Are CNS neurons polyploid? A critical analysis based upon cytophotometric study of the DNA content of cerebellar and olfactory bulbar neurons of the bat

Swartz, Frank J.; Bhatnagar, Kunwar P.

doi:10.1016/0006-8993(81)90557-6

Cited by 38 publications

(20 citation statements)

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“…The issue of the polyploidy of cerebral cortical and Purkinje neurons is controversial (Bregnard et al, 1975;Swartz and Bhatnagar, 1981). Here, we clearly show that the chromosome complements of the cerebral cortical neurons and cerebellar Purkinje neurons are basically diploid, but that they display condensation defects and aneuploidy.…”

Section: Discussionmentioning

confidence: 69%

“…Postmitotic neuronal nuclei are known to have unique nuclear chromatin domains and specific gene-expression machinery (Akhmanova et al, 2000;Yoshikawa, 2000;Ballas et al, 2001;Diez del Corral and Storey, 2001). Whether adult neurons are diploid or polyploid remains controversial (Bregnard et al, 1975;Swartz and Bhatnagar, 1981).…”

confidence: 99%

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Adult murine neurons: their chromatin and chromosome changes and failure to support embryonic development as revealed by nuclear transfer

Osada

Kusakabe

Akutsu

et al. 2002

Cytogenet Genome Res

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Fully differentiated neurons in adult mammalian brains do not divide; consequently, their metaphase chromosomes have never been examined. Here we report metaphase chromosome constitutions of cortical neurons in adult mice visualized by a nuclear transfer technique. We found that although some reconstructed oocytes cloned from neuronal nuclei have an apparently normal karyotype, the majority do not. Regardless of chromosome morphology, nuclei of adult neurons totally lack the ability to support embryonic development. These findings support the hypothesis that fully differentiated neurons in adult mammalian brains are genomically altered.

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Section: Discussionmentioning

confidence: 69%

confidence: 99%

Adult murine neurons: their chromatin and chromosome changes and failure to support embryonic development as revealed by nuclear transfer

Osada

Kusakabe

Akutsu

et al. 2002

Cytogenet Genome Res

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“…It has been long debated whether the mammalian brain is populated by cells with abnormal chromosome numbers (polyploid cells) [7,29-31]. However, these observations were not definitive, inasmuch as there were not a technique for direct analysis of chromosomes in non-dividing interphase cells [7,9,12,16].…”

Section: Aneuploidy In the Human Brain: Cell Fate And Ontogenymentioning

confidence: 99%

GIN'n'CIN hypothesis of brain aging: deciphering the role of somatic genetic instabilities and neural aneuploidy during ontogeny

Yurov

Iourov

2009

Mol Cytogenet

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Genomic instability (GIN) and chromosome instability (CIN) are two closely related ways to produce a variety of pathogenic conditions, i.e. cancer, neurodegeneration, chromosomal and genomic diseases. The GIN and CIN manifestation that possesses the most appreciable impact on cell physiology and viability is aneuploidy. The latter has been consistently shown to be associated with aging. Classically, it has been considered that a failure of mitotic machinery leads to aneuploidy acquiring throughout aging in dividing cells. Paradoxically, this model is inapplicable for the human brain, which is composed of post-mitotic cells persisting throughout the lifetime. To solve this paradox, we have focused on mosaic neural aneuploidy, a remarkable biomarker of GIN and CIN in the normal and diseased brain (i.e. Alzheimer's disease and ataxia-telangiectasia). Looking through the available data on genomic variations in the developing and adult human central nervous system, we were able to propose a hypothesis suggesting that neural aneuploidy produced during early brain development plays a crucial role of genetic determinant of aging in the healthy and diseased brain.

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“…Nevertheless, technical limitations prevented a clear conclusion at that time (1). The current belief is that some neurons in the normal vertebrate nervous system are tetraploid (2), but the mechanism leading to this condition remains unclear.…”

mentioning

confidence: 99%

Somatic tetraploidy in specific chick retinal ganglion cells induced by nerve growth factor

Morillo

Escoll

Hera

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

115

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A subset of neurons in the normal vertebrate nervous system contains double the normal amount of DNA in their nuclei. These neurons are all thought to derive from aberrant mitoses in neuronal precursor cells. Here we show that endogenous NGF induces DNA replication in a subpopulation of differentiating chick retinal ganglion cells that express both the neurotrophin receptor p75 and the E2F1 transcription factor, but that lack the retinoblastoma protein. Many of these neurons avoid G2/M transition and remain alive in the retina as tetraploid cells with large cell somas and extensive dendritic trees, and most of them express β2 nicotinic acetylcholine receptor subunits, a specific marker of retinal ganglion cells innervating lamina F in the stratum-griseum-et-fibrosum-superficiale of the tectal cortex. Tetraploid neurons were also observed in the adult mouse retina. Thus, a developmental program leading to somatic tetraploidy in specific retinal neurons exists in vertebrates. This program might occur in other vertebrate neurons during normal or pathological situations.AChR | cell cycle | dendritic tree | p75NTR | tectum

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Are CNS neurons polyploid? A critical analysis based upon cytophotometric study of the DNA content of cerebellar and olfactory bulbar neurons of the bat

Cited by 38 publications

References 20 publications

Adult murine neurons: their chromatin and chromosome changes and failure to support embryonic development as revealed by nuclear transfer

Adult murine neurons: their chromatin and chromosome changes and failure to support embryonic development as revealed by nuclear transfer

GIN'n'CIN hypothesis of brain aging: deciphering the role of somatic genetic instabilities and neural aneuploidy during ontogeny

Somatic tetraploidy in specific chick retinal ganglion cells induced by nerve growth factor

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