Increased truncated TrkB receptor expression and decreased BDNF/TrkB signaling in the frontal cortex of reeler mouse model of schizophrenia
Abstract Heterozygous reeler mouse has been used as an animal model for schizophrenia based on several neuropathological and behavioral abnormalities homologous to schizophrenia. Since some of these abnormalities are primarily associated with altered BDNF signaling we investigated BDNF signaling in...
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| description | Abstract Heterozygous reeler mouse has been used as an animal model for schizophrenia based on several neuropathological and behavioral abnormalities homologous to schizophrenia. Since some of these abnormalities are primarily associated with altered BDNF signaling we investigated BDNF signaling in the frontal cortex of reeler mice in order to shed some light on the neuropathology and treatment of schizophrenia. BDNF, TrkB receptor isoforms (full-length and truncated), reelin, GAD67, GAD65, p75NTR, and NRH-2 levels were measured in the frontal cortex samples from reeler (B6C3Fe a/a-Relnrl /+) and wild-type (WT) mice. BDNF protein levels were significantly higher in reeler compared to WT. The protein levels of full-length TrkB were not altered in reeler mice, but both mRNA and protein levels of truncated TrkB were significantly higher. Protein analysis showed that TrkB activity, as indicated by the levels of tyrosine-phosphorylated TrkB, was lower in reeler mice. We did not find any significant change in the levels of p75NTR and NRH-2, regulatory proteins of TrkB signaling, in the reeler mice. Furthermore, we found significant reduction in reelin and GAD67 expressions, but not GAD65 expression in reeler compared to WT mice. In summary, molecular processes associated with defective BDNF signaling in reeler mice provide new therapeutic targets for neuroprotective pharmacotherapy for schizophrenia. |
| doi_str_mv | 10.1016/j.schres.2007.11.030 |
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Since some of these abnormalities are primarily associated with altered BDNF signaling we investigated BDNF signaling in the frontal cortex of reeler mice in order to shed some light on the neuropathology and treatment of schizophrenia. BDNF, TrkB receptor isoforms (full-length and truncated), reelin, GAD67, GAD65, p75NTR, and NRH-2 levels were measured in the frontal cortex samples from reeler (B6C3Fe a/a-Relnrl /+) and wild-type (WT) mice. BDNF protein levels were significantly higher in reeler compared to WT. The protein levels of full-length TrkB were not altered in reeler mice, but both mRNA and protein levels of truncated TrkB were significantly higher. Protein analysis showed that TrkB activity, as indicated by the levels of tyrosine-phosphorylated TrkB, was lower in reeler mice. We did not find any significant change in the levels of p75NTR and NRH-2, regulatory proteins of TrkB signaling, in the reeler mice. Furthermore, we found significant reduction in reelin and GAD67 expressions, but not GAD65 expression in reeler compared to WT mice. In summary, molecular processes associated with defective BDNF signaling in reeler mice provide new therapeutic targets for neuroprotective pharmacotherapy for schizophrenia.</description><identifier>ISSN: 0920-9964</identifier><identifier>EISSN: 1573-2509</identifier><identifier>DOI: 10.1016/j.schres.2007.11.030</identifier><identifier>PMID: 18187310</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Adult and adolescent clinical studies ; Animal model ; Animals ; BDNF signaling ; Biological and medical sciences ; Blotting, Western ; Brain-Derived Neurotrophic Factor - genetics ; Brain-Derived Neurotrophic Factor - metabolism ; Brain-Derived Neurotrophic Factor - physiology ; Cell Adhesion Molecules, Neuronal - analysis ; Cell Adhesion Molecules, Neuronal - metabolism ; Cell Adhesion Molecules, Neuronal - physiology ; Disease Models, Animal ; Extracellular Matrix Proteins - analysis ; Extracellular Matrix Proteins - metabolism ; Extracellular Matrix Proteins - physiology ; Frontal Lobe - chemistry ; Frontal Lobe - metabolism ; Frontal Lobe - physiopathology ; gamma-Aminobutyric Acid - analysis ; gamma-Aminobutyric Acid - genetics ; Gene Expression ; Glutamate Decarboxylase - genetics ; Glutamate Decarboxylase - metabolism ; Heterozygote ; Humans ; Immunoassay ; Intracellular Signaling Peptides and Proteins - analysis ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Medical sciences ; Mice ; Mice, Neurologic Mutants ; Nerve Tissue