Catecholaminergic neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia
The precise aetiology of schizophrenia remains unclear. The neurodevelopmental hypothesis of schizophrenia has been proposed based on the accumulation of genomic or neuroimaging studies. In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizo...
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| Veröffentlicht in: | Acta neuropsychiatrica 2016-04, Vol.28 (2), p.117-123 |
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| container_title | Acta neuropsychiatrica |
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| creator | Iritani, Shuji Sekiguchi, Hirotaka Habuchi, Chikako Torii, Youta Kuroda, Keisuke Kaibuchi, Kozo Ozaki, Norio |
| description | The precise aetiology of schizophrenia remains unclear. The neurodevelopmental hypothesis of schizophrenia has been proposed based on the accumulation of genomic or neuroimaging studies.
In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizophrenia 1 (DISC1) knockout (KO) mice, which are considered to be a useful model of schizophrenia.
Six DISC1 homozygous KO mice and six age-matched littermates were used. The animals' brains were cut into 20-μm-thick slices, which were then immunohistochemically stained using an anti-tyrosine hydroxylase (TH) monoclonal antibody.
The TH-immunopositive fibres detected in the orbitofrontal cortices of the DISC1 KO mice were significantly shorter than those seen in the wild-type mice.
These neuropathological findings indicate that the hypofrontal symptoms of schizophrenia are associated with higher mental function deficiencies or cognitive dysfunction such as a loss of working memory. |
| doi_str_mv | 10.1017/neu.2015.51 |
| format | Article |
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In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizophrenia 1 (DISC1) knockout (KO) mice, which are considered to be a useful model of schizophrenia.
Six DISC1 homozygous KO mice and six age-matched littermates were used. The animals' brains were cut into 20-μm-thick slices, which were then immunohistochemically stained using an anti-tyrosine hydroxylase (TH) monoclonal antibody.
The TH-immunopositive fibres detected in the orbitofrontal cortices of the DISC1 KO mice were significantly shorter than those seen in the wild-type mice.
These neuropathological findings indicate that the hypofrontal symptoms of schizophrenia are associated with higher mental function deficiencies or cognitive dysfunction such as a loss of working memory.</description><identifier>ISSN: 0924-2708</identifier><identifier>EISSN: 1601-5215</identifier><identifier>DOI: 10.1017/neu.2015.51</identifier><identifier>PMID: 26333915</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>Animal cognition ; Animals ; Antibodies ; Brain ; Confounding (Statistics) ; Digital cameras ; Digital maps ; Disease Models, Animal ; Female ; Gender ; Genes ; Investigations ; Kinases ; Laboratories ; Male ; Mice ; Mice, Knockout ; Nerve Tissue Proteins - genetics ; Neuropathology ; Pathogenesis ; Pathophysiology ; Prefrontal Cortex - metabolism ; Prefrontal Cortex - pathology ; Prefrontal Cortex - physiopathology ; Schizophrenia ; Schizophrenia - genetics ; Schizophrenia - pathology ; Schizophrenia - physiopathology ; Short Communications ; Software packages ; Stem cells ; Tyrosine 3-Monooxygenase - metabolism</subject><ispartof>Acta neuropsychiatrica, 2016-04, Vol.28 (2), p.117-123</ispartof><rights>Scandinavian College of Neuropsychopharmacology 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-572c149dc45b913d251cf79d5858894473f32eeda46447bb8a435769da53f5143</citedby><cites>FETCH-LOGICAL-c454t-572c149dc45b913d251cf79d5858894473f32eeda46447bb8a435769da53f5143</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.cambridge.org/core/product/identifier/S0924270815000514/type/journal_article$$EHTML$$P50$$Gcambridge$$H</linktohtml><link.rule.ids>164,314,776,780,27901,27902,55603</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26333915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Iritani, Shuji</creatorcontrib><creatorcontrib>Sekiguchi, Hirotaka</creatorcontrib><creatorcontrib>Habuchi, Chikako</creatorcontrib><creatorcontrib>Torii, Youta</creatorcontrib><creatorcontrib>Kuroda, Keisuke</creatorcontrib><creatorcontrib>Kaibuchi, Kozo</creatorcontrib><creatorcontrib>Ozaki, Norio</creatorcontrib><title>Catecholaminergic neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia</title><title>Acta neuropsychiatrica</title><addtitle>Acta Neuropsychiatr</addtitle><description>The precise aetiology of schizophrenia remains unclear. The neurodevelopmental hypothesis of schizophrenia has been proposed based on the accumulation of genomic or neuroimaging studies.
