A novel, rapid, quantitative cell-counting method reveals oligodendroglial reduction in the frontopolar cortex in major depressive disorder

Hayashi, Yoshitaka; Nihonmatsu-Kikuchi, Naomi; Yu, Xinguang; Ishimoto, Keiko; Hisanaga, S-I; Tatebayashi, Yoshitaka

doi:10.1038/mp.2011.84

Cited by 41 publications

(38 citation statements)

References 10 publications

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“…From the nuclei suspension, aliquots are taken, placed into a hemocytometer, and counted at the fluorescence microscope. Similar results were obtained by running the suspension through a flow cytometer (Collins et al, 2010;Hayashi et al, 2011).…”

Section: Discussionsupporting

confidence: 80%

“…The technique starts by homogenizing the tissue as much as to rupture cell membranes but not nuclear membranes. We usually employ aldehyde-fixed tissue (HerculanoHouzel and Lent, 2005;Herculano-Houzel et al, 2006;Azevedo et al, 2009), but fresh material has been employed successfully as well (Hayashi et al, 2011). As a result, a nuclei suspension is obtained, DNA-stained for better visualization, and immunostained to reveal a neuron-specific antigen and thus discern neuronal from non-neuronal nuclei.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to the popular stereological techniques (Schmitz and Hof, 2005), an alternative method has been proposed, tailored for large anisotropic tissues as is the case of most brain regions: the isotropic fractionator (Herculano-Houzel and Lent, 2005;Collins et al, 2010;Hayashi et al, 2011). In short, the rationale of this new method is to transform any dissectable region of the brain into an isotropic suspension of cell nuclei that can be immunostained and counted in a hemocytometer at a fluorescent microscope, or by use of flow cytometry.…”

Section: Introductionmentioning

confidence: 98%

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Automatic isotropic fractionation for large-scale quantitative cell analysis of nervous tissue

Azevedo

Andrade-Moraes

Curado

et al. 2013

Journal of Neuroscience Methods

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

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Automatic isotropic fractionation for large-scale quantitative cell analysis of nervous tissue

Azevedo

Andrade-Moraes

Curado

et al. 2013

Journal of Neuroscience Methods

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“…These approaches should be, in principle, also applicable to capture selected interneuron subtypes or other neuronal subpopulations. Related approaches were recently employed to sort-specific subtypes of non-neuronal cells, including oligodendroglia (Hayashi et al, 2011). One important limitation of the nuclei sorting approach is the need for epitopes that are selectively expressed in the nucleus of the cell type-of-interest, and sufficiently stable to maintain robust immunoreactivity during tissue autolysis.…”

Section: Cellular Specificity Of Epigenetic Markingsmentioning

confidence: 99%

Epigenetics in the Human Brain

Houston

Peter

Mitchell

et al. 2012

Neuropsychopharmacol

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Many cellular constituents in the human brain permanently exit from the cell cycle during pre-or early postnatal development, but little is known about epigenetic regulation of neuronal and glial epigenomes during maturation and aging, including changes in mood and psychosis spectrum disorders and other cognitive or emotional disease. Here, we summarize the current knowledge base as it pertains to genome organization in the human brain, including the regulation of DNA cytosine methylation and hydroxymethylation, and a subset of (altogether 4100) residue-specific histone modifications associated with gene expression, and silencing and various other functional chromatin states. We propose that high-resolution mapping of epigenetic markings in postmortem brain tissue or neural cultures derived from induced pluripotent cells (iPS), in conjunction with transcriptome profiling and whole-genome sequencing, will increasingly be used to define the molecular pathology of specific cases diagnosed with depression, schizophrenia, autism, or other major psychiatric disease. We predict that these highly integrative explorations of genome organization and function will provide an important alternative to conventional approaches in human brain studies, which mainly are aimed at uncovering group effects by diagnosis but generally face limitations because of cohort size.

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“…Furthermore, growing evidence from studies of postmortem human tissue microarrays [9,10], histopathology [11,12] and neuroimaging [9] suggests that oligodendrocytes (ODCs) and myelin dysfunction play an important role in the pathophysiology of depression and antidepressant treatment response [9]. Rajkowska et al proposed that the combination All patients were treated with single antidepressant drugs (SSRI or SNRI) according to current clinical practice.…”

Section: Introductionmentioning

confidence: 99%

Influence of Childhood Physical Neglect on Depression: Potential Moderation by a Polymorphism in the QKI Gene

Geng¹,

Shi²

2016

J Depress Anxiety

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of genetic and environmental factors (e.g., stress) could initially lead to glial cell pathology and consequently contribute to neuronal pathology later in life, as depressive illnesses progresses [13].For these reasons, the present study sought to (i) examine the potential impact of CPN on general functioning, adult depressive symptoms and antidepressant treatment response, and (ii) test whether genetic polymorphisms related to ODC and myelin function interact with CPN to affect adult depressive symptoms and antidepressant response. Methods Study design and subjectsSubjects were Chinese Han individuals aged between 18 to 60 years, with a diagnosis of new or recently relapsed major depression disorder (MDD). The baseline scores on the 17-item Hamilton Depression Rating Scale (HAMD-17) were>17. Exclusion criteria used for this study have been previously reported [14]. All of the subjects were informed of the potential risks and benefits of the study and gave their informed consent prior to their participation in the study. AbstractObjective: Childhood physical neglect (CPN) is a common but often overlooked form of abuse that may contribute to depression. We aimed at examining the potential impact of CPN and its interactions with genes related to oligodendrocytes (ODCs) and myelin function on adult depressive symptoms and antidepressant treatment response.Methods: A group of 209 Chinese Han patients with major depressive disorder (MDD) completed the Hamilton Depression Scale-17 (HAMD-17) at baseline and after 8 weeks antidepressant treatment. The Childhood Trauma Questionnaire was used to evaluate the occurrence of childhood physical neglect. Twelve single nucleotide polymorphisms (SNPs) in functional regions were successfully genotyped in seven genes associated with ODCs and myelin function. Results:Childhood physical neglect is related to education and social support, especially the subjective social support of those who experience CPN. The GG genotype of the 3'UTR functional polymorphism rs715020 in the QKI gene showed significant association with diminished effects of childhood physical neglect on adult depressive symptoms(P=.003) even after the Bonferroni correction. No significant interactions between candidate genes and CPN on antidepressant response were observed. Conclusion:These results indicate that CPN are potentially associated with ODCs and myelin-related gene QKI, and may influence adult depressive symptoms in major depression disorder (MDD) patients. This finding needs to be further replicated in a larger sample.

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A novel, rapid, quantitative cell-counting method reveals oligodendroglial reduction in the frontopolar cortex in major depressive disorder

Cited by 41 publications

References 10 publications

Automatic isotropic fractionation for large-scale quantitative cell analysis of nervous tissue

Automatic isotropic fractionation for large-scale quantitative cell analysis of nervous tissue

Epigenetics in the Human Brain

Influence of Childhood Physical Neglect on Depression: Potential Moderation by a Polymorphism in the QKI Gene

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