Proteins - analysis ; Nerve Tissue Proteins - metabolism ; Nerve Tissue Proteins - physiology ; Neurons - metabolism ; Neurons - physiology ; Prefrontal Cortex - metabolism ; Prefrontal Cortex - physiopathology ; Protein Isoforms - genetics ; Protein Isoforms - metabolism ; Protein Isoforms - physiology ; Psychiatry ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychoses ; Receptor, trkB - genetics ; Receptor, trkB - metabolism ; Receptor, trkB - physiology ; Receptors, GABA - genetics ; Receptors, GABA - physiology ; Reeler mice ; Schizophrenia ; Schizophrenia - genetics ; Schizophrenia - metabolism ; Schizophrenia - physiopathology ; Serine Endopeptidases - analysis ; Serine Endopeptidases - metabolism ; Serine Endopeptidases - physiology ; Signal Transduction - genetics ; Signal Transduction - physiology ; TrkB receptor isoforms</subject><ispartof>Schizophrenia research, 2008-03, Vol.100 (1), p.325-333</ispartof><rights>Elsevier B.V.</rights><rights>2007 Elsevier B.V.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-dd8a7207c443f17c8fb44bfd224fac4f94ff66ee1f3705df7a340b044be151f3</citedby><cites>FETCH-LOGICAL-c511t-dd8a7207c443f17c8fb44bfd224fac4f94ff66ee1f3705df7a340b044be151f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.schres.2007.11.030$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20184966$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18187310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pillai, Anilkumar</creatorcontrib><creatorcontrib>Mahadik, Sahebarao P</creatorcontrib><title>Increased truncated TrkB receptor expression and decreased BDNF/TrkB signaling in the frontal cortex of reeler mouse model of schizophrenia</title><title>Schizophrenia research</title><addtitle>Schizophr Res</addtitle><description>Abstract Heterozygous reeler mouse has been used as an animal model for schizophrenia based on several neuropathological and behavioral abnormalities homologous to schizophrenia. Since some of these abnormalities are primarily associated with altered BDNF signaling we investigated BDNF signaling in the frontal cortex of reeler mice in order to shed some light on the neuropathology and treatment of schizophrenia. BDNF, TrkB receptor isoforms (full-length and truncated), reelin, GAD67, GAD65, p75NTR, and NRH-2 levels were measured in the frontal cortex samples from reeler (B6C3Fe a/a-Relnrl /+) and wild-type (WT) mice. BDNF protein levels were significantly higher in reeler compared to WT. The protein levels of full-length TrkB were not altered in reeler mice, but both mRNA and protein levels of truncated TrkB were significantly higher. Protein analysis showed that TrkB activity, as indicated by the levels of tyrosine-phosphorylated TrkB, was lower in reeler mice. We did not find any significant change in the levels of p75NTR and NRH-2, regulatory proteins of TrkB signaling, in the reeler mice. Furthermore, we found significant reduction in reelin and GAD67 expressions, but not GAD65 expression in reeler compared to WT mice. In summary, molecular processes associated with defective BDNF signaling in reeler mice provide new therapeutic targets for neuroprotective pharmacotherapy for schizophrenia.</description><subject>Adult and adolescent clinical studies</subject><subject>Animal model</subject><subject>Animals</subject><subject>BDNF signaling</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Brain-Derived Neurotrophic Factor - genetics</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Brain-Derived Neurotrophic Factor - physiology</subject><subject>Cell Adhesion Molecules, Neuronal - analysis</subject><subject>Cell Adhesion Molecules, Neuronal - metabolism</subject><subject>Cell Adhesion Molecules, Neuronal - physiology</subject><subject>Disease Models, Animal</subject><subject>Extracellular Matrix Proteins - analysis</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Extracellular Matrix Proteins - physiology</subject><subject>Frontal Lobe - chemistry</subject><subject>Frontal Lobe - metabolism</subject><subject>Frontal Lobe - physiopathology</subject><subject>gamma-Aminobutyric Acid - analysis</subject><subject>gamma-Aminobutyric Acid - genetics</subject><subject>Gene Expression</subject><subject>Glutamate Decarboxylase - genetics</subject><subject>Glutamate Decarboxylase - metabolism</subject><subject>Heterozygote</subject><subject>Humans</subject><subject>Immunoassay</subject><subject>Intracellular Signaling Peptides and Proteins - analysis</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Neurologic