Increased stress response and β-phenylethylamine in MAOB -deficient mice
MAOA and MAOB are key iso-enzymes that degrade biogenic and dietary amines 1–5 . MAOA preferentially oxidizes serotonin (5-hydroxytryptamine, or 5-HT) and nore-pinephrine (NE), whereas MAOB preferentially oxidizes β-phenylethylamine (PEA). Both forms can oxidize dopamine (DA). A mutation in MAOA res...
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| Veröffentlicht in: | Nature genetics 1997-10, Vol.17 (2), p.206-210 |
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| creator | Grimsby, Joseph Toth, Miklos Chen, Kevin Kumazawa, Takeshi Klaidman, Lori Adams, James D Karoum, Farouk Gal, Judit Shih, Jean C |
| description | MAOA and MAOB are key iso-enzymes that degrade biogenic and dietary amines
1–5
. MAOA preferentially oxidizes serotonin (5-hydroxytryptamine, or 5-HT) and nore-pinephrine (NE), whereas MAOB preferentially oxidizes β-phenylethylamine (PEA). Both forms can oxidize dopamine (DA). A mutation in
MAOA
results in a clinical phenotype characterized by borderline mental retardation and impaired impulse control
6,7
. X-chromosomal deletions which include
MAOB
were found in patients suffering from atypical Norrie's disease
8,9
, which is characterized by blindness and impaired hearing. Reduced MAOB activity has been found in type-ll alcoholism and in cigarette smokers
10,11
. Because most alcoholics smoke, the effects of alcohol on MAOB activity remain to be determined. Here we show that targetted inactivation of
MAOB
in mice increases levels of PEA but not those of 5-HT, NE and DA, demonstrating a primary role for
MAOB
in the metabolism of PEA. PEA has been implicated in modulating mood and affect
12,13
. Indeed,
MAOB
-deficient mice showed an increased reactivity to stress. In addition, mutant mice were resistant to the neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease. |
| doi_str_mv | 10.1038/ng1097-206 |
| format | Article |
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1–5
. MAOA preferentially oxidizes serotonin (5-hydroxytryptamine, or 5-HT) and nore-pinephrine (NE), whereas MAOB preferentially oxidizes β-phenylethylamine (PEA). Both forms can oxidize dopamine (DA). A mutation in
MAOA
results in a clinical phenotype characterized by borderline mental retardation and impaired impulse control
6,7
. X-chromosomal deletions which include
MAOB
were found in patients suffering from atypical Norrie's disease
8,9
, which is characterized by blindness and impaired hearing. Reduced MAOB activity has been found in type-ll alcoholism and in cigarette smokers
10,11
. Because most alcoholics smoke, the effects of alcohol on MAOB activity remain to be determined. Here we show that targetted inactivation of
MAOB
in mice increases levels of PEA but not those of 5-HT, NE and DA, demonstrating a primary role for
MAOB
in the metabolism of PEA. PEA has been implicated in modulating mood and affect
12,13
. Indeed,
MAOB
-deficient mice showed an increased reactivity to stress. In addition, mutant mice were resistant to the neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease.</description><identifier>ISSN: 1061-4036</identifier><identifier>EISSN: 1546-1718</identifier><identifier>DOI: 10.1038/ng1097-206</identifier><identifier>PMID: 9326944</identifier><identifier>CODEN: NGENEC</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Agriculture ; Animal Genetics and Genomics ; Animals ; Base Sequence ; Biogenic Monoamines - metabolism ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Brain - drug effects ; Brain - metabolism ; Cancer Research ; DNA Primers - genetics ; Female ; Gene Function ; Human Genetics ; Humans ; letter ; Male ; Malformations of the eye ; Medical sciences ; Mice ; Mice, Knockout ; Monoamine Oxidase - deficiency ; Monoamine Oxidase - genetics ; Motor Activity - genetics ; Motor Activity - physiology ; MPTP Poisoning ; Ophthalmology ; Oxidation-Reduction ; Phenethylamines - metabolism ; Polymerase Chain Reaction ; Restriction Mapping ; Stress, Physiological - enzymology ; Stress, Physiological - genetics ; Stress, Physiological - physiopathology ; X Chromosome - genetics</subject><ispartof>Nature genetics, 1997-10, Vol.17 (2), p.206-210</ispartof><rights>Springer Nature America, Inc. 