In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizophrenia 1 (DISC1) knockout (KO) mice, which are considered to be a useful model of schizophrenia.
Six DISC1 homozygous KO mice and six age-matched littermates were used. The animals' brains were cut into 20-μm-thick slices, which were then immunohistochemically stained using an anti-tyrosine hydroxylase (TH) monoclonal antibody.
The TH-immunopositive fibres detected in the orbitofrontal cortices of the DISC1 KO mice were significantly shorter than those seen in the wild-type mice.
These neuropathological findings indicate that the hypofrontal symptoms of schizophrenia are associated with higher mental function deficiencies or cognitive dysfunction such as a loss of working memory.</description><subject>Animal cognition</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Brain</subject><subject>Confounding (Statistics)</subject><subject>Digital cameras</subject><subject>Digital maps</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Gender</subject><subject>Genes</subject><subject>Investigations</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Neuropathology</subject><subject>Pathogenesis</subject><subject>Pathophysiology</subject><subject>Prefrontal Cortex - metabolism</subject><subject>Prefrontal Cortex - pathology</subject><subject>Prefrontal Cortex - physiopathology</subject><subject>Schizophrenia</subject><subject>Schizophrenia - genetics</subject><subject>Schizophrenia - pathology</subject><subject>Schizophrenia - physiopathology</subject><subject>Short Communications</subject><subject>Software packages</subject><subject>Stem cells</subject><subject>Tyrosine 3-Monooxygenase - metabolism</subject><issn>0924-2708</issn><issn>1601-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkc2LFDEQxYMo7uzqybs0eBGWHlNJp9M5yuAXLHjRc0gn1TNZuztj0s2y_vXWsKOCCF4qKfLLq-I9xl4A3wIH_WbGdSs4qK2CR2wDLYdaCVCP2YYb0dRC8-6CXZZyy4k2XDxlF6KVUhpQGzbu3IL-kEY3xRnzPvqK9HKa3UiX5S7lb1W4L8M6-yWmuYpztRywGohYCBlTj1UaKlftkXD6PaW1INWA4-mh-EP8kY6HjHN0z9iTwY0Fn5_PK_b1_bsvu4_1zecPn3Zvb2rfqGaplRYeGhOo6w3IIBT4QZugOtV1pmm0HKRADK5pqen7zjVS6dYEp-SgoJFX7PWD7jGn7yuWxU6xeBxHNyOtZ6ED6EwL3Pwf1WSfpqoJffUXepvWTEYVK3RHu2kjBVHXD5TPqZSMgz3mOLl8b4HbU16W_LWnvKwCol-eNdd-wvCb_RUQAfVZzk19jmGPf6b-S_Any6ufIg</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Iritani, Shuji</creator><creator>Sekiguchi, Hirotaka</creator><creator>Habuchi, Chikako</creator><creator>Torii, Youta</creator><creator>Kuroda, Keisuke</creator><creator>Kaibuchi, Kozo</creator><creator>Ozaki, Norio</creator><general>Cambridge University Press</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20160401</creationdate><title>Catecholaminergic neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia</title><author>Iritani, Shuji ; Sekiguchi, Hirotaka ; Habuchi, Chikako ; Torii, Youta ; Kuroda, Keisuke ; Kaibuchi, Kozo ; Ozaki, Norio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-572c149dc45b913d251cf79d5858894473f32eeda46447bb8a435769da53f5143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animal cognition</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Brain</topic><topic>Confounding (Statistics)</topic><topic>Digital cameras</topic><topic>Digital maps</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Gender</topic><topic>Genes</topic><topic>Investigations</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Neuropathology</topic><topic>Pathogenesis</topic><topic>Pathophysiology</topic><topic>Prefrontal Cortex - metabolism</topic><topic>Prefrontal Cortex - pathology</topic><topic>Prefrontal