri:cityArea>Department of Human Genetics, Emory University School of Medicine, Atlanta</wicri:cityArea></affiliation></author><author><name sortKey="Sumiyoshi, Tomiki" sort="Sumiyoshi, Tomiki" uniqKey="Sumiyoshi T" first="Tomiki" last="Sumiyoshi">Tomiki Sumiyoshi</name><affiliation wicri:level="1"><mods:affiliation>Department of Neuropsychiatry, Toyama University School of Medicine, Toyama 930‐0194, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neuropsychiatry, Toyama University School of Medicine, Toyama 930‐0194</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="ISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-09-15">2006-09-15</date><biblScope unit="volume">60</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="319">319</biblScope><biblScope unit="page" to="346">346</biblScope></imprint><idno type="ISSN">0887-4476</idno></series><idno type="istex">BC1CE7E0E5869A56CF127423D4E692C06FF8169B</idno><idno type="DOI">10.1002/syn.20303</idno><idno type="ArticleID">SYN20303</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0887-4476</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>D2High receptors</term><term>amphetamine</term><term>degenerative brain</term><term>dopamine receptors</term><term>dopamine supersensitivity</term><term>gene knockouts</term><term>gene mutations</term><term>phencyclidine</term><term>psychosis</term><term>psychosis biomarker</term><term>schizophrenia</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The objective of this review is to identify a target or biomarker of altered neurochemical sensitivity that is common to the many animal models of human psychoses associated with street drugs, brain injury, steroid use, birth injury, and gene alterations. Psychosis in humans can be caused by amphetamine, phencyclidine, steroids, ethanol, and brain lesions such as hippocampal, cortical, and entorhinal lesions. Strikingly, all of these drugs and lesions in rats lead to dopamine supersensitivity and increase the high‐affinity states of dopamine D2 receptors, or D2High, by 200–400% in striata. Similar supersensitivity and D2High elevations occur in rats born by Caesarian section and in rats treated with corticosterone or antipsychotics such as reserpine, risperidone, haloperidol, olanzapine, quetiapine, and clozapine, with the latter two inducing elevated D2High states less than that caused by haloperidol or olanzapine. Mice born with gene knockouts of some possible schizophrenia susceptibility genes are dopamine supersensitive, and their striata reveal markedly elevated D2High states; suchgenes include dopamine‐β‐hydroxylase, dopamine D4 receptors, G protein receptor kinase 6, tyrosine hydroxylase, catechol‐O‐methyltransferase, the trace amine‐1 receptor, regulator of G protein signaling RGS9, and the RIIβ form of cAMP‐dependent protein kinase (PKA). Striata from mice that are not dopamine supersensitive did not reveal elevated D2High states; these include mice with knockouts of adenosine A2A receptors, glycogen synthase kinase GSK3β, metabotropic glutamate receptor 5, dopamine D1 or D3 receptors, histamine H1, H2, or H3 receptors, and rats treated with ketanserin or aD1 antagonist. The evidence suggests that there are multiple pathways that convergetoelevate the D2High state in brain regions and that this elevation may elicit psychosis. This proposition is supported by the dopamine supersensitivity that is a common feature of schizophrenia and that also occurs in many types of genetically altered, drug‐altered, and lesion‐altered animals. Dopamine supersensitivity, in turn, correlates with D2High states. The finding that all antipsychotics, traditional and recent ones, act on D2High dopamine receptors further supports the proposition. Synapse 60: 319–346, 2006. © 2006 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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