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Alterations in dendrite and spine morphology of cortical pyramidal neurons in DISC1-binding zinc finger protein (DBZ) knockout mice
Dendrite and dendritic spine formation are crucial for proper brain function. DISC1-binding zinc finger protein (DBZ) was first identified as a Disrupted-In-Schizophrenia1 (DISC1) binding partner. DBZ is highly expressed in the cerebral cortex of developing and adult rodents and is involved in neuri...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4415407/ https://www.ncbi.nlm.nih.gov/pubmed/25983680 http://dx.doi.org/10.3389/fnana.2015.00052 |
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author | Koyama, Yoshihisa Hattori, Tsuyoshi Nishida, Tomoki Hori, Osamu Tohyama, Masaya |
author_facet | Koyama, Yoshihisa Hattori, Tsuyoshi Nishida, Tomoki Hori, Osamu Tohyama, Masaya |
author_sort | Koyama, Yoshihisa |
collection | PubMed |
description | Dendrite and dendritic spine formation are crucial for proper brain function. DISC1-binding zinc finger protein (DBZ) was first identified as a Disrupted-In-Schizophrenia1 (DISC1) binding partner. DBZ is highly expressed in the cerebral cortex of developing and adult rodents and is involved in neurite formation, cell positioning, and the development of interneurons and oligodendrocytes. The functional roles of DBZ in postnatal brain remain unknown; thus we investigated cortical pyramidal neuron morphology in DBZ knockout (KO) mice. Morphological analyses by Golgi staining alone in DBZ KO mice revealed decreased dendritic arborization, increased spine density. A morphological analysis of the spines revealed markedly increased numbers of thin spines. To investigate whole spine structure in detail, electron tomographic analysis using ultra-high voltage electron microscopy (UHVEM) combined with Golgi staining was performed. Tomograms and three-dimensional models of spines revealed that the spines of DBZ KO mice exhibited two types of characteristic morphology, filopodia-like spines and abnormal thin-necked spines having an extremely thin spine neck. Moreover, conventional electron microscopy revealed significantly decreased number of postsynaptic densities (PSDs) in spines of DBZ KO mice. In conclusion, DBZ deficiency impairs the morphogenesis of dendrites and spines in cortical pyramidal neurons. |
format | Online Article Text |
id | pubmed-4415407 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-44154072015-05-15 Alterations in dendrite and spine morphology of cortical pyramidal neurons in DISC1-binding zinc finger protein (DBZ) knockout mice Koyama, Yoshihisa Hattori, Tsuyoshi Nishida, Tomoki Hori, Osamu Tohyama, Masaya Front Neuroanat Neuroscience Dendrite and dendritic spine formation are crucial for proper brain function. DISC1-binding zinc finger protein (DBZ) was first identified as a Disrupted-In-Schizophrenia1 (DISC1) binding partner. DBZ is highly expressed in the cerebral cortex of developing and adult rodents and is involved in neurite formation, cell positioning, and the development of interneurons and oligodendrocytes. The functional roles of DBZ in postnatal brain remain unknown; thus we investigated cortical pyramidal neuron morphology in DBZ knockout (KO) mice. Morphological analyses by Golgi staining alone in DBZ KO mice revealed decreased dendritic arborization, increased spine density. A morphological analysis of the spines revealed markedly increased numbers of thin spines. To investigate whole spine structure in detail, electron tomographic analysis using ultra-high voltage electron microscopy (UHVEM) combined with Golgi staining was performed. Tomograms and three-dimensional models of spines revealed that the spines of DBZ KO mice exhibited two types of characteristic morphology, filopodia-like spines and abnormal thin-necked spines having an extremely thin spine neck. Moreover, conventional electron microscopy revealed significantly decreased number of postsynaptic densities (PSDs) in spines of DBZ KO mice. In conclusion, DBZ deficiency impairs the morphogenesis of dendrites and spines in cortical pyramidal neurons. Frontiers Media S.A. 2015-04-30 /pmc/articles/PMC4415407/ /pubmed/25983680 http://dx.doi.org/10.3389/fnana.2015.00052 Text en Copyright © 2015 Koyama, Hattori, Nishida, Hori and Tohyama. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Koyama, Yoshihisa Hattori, Tsuyoshi Nishida, Tomoki Hori, Osamu Tohyama, Masaya Alterations in dendrite and spine morphology of cortical pyramidal neurons in DISC1-binding zinc finger protein (DBZ) knockout mice |
title | Alterations in dendrite and spine morphology of cortical pyramidal neurons in DISC1-binding zinc finger protein (DBZ) knockout mice |
title_full | Alterations in dendrite and spine morphology of cortical pyramidal neurons in DISC1-binding zinc finger protein (DBZ) knockout mice |
title_fullStr | Alterations in dendrite and spine morphology of cortical pyramidal neurons in DISC1-binding zinc finger protein (DBZ) knockout mice |
title_full_unstemmed | Alterations in dendrite and spine morphology of cortical pyramidal neurons in DISC1-binding zinc finger protein (DBZ) knockout mice |
title_short | Alterations in dendrite and spine morphology of cortical pyramidal neurons in DISC1-binding zinc finger protein (DBZ) knockout mice |
title_sort | alterations in dendrite and spine morphology of cortical pyramidal neurons in disc1-binding zinc finger protein (dbz) knockout mice |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4415407/ https://www.ncbi.nlm.nih.gov/pubmed/25983680 http://dx.doi.org/10.3389/fnana.2015.00052 |
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