Mutants</subject><subject>Nerve Tissue Proteins - analysis</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>Neurons - metabolism</subject><subject>Neurons - physiology</subject><subject>Prefrontal Cortex - metabolism</subject><subject>Prefrontal Cortex - physiopathology</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Protein Isoforms - physiology</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychoses</subject><subject>Receptor, trkB - genetics</subject><subject>Receptor, trkB - metabolism</subject><subject>Receptor, trkB - physiology</subject><subject>Receptors, GABA - genetics</subject><subject>Receptors, GABA - physiology</subject><subject>Reeler mice</subject><subject>Schizophrenia</subject><subject>Schizophrenia - genetics</subject><subject>Schizophrenia - metabolism</subject><subject>Schizophrenia - physiopathology</subject><subject>Serine Endopeptidases - analysis</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Serine Endopeptidases - physiology</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - physiology</subject><subject>TrkB receptor isoforms</subject><issn>0920-9964</issn><issn>1573-2509</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks9u1DAQxi0EokvhDRDyBW5Jx4kTJxckWihUquDA3i2vPW69zdrBTqqWV-Cl63QXkLhwsa3Rb77585mQ1wxKBqw92ZZJX0dMZQUgSsZKqOEJWbFG1EXVQP-UrKCvoOj7lh-RFyltAYA1IJ6TI9axTtQMVuTXhdcRVUJDpzh7rab8WsebUxpR4ziFSPFuzGWSC54qb6jB3wmnH7-enzyyyV15NTh_RZ2n0zVSG4Of1EB1iBPe0WCzHA4Y6S7MCfNpcFiieQT3M4x5Du_US_LMqiHhq8N9TNbnn9ZnX4rLb58vzj5cFrphbCqM6ZSoQGjOa8uE7uyG8401VcWt0tz23Nq2RWS2FtAYK1TNYQOZQdbk4DF5t5cdY_gxY5rkziWNw6A85u6kgFq0TddkkO9BHUNKEa0co9upeC8ZyMUDuZV7D-TigWRMZg9y2puD_rzZofmbdFh6Bt4eAJW0GmxUXrv0h6uAdbxv28y933OYl3HrMOZqDr1G47I5kzTB_a-TfwV0Nsnlmjd4j2kb5phtS5LJVEmQ35f_snwXEAANh7p-AAo6vlM</recordid><startdate>20080301</startdate><enddate>20080301</enddate><creator>Pillai, Anilkumar</creator><creator>Mahadik, Sahebarao P</creator><general>Elsevier B.V</general><general>Elsevier Science</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>7X8</scope></search><sort><creationdate>20080301</creationdate><title>Increased truncated TrkB receptor expression and decreased BDNF/TrkB signaling in the frontal cortex of reeler mouse model of schizophrenia</title><author>Pillai, Anilkumar ; Mahadik, Sahebarao P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-dd8a7207c443f17c8fb44bfd224fac4f94ff66ee1f3705df7a340b044be151f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult and adolescent clinical studies</topic><topic>Animal model</topic><topic>Animals</topic><topic>BDNF signaling</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Brain-Derived Neurotrophic Factor - genetics</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Brain-Derived Neurotrophic Factor - physiology</topic><topic>Cell Adhesion Molecules, Neuronal - analysis</topic><topic>Cell Adhesion Molecules, Neuronal - metabolism</topic><topic>Cell Adhesion Molecules, Neuronal - physiology</topic><topic>Disease Models, Animal</topic><topic>Extracellular Matrix Proteins - analysis</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Extracellular Matrix Proteins - physiology</topic><topic>Frontal Lobe - chemistry</topic><topic>Frontal Lobe - metabolism</topic><topic>Frontal Lobe - physiopathology</topic><topic>gamma-Aminobutyric Acid - analysis</topic><topic>gamma-Aminobutyric Acid - genetics</topic><topic>Gene Expression</topic><topic>Glutamate Decarboxylase - genetics</topic><topic>Glutamate Decarboxylase - metabolism</topic><topic>Heterozygote</topic><topic>Humans</topic><topic>Immunoassay</topic><topic>Intracellular Signaling Peptides and Proteins - analysis</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Neurologic Mutants</topic><topic>Nerve Tissue Proteins - analysis</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>Prefrontal Cortex - metabolism</topic><topic>Prefrontal Cortex - physiopathology</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - metabolism</topic><topic>Protein Isoforms - physiology</topic><topic>Psychiatry</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychoses</topic><topic>Receptor, trkB - genetics</topic><topic>Receptor, trkB - metabolism</topic><topic>Receptor, trkB - physiology</topic><topic>Receptors, GABA - genetics</topic><topic>Receptors, GABA - physiology</topic><topic>Reeler mice</topic><topic>Schizophrenia</topic><topic>Schizophrenia - genetics</topic><topic>Schizophrenia - metabolism</topic><topic>Schizophrenia - physiopathology</topic><topic>Serine Endopeptidases - analysis</topic><topic>Serine Endopeptidases - metabolism</topic><topic>Serine Endopeptidases - physiology</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - physiology</topic><topic>TrkB receptor isoforms</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pillai, Anilkumar</creatorcontrib><creatorcontrib>Mahadik, Sahebarao P</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>MEDLINE - Academic</collection><jtitle>Schizophrenia research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pillai, Anilkumar</au><au>Mahadik, Sahebarao P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased truncated TrkB receptor expression and decreased BDNF/TrkB signaling in the frontal cortex of reeler mouse model of schizophrenia</atitle><jtitle>Schizophrenia research</jtitle><addtitle>Schizophr Res</addtitle><date>2008-03-01</date><risdate>2008</risdate><volume>100</volume><issue>1</issue><spage>325</spage><epage>333</epage><pages>325-333</pages><issn>0920-9964</issn><eissn>1573-2509</eissn><abstract>Abstract Heterozygous reeler mouse has been used as an animal model for schizophrenia based on several neuropathological and behavioral abnormalities homologous to schizophrenia. Since some of these abnormalities are primarily associated with altered BDNF signaling we investigated BDNF signaling in the frontal cortex of reeler mice in order to shed some light on the neuropathology and treatment of schizophrenia. BDNF, TrkB receptor isoforms (full-length and truncated), reelin, GAD67, GAD65, p75NTR, and NRH-2 levels were measured in the frontal cortex samples from reeler (B6C3Fe a/a-Relnrl /+) and wild-type (WT) mice. BDNF protein levels were significantly higher in reeler compared to WT. The protein levels of full-length TrkB were not altered in reeler mice, but both mRNA and protein levels of truncated TrkB were significantly higher. Protein analysis showed that TrkB activity, as indicated by the levels of tyrosine-phosphorylated TrkB, was lower in reeler mice. We did not find any significant change in the levels of p75NTR and NRH-2, regulatory proteins of TrkB signaling, in the reeler mice. Furthermore, we found significant reduction in reelin and GAD67 expressions, but not GAD65 expression in reeler compared to WT mice. In summary, molecular processes associated with defective BDNF signaling in reeler mice provide new therapeutic targets for neuroprotective pharmacotherapy for schizophrenia.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>18187310</pmid><doi>10.1016/j.schres.2007.11.030</doi><tpages>9</tpages></addata></record> |
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| subjects | Adult and adolescent clinical studies Animal model Animals BDNF signaling Biological and medical sciences Blotting, Western Brain-Derived Neurotrophic Factor - genetics Brain-Derived Neurotrophic Factor - metabolism Brain-Derived Neurotrophic Factor - physiology Cell Adhesion Molecules, Neuronal - analysis Cell Adhesion Molecules, Neuronal - metabolism Cell Adhesion Molecules, Neuronal - physiology Disease Models, Animal Extracellular Matrix Proteins - analysis Extracellular Matrix Proteins - metabolism Extracellular Matrix Proteins - physiology Frontal Lobe - chemistry Frontal Lobe - metabolism Frontal Lobe - physiopathology gamma-Aminobutyric Acid - analysis gamma-Aminobutyric Acid - genetics Gene Expression Glutamate Decarboxylase - genetics Glutamate Decarboxylase - metabolism Heterozygote Humans Immunoassay Intracellular Signaling Peptides and Proteins - analysis Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Medical sciences Mice Mice, Neurologic Mutants Nerve Tissue Proteins - analysis Nerve Tissue Proteins - metabolism Nerve Tissue Proteins - physiology Neurons - metabolism Neurons - physiology Prefrontal Cortex - metabolism Prefrontal Cortex - physiopathology Protein Isoforms - genetics Protein Isoforms - metabolism Protein Isoforms - physiology Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Receptor, trkB - genetics Receptor, trkB - metabolism Receptor, trkB - physiology Receptors, GABA - genetics Receptors, GABA - physiology Reeler mice Schizophrenia Schizophrenia - genetics Schizophrenia - metabolism Schizophrenia - physiopathology Serine Endopeptidases - analysis Serine Endopeptidases - metabolism Serine Endopeptidases - physiology Signal Transduction - genetics Signal Transduction - physiology TrkB receptor isoforms |
| title | Increased truncated TrkB receptor expression and decreased BDNF/TrkB signaling in the frontal cortex of reeler mouse model of schizophrenia |
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