Antipsychotic drugs increase N‐acetylaspartate and N‐acetylaspartylglutamate in SH‐SY5Y human neuroblastoma cells
N‐Acetylaspartate (NAA) and N‐acetylaspartylglutamate (NAAG) are related neuronal metabolites associated with the diagnosis and treatment of schizophrenia. NAA is a valuable marker of neuronal viability in magnetic resonance spectroscopy, a technique which has consistently shown NAA levels to be mod...
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| Veröffentlicht in: | Journal of neurochemistry 2008-08, Vol.106 (4), p.1669-1680 |
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| creator | Arun, Peethambaran Madhavarao, Chikkathur N. Moffett, John R. Namboodiri, Aryan M. A. |
| description | N‐Acetylaspartate (NAA) and N‐acetylaspartylglutamate (NAAG) are related neuronal metabolites associated with the diagnosis and treatment of schizophrenia. NAA is a valuable marker of neuronal viability in magnetic resonance spectroscopy, a technique which has consistently shown NAA levels to be modestly decreased in the brains of schizophrenia patients. However, there are conflicting reports on the changes in brain NAA levels after treatment with antipsychotic drugs, which exert their therapeutic effects in part by blocking dopamine D2 receptors. NAAG is reported to be an agonist of the metabotropic glutamate 2/3 receptor, which is linked to neurotransmitter release modulation, including glutamate release. Alterations in NAAG metabolism have been implicated in the development of schizophrenia possibly via dysregulation of glutamate neurotransmission. In the present study we have used high performance liquid chromatography to determine the effects of the antipsychotic drugs haloperidol and clozapine on NAA and NAAG levels in SH‐SY5Y human neuroblastoma cells, a model system used to test the responses of dopaminergic neurons in vitro. The results indicate that the antipsychotic drugs haloperidol and clozapine increase both NAA and NAAG levels in SH‐SY5Y cells in a dose and time dependant manner, providing evidence that NAA and NAAG metabolism in neurons is responsive to antipsychotic drug treatment. |
| doi_str_mv | 10.1111/j.1471-4159.2008.05524.x |
| format | Article |
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A.</creator><creatorcontrib>Arun, Peethambaran ; Madhavarao, Chikkathur N. ; Moffett, John R. ; Namboodiri, Aryan M. A.</creatorcontrib><description>N‐Acetylaspartate (NAA) and N‐acetylaspartylglutamate (NAAG) are related neuronal metabolites associated with the diagnosis and treatment of schizophrenia. NAA is a valuable marker of neuronal viability in magnetic resonance spectroscopy, a technique which has consistently shown NAA levels to be modestly decreased in the brains of schizophrenia patients. However, there are conflicting reports on the changes in brain NAA levels after treatment with antipsychotic drugs, which exert their therapeutic effects in part by blocking dopamine D2 receptors. NAAG is reported to be an agonist of the metabotropic glutamate 2/3 receptor, which is linked to neurotransmitter release modulation, including glutamate release. Alterations in NAAG metabolism have been implicated in the development of schizophrenia possibly via dysregulation of glutamate neurotransmission. In the present study we have used high performance liquid chromatography to determine the effects of the antipsychotic drugs haloperidol and clozapine on NAA and NAAG levels in SH‐SY5Y human neuroblastoma cells, a model system used to test the responses of dopaminergic neurons in vitro. The results indicate that the antipsychotic drugs haloperidol and clozapine increase both NAA and NAAG levels in SH‐SY5Y cells in a dose and time dependant manner, providing evidence that NAA and NAAG metabolism in neurons is responsive to antipsychotic drug treatment.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2008.05524.x</identifier><identifier>PMID: 18631215</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult and adolescent clinical studies ; Antipsychotic Agents - pharmacology ; antipsychotics ; Aspartic Acid - analogs & derivatives ; Aspartic Acid - analysis ; Aspartic Acid - metabolism ; Biochemistry ; Biological and medical sciences ; Cell Line, Tumor ; clozapine ; Clozapine - pharmacology ; Dipeptides - analysis ; Dipeptides - metabolism ; Dose-Response Relationship, Drug ; haloperidol ; Haloperidol - pharmacology ; Humans ; Medical sciences ; Neuroblastoma - metabolism ; Neurology ; Neurons - drug effects ; Neurons - metabolism ; NMR ; Nuclear magnetic resonance ; N‐acetylaspartate ; N‐acetylaspartylglutamate ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychoses ; Psychotropic drugs ; Schizophrenia ; Spectrum analysis ; Tumors of the nervous system. Phacomatoses</subject><ispartof>Journal of neurochemistry, 2008-08, Vol.106 (4), p.1669-1680</ispartof><rights>2008 International Society for Neurochemistry. 