1997</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3186-13777b2b4fd50f1920c061b206eadc53b85ac4ff521a46d729631853345407773</citedby><cites>FETCH-LOGICAL-c3186-13777b2b4fd50f1920c061b206eadc53b85ac4ff521a46d729631853345407773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ng1097-206$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ng1097-206$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,2725,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2847197$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9326944$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Grimsby, Joseph</creatorcontrib><creatorcontrib>Toth, Miklos</creatorcontrib><creatorcontrib>Chen, Kevin</creatorcontrib><creatorcontrib>Kumazawa, Takeshi</creatorcontrib><creatorcontrib>Klaidman, Lori</creatorcontrib><creatorcontrib>Adams, James D</creatorcontrib><creatorcontrib>Karoum, Farouk</creatorcontrib><creatorcontrib>Gal, Judit</creatorcontrib><creatorcontrib>Shih, Jean C</creatorcontrib><title>Increased stress response and β-phenylethylamine in MAOB -deficient mice</title><title>Nature genetics</title><addtitle>Nat Genet</addtitle><addtitle>Nat Genet</addtitle><description>MAOA and MAOB are key iso-enzymes that degrade biogenic and dietary amines
1–5
. MAOA preferentially oxidizes serotonin (5-hydroxytryptamine, or 5-HT) and nore-pinephrine (NE), whereas MAOB preferentially oxidizes β-phenylethylamine (PEA). Both forms can oxidize dopamine (DA). A mutation in
MAOA
results in a clinical phenotype characterized by borderline mental retardation and impaired impulse control
6,7
. X-chromosomal deletions which include
MAOB
were found in patients suffering from atypical Norrie's disease
8,9
, which is characterized by blindness and impaired hearing. Reduced MAOB activity has been found in type-ll alcoholism and in cigarette smokers
10,11
. Because most alcoholics smoke, the effects of alcohol on MAOB activity remain to be determined. Here we show that targetted inactivation of
MAOB
in mice increases levels of PEA but not those of 5-HT, NE and DA, demonstrating a primary role for
MAOB
in the metabolism of PEA. PEA has been implicated in modulating mood and affect
12,13
. Indeed,
MAOB
-deficient mice showed an increased reactivity to stress. In addition, mutant mice were resistant to the neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease.</description><subject>Agriculture</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Biogenic Monoamines - metabolism</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Cancer Research</subject><subject>DNA Primers - genetics</subject><subject>Female</subject><subject>Gene Function</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>letter</subject><subject>Male</subject><subject>Malformations of the eye</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Monoamine Oxidase - deficiency</subject><subject>Monoamine Oxidase - genetics</subject><subject>Motor Activity - genetics</subject><subject>Motor Activity - physiology</subject><subject>MPTP Poisoning</subject><subject>Ophthalmology</subject><subject>Oxidation-Reduction</subject><subject>Phenethylamines - metabolism</subject><subject>Polymerase Chain Reaction</subject><subject>Restriction Mapping</subject><subject>Stress, Physiological - enzymology</subject><subject>Stress, Physiological - genetics</subject><subject>Stress, Physiological - physiopathology</subject><subject>X Chromosome - genetics</subject><issn>1061-4036</issn><issn>1546-1718</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkTtPwzAUhS0EKlBY2JE8IAZQwK-8xlLxqFTUBWbLcW7aVIkT7GTo3-KH8JtwlagsLLal891zj44RuqLkgRKePJo1JWkcMBIdoTMaiiigMU2O_ZtENBCER6fo3LktIVQIkkzQJOUsSoU4Q4uF0RaUgxy7zoJz2B9tYxxgZXL88x20GzC7CrrNrlJ1aQCXBr_PVk84yKEodQmmw3Wp4QKdFKpycDneU_T58vwxfwuWq9fFfLYMNKeJT8bjOM5YJoo8JAVNGdE-ZOazg8p1yLMkVFoURcioElEeszTycyHnIhTEj_Ipuh18W9t89eA6WZdOQ1UpA03vJI0ZiyhnHrwbQG0b5ywUsrVlrexOUiL3vcmhN-l3e_h6dO2zGvIDOhbl9ZtRV06rqrDK6NIdMJaImKb7cPcD5rxi1mDltumt8X38vxQPtFFdb-Hg9vef_BdRW4wy</recordid><startdate>19971001</startdate><enddate>19971001</enddate><creator>Grimsby, Joseph</creator><creator>Toth, Miklos</creator><creator>Chen, Kevin</creator><creator>Kumazawa, Takeshi</creator><creator>Klaidman, Lori</creator><creator>Adams, James D</creator><creator>Karoum, Farouk</creator><creator>Gal, Judit</creator><creator>Shih, Jean C</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>19971001</creationdate><title>Increased stress response and β-phenylethylamine in MAOB -deficient mice</title><author>Grimsby, Joseph ; Toth, Miklos ; Chen, Kevin ; Kumazawa, Takeshi ; Klaidman, Lori ; Adams, James D ; Karoum, Farouk ; Gal, Judit ; Shih, Jean C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3186-13777b2b4fd50f1920c061b206eadc53b85ac4ff521a46d729631853345407773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Agriculture</topic><topic>Animal