Cortex - physiopathology</topic><topic>Schizophrenia</topic><topic>Schizophrenia - genetics</topic><topic>Schizophrenia - pathology</topic><topic>Schizophrenia - physiopathology</topic><topic>Short Communications</topic><topic>Software packages</topic><topic>Stem cells</topic><topic>Tyrosine 3-Monooxygenase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Iritani, Shuji</creatorcontrib><creatorcontrib>Sekiguchi, Hirotaka</creatorcontrib><creatorcontrib>Habuchi, Chikako</creatorcontrib><creatorcontrib>Torii, Youta</creatorcontrib><creatorcontrib>Kuroda, Keisuke</creatorcontrib><creatorcontrib>Kaibuchi, Kozo</creatorcontrib><creatorcontrib>Ozaki, Norio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Psychology Database (Alumni)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest Psychology</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Acta neuropsychiatrica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Iritani, Shuji</au><au>Sekiguchi, Hirotaka</au><au>Habuchi, Chikako</au><au>Torii, Youta</au><au>Kuroda, Keisuke</au><au>Kaibuchi, Kozo</au><au>Ozaki, Norio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Catecholaminergic neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia</atitle><jtitle>Acta neuropsychiatrica</jtitle><addtitle>Acta Neuropsychiatr</addtitle><date>2016-04-01</date><risdate>2016</risdate><volume>28</volume><issue>2</issue><spage>117</spage><epage>123</epage><pages>117-123</pages><issn>0924-2708</issn><eissn>1601-5215</eissn><abstract>The precise aetiology of schizophrenia remains unclear. The neurodevelopmental hypothesis of schizophrenia has been proposed based on the accumulation of genomic or neuroimaging studies.
In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizophrenia 1 (DISC1) knockout (KO) mice, which are considered to be a useful model of schizophrenia.
Six DISC1 homozygous KO mice and six age-matched littermates were used. The animals' brains were cut into 20-μm-thick slices, which were then immunohistochemically stained using an anti-tyrosine hydroxylase (TH) monoclonal antibody.
The TH-immunopositive fibres detected in the orbitofrontal cortices of the DISC1 KO mice were significantly shorter than those seen in the wild-type mice.
These neuropathological findings indicate that the hypofrontal symptoms of schizophrenia are associated with higher mental function deficiencies or cognitive dysfunction such as a loss of working memory.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>26333915</pmid><doi>10.1017/neu.2015.51</doi><tpages>7</tpages></addata></record> |
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| ispartof | Acta neuropsychiatrica, 2016-04, Vol.28 (2), p.117-123 |
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| source | MEDLINE; Cambridge University Press Journals Complete |
| subjects | Animal cognition Animals Antibodies Brain Confounding (Statistics) Digital cameras Digital maps Disease Models, Animal Female Gender Genes Investigations Kinases Laboratories Male Mice Mice, Knockout Nerve Tissue Proteins - genetics Neuropathology Pathogenesis Pathophysiology Prefrontal Cortex - metabolism Prefrontal Cortex - pathology Prefrontal Cortex - physiopathology Schizophrenia Schizophrenia - genetics Schizophrenia - pathology Schizophrenia - physiopathology Short Communications Software packages Stem cells Tyrosine 3-Monooxygenase - metabolism |
| title | Catecholaminergic neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia |
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