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A.</creatorcontrib><title>Antipsychotic drugs increase N‐acetylaspartate and N‐acetylaspartylglutamate in SH‐SY5Y human neuroblastoma cells</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>N‐Acetylaspartate (NAA) and N‐acetylaspartylglutamate (NAAG) are related neuronal metabolites associated with the diagnosis and treatment of schizophrenia. NAA is a valuable marker of neuronal viability in magnetic resonance spectroscopy, a technique which has consistently shown NAA levels to be modestly decreased in the brains of schizophrenia patients. However, there are conflicting reports on the changes in brain NAA levels after treatment with antipsychotic drugs, which exert their therapeutic effects in part by blocking dopamine D2 receptors. NAAG is reported to be an agonist of the metabotropic glutamate 2/3 receptor, which is linked to neurotransmitter release modulation, including glutamate release. Alterations in NAAG metabolism have been implicated in the development of schizophrenia possibly via dysregulation of glutamate neurotransmission. In the present study we have used high performance liquid chromatography to determine the effects of the antipsychotic drugs haloperidol and clozapine on NAA and NAAG levels in SH‐SY5Y human neuroblastoma cells, a model system used to test the responses of dopaminergic neurons in vitro. The results indicate that the antipsychotic drugs haloperidol and clozapine increase both NAA and NAAG levels in SH‐SY5Y cells in a dose and time dependant manner, providing evidence that NAA and NAAG metabolism in neurons is responsive to antipsychotic drug treatment.</description><subject>Adult and adolescent clinical studies</subject><subject>Antipsychotic Agents - pharmacology</subject><subject>antipsychotics</subject><subject>Aspartic Acid - analogs & derivatives</subject><subject>Aspartic Acid - analysis</subject><subject>Aspartic Acid - metabolism</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Tumor</subject><subject>clozapine</subject><subject>Clozapine - pharmacology</subject><subject>Dipeptides - analysis</subject><subject>Dipeptides - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>haloperidol</subject><subject>Haloperidol - pharmacology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Neuroblastoma - metabolism</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>N‐acetylaspartate</subject><subject>N‐acetylaspartylglutamate</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychoses</subject><subject>Psychotropic drugs</subject><subject>Schizophrenia</subject><subject>Spectrum analysis</subject><subject>Tumors of the nervous system. Phacomatoses</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcFO3DAURa0KVAbaX6isSnSX1HbsTLzoAo0oUCG6oF2wst54niGjxJnaiSC7fkK_kS8hZkZUopt6Yz_f866udAmhnOV8Op_XOZdznkmudC4Yq3KmlJD5wxsyexH2yIwxIbKCSXFADmNcM8ZLWfK35IBXZcEFVzNyf-L7ehNHe9f1taWrMNxGWnsbECLSq8fff8BiPzYQNxB66JGCX_3zPza3zdBDm_Ta0-vzSb--UTf0bmjBU49D6JYT23ctUItNE9-RfQdNxPe7-4j8_Hr6Y3GeXX4_u1icXGZWCS4zJXFpXWEtF7qyFSCoabZMO8kqVjmJhdICuVRcC6aVU85pp0AUiDh3ojgin7a-m9D9GjD2pq1jSgAeuyEawZmYV7ycwI-vwHU3BD9lM4KVSupCJ7dqC9nQxRjQmU2oWwij4cykZszapAJMKsCkZsxzM-ZhWv2w8x-WLa7-Lu6qmIDjHQDRQuMCeFvHF04wNS9LkTJ82XL3dYPjfwcw364W6VU8Ac89rhM</recordid><startdate>200808</startdate><enddate>200808</enddate><creator>Arun, Peethambaran</creator><creator>Madhavarao, Chikkathur N.</creator><creator>Moffett, John R.</creator><creator>Namboodiri, Aryan M. A.