Genetics and Genomics</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Biogenic Monoamines - metabolism</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Cancer Research</topic><topic>DNA Primers - genetics</topic><topic>Female</topic><topic>Gene Function</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>letter</topic><topic>Male</topic><topic>Malformations of the eye</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Monoamine Oxidase - deficiency</topic><topic>Monoamine Oxidase - genetics</topic><topic>Motor Activity - genetics</topic><topic>Motor Activity - physiology</topic><topic>MPTP Poisoning</topic><topic>Ophthalmology</topic><topic>Oxidation-Reduction</topic><topic>Phenethylamines - metabolism</topic><topic>Polymerase Chain Reaction</topic><topic>Restriction Mapping</topic><topic>Stress, Physiological - enzymology</topic><topic>Stress, Physiological - genetics</topic><topic>Stress, Physiological - physiopathology</topic><topic>X Chromosome - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Grimsby, Joseph</creatorcontrib><creatorcontrib>Toth, Miklos</creatorcontrib><creatorcontrib>Chen, Kevin</creatorcontrib><creatorcontrib>Kumazawa, Takeshi</creatorcontrib><creatorcontrib>Klaidman, Lori</creatorcontrib><creatorcontrib>Adams, James D</creatorcontrib><creatorcontrib>Karoum, Farouk</creatorcontrib><creatorcontrib>Gal, Judit</creatorcontrib><creatorcontrib>Shih, Jean C</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Nature genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Grimsby, Joseph</au><au>Toth, Miklos</au><au>Chen, Kevin</au><au>Kumazawa, Takeshi</au><au>Klaidman, Lori</au><au>Adams, James D</au><au>Karoum, Farouk</au><au>Gal, Judit</au><au>Shih, Jean C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased stress response and β-phenylethylamine in MAOB -deficient mice</atitle><jtitle>Nature genetics</jtitle><stitle>Nat Genet</stitle><addtitle>Nat Genet</addtitle><date>1997-10-01</date><risdate>1997</risdate><volume>17</volume><issue>2</issue><spage>206</spage><epage>210</epage><pages>206-210</pages><issn>1061-4036</issn><eissn>1546-1718</eissn><coden>NGENEC</coden><abstract>MAOA and MAOB are key iso-enzymes that degrade biogenic and dietary amines
1–5
. MAOA preferentially oxidizes serotonin (5-hydroxytryptamine, or 5-HT) and nore-pinephrine (NE), whereas MAOB preferentially oxidizes β-phenylethylamine (PEA). Both forms can oxidize dopamine (DA). A mutation in
MAOA
results in a clinical phenotype characterized by borderline mental retardation and impaired impulse control
6,7
. X-chromosomal deletions which include
MAOB
were found in patients suffering from atypical Norrie's disease
8,9
, which is characterized by blindness and impaired hearing. Reduced MAOB activity has been found in type-ll alcoholism and in cigarette smokers
10,11
. Because most alcoholics smoke, the effects of alcohol on MAOB activity remain to be determined. Here we show that targetted inactivation of
MAOB
in mice increases levels of PEA but not those of 5-HT, NE and DA, demonstrating a primary role for
MAOB
in the metabolism of PEA. PEA has been implicated in modulating mood and affect
12,13
. Indeed,
MAOB
-deficient mice showed an increased reactivity to stress. In addition, mutant mice were resistant to the neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>9326944</pmid><doi>10.1038/ng1097-206</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1061-4036 |
| ispartof | Nature genetics, 1997-10, Vol.17 (2), p.206-210 |
| issn | 1061-4036 1546-1718 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_17226132 |
| source | MEDLINE; Nature; SpringerLink Journals - AutoHoldings |
| subjects | Agriculture Animal Genetics and Genomics Animals Base Sequence Biogenic Monoamines - metabolism Biological and medical sciences Biomedical and Life Sciences Biomedicine Brain - drug effects Brain - metabolism Cancer Research DNA Primers - genetics Female Gene Function Human Genetics Humans letter Male Malformations of the eye Medical sciences Mice Mice, Knockout Monoamine Oxidase - deficiency Monoamine Oxidase - genetics Motor Activity - genetics Motor Activity - physiology MPTP Poisoning Ophthalmology Oxidation-Reduction Phenethylamines - metabolism Polymerase Chain Reaction Restriction Mapping Stress, Physiological - enzymology Stress, Physiological - genetics Stress, Physiological - physiopathology X Chromosome - genetics |
| title | Increased stress response and β-phenylethylamine in MAOB -deficient mice |
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