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>200808</creationdate><title>Antipsychotic drugs increase N‐acetylaspartate and N‐acetylaspartylglutamate in SH‐SY5Y human neuroblastoma cells</title><author>Arun, Peethambaran ; Madhavarao, Chikkathur N. ; Moffett, John R. ; Namboodiri, Aryan M. A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5214-54ebcf3cc1298c8aea5bcfc09f40808f4e3592e145192095f5ff9f5a23eee7f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult and adolescent clinical studies</topic><topic>Antipsychotic Agents - pharmacology</topic><topic>antipsychotics</topic><topic>Aspartic Acid - analogs & derivatives</topic><topic>Aspartic Acid - analysis</topic><topic>Aspartic Acid - metabolism</topic><topic>Biochemistry</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Tumor</topic><topic>clozapine</topic><topic>Clozapine - pharmacology</topic><topic>Dipeptides - analysis</topic><topic>Dipeptides - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>haloperidol</topic><topic>Haloperidol - pharmacology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Neuroblastoma - metabolism</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>NMR</topic><topic>Nuclear magnetic resonance</topic><topic>N‐acetylaspartate</topic><topic>N‐acetylaspartylglutamate</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychoses</topic><topic>Psychotropic drugs</topic><topic>Schizophrenia</topic><topic>Spectrum analysis</topic><topic>Tumors of the nervous system. Phacomatoses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arun, Peethambaran</creatorcontrib><creatorcontrib>Madhavarao, Chikkathur N.</creatorcontrib><creatorcontrib>Moffett, John R.</creatorcontrib><creatorcontrib>Namboodiri, Aryan M. A.</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arun, Peethambaran</au><au>Madhavarao, Chikkathur N.</au><au>Moffett, John R.</au><au>Namboodiri, Aryan M. A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antipsychotic drugs increase N‐acetylaspartate and N‐acetylaspartylglutamate in SH‐SY5Y human neuroblastoma cells</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2008-08</date><risdate>2008</risdate><volume>106</volume><issue>4</issue><spage>1669</spage><epage>1680</epage><pages>1669-1680</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>N‐Acetylaspartate (NAA) and N‐acetylaspartylglutamate (NAAG) are related neuronal metabolites associated with the diagnosis and treatment of schizophrenia. NAA is a valuable marker of neuronal viability in magnetic resonance spectroscopy, a technique which has consistently shown NAA levels to be modestly decreased in the brains of schizophrenia patients. However, there are conflicting reports on the changes in brain NAA levels after treatment with antipsychotic drugs, which exert their therapeutic effects in part by blocking dopamine D2 receptors. NAAG is reported to be an agonist of the metabotropic glutamate 2/3 receptor, which is linked to neurotransmitter release modulation, including glutamate release. Alterations in NAAG metabolism have been implicated in the development of schizophrenia possibly via dysregulation of glutamate neurotransmission. In the present study we have used high performance liquid chromatography to determine the effects of the antipsychotic drugs haloperidol and clozapine on NAA and NAAG levels in SH‐SY5Y human neuroblastoma cells, a model system used to test the responses of dopaminergic neurons in vitro. The results indicate that the antipsychotic drugs haloperidol and clozapine increase both NAA and NAAG levels in SH‐SY5Y cells in a dose and time dependant manner, providing evidence that NAA and NAAG metabolism in neurons is responsive to antipsychotic drug treatment.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>18631215</pmid><doi>10.1111/j.1471-4159.2008.05524.x</doi><tpages>12</tpages></addata></record> |
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| subjects | Adult and adolescent clinical studies Antipsychotic Agents - pharmacology antipsychotics Aspartic Acid - analogs & derivatives Aspartic Acid - analysis Aspartic Acid - metabolism Biochemistry Biological and medical sciences Cell Line, Tumor clozapine Clozapine - pharmacology Dipeptides - analysis Dipeptides - metabolism Dose-Response Relationship, Drug haloperidol Haloperidol - pharmacology Humans Medical sciences Neuroblastoma - metabolism Neurology Neurons - drug effects Neurons - metabolism NMR Nuclear magnetic resonance N‐acetylaspartate N‐acetylaspartylglutamate Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Psychotropic drugs Schizophrenia Spectrum analysis Tumors of the nervous system. Phacomatoses |
| title | Antipsychotic drugs increase N‐acetylaspartate and N‐acetylaspartylglutamate in SH‐SY5Y human neuroblastoma cells |
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