関: ependymal

WordNet

thin epithelial membrane lining the ventricles of the brain and the spinal cord canal

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/10/04 22:10:27」(JST)

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Ependyma is the thin epithelial membrane lining the ventricular system of the brain and the spinal cord. Ependyma is one of the four types of neuroglia in the central nervous system. It is involved in the production of cerebrospinal fluid (CSF).

Ependymal Cells

The ependyma is made up of ependymal cells. These are the epithelial-like cells that line the CSF-filled ventricles in the brain and the central canal of the spinal cord. The cells are ciliated simple cuboidal epithelium-like cells. Their apical surfaces are covered in a layer of cilia, which circulate CSF around the central nervous system. Their apical surfaces are also covered with microvilli, which absorb CSF. Ependymal cells are a type of Glial cell and are also CSF producing cells. Within the brain's ventricles, a population of modified ependymal cells and capillaries together form a system called the choroid plexus, which produces the CSF.

Tight junctions, zonae occludentes, between ependymal cells control fluid release across the epithelium. This release allows free exchange between CSF and nervous tissue of brain and spinal cord. This is why sampling of CSF (e.g. through a "spinal tap") gives one window to CNS.

The basal membrane of these cells are caracterized by tentacles like extensions that attach to astrocytes. they are not epithelial cells because they do not have a basement membrane.

Pathology

Ependymoma is a tumor of the ependymal cells most commonly found in 4th ventricle.

Stem cells

Jonas Frisén and his colleagues at the Karolinska Institute in Stockholm provided evidence that ependymal cells act as reservoir cells in the forebrain, which can be activated after stroke and as in vivo and in vitro stem cells in the spinal cord.^[1] ^[2] One study observed that ependymal cells from the lining of the lateral ventricle might be a source for cells which can be transplanted into the cochlea to reverse hearing loss.^[3]

Ependyma and Neurodegeneration

In 2004, Dr. Milan Radojicic proposed the stem cell niche disruption hypothesis, highlighting the role of local ischemia, cerebrospinal fluid dynamics and cytotoxic factors in disrupting the ependymal stromal epithelium, along with periependymal stem/progenitor cells, thereby tipping the balance between injury and self-repair (i.e., neurogenesis and gliogenesis) in the central nervous system toward further degeneration over time.^{[citation needed]}

References

^ Johansson CB, Momma S, Clarke DL, Risling M, Lendahl U, Frisen J (1999). "Identification of a neural stem cell in the adult mammalian central nervous system". Cell 96 (1): 25–34. doi:10.1016/S0092-8674(00)80956-3. PMID 9989494.
^ Carlén M, Meletis K, Göritz C, Darsalia V, Evergren E, Tanigaki K, Amendola M, Barnabé-Heider F, Yeung MS, Naldini L, Honjo T, Kokaia Z, Shupliakov O, Cassidy RM, Lindvall O, Frisén J. (2009). "Forebrain ependymal cells are Notch-dependent and generate neuroblasts and astrocytes after stroke.". Nature Neuroscience 12 (3): 259–267. doi:10.1038/nn.2268. PMID 19234458.
^ "Brain cell hope for hearing loss". BBC News. 2008-12-09. http://news.bbc.co.uk/2/hi/health/7770665.stm. Retrieved 2008-12-09.

External links

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1. 新生児における細菌性髄膜炎：神経学的合併症 bacterial meningitis in the neonate neurologic complications
2. 神経管欠損および脳室拡大を除く中枢神経系異常の出生前診断 prenatal diagnosis of cns anomalies other than neural tube defects and ventriculomegaly
3. 水頭症 hydrocephalus

English Journal

MCT8 in human fetal cerebral cortex is reduced in severe intrauterine growth restriction.

Chan SY, Hancox LA, Martín-Santos A, Loubière LS, Walter MN, Gonzalez AM, Cox PM, Logan A, McCabe CJ, Franklyn JA, Kilby M.Author information S Chan, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, B15 2TT, United Kingdom.AbstractThe importance of the thyroid hormone (TH) transporter, monocarboxylate transporter (MCT8), to human neurodevelopment is highlighted by findings of severe global neurological impairment in subjects with MCT8 mutations. Intrauterine growth restriction (IUGR), usually due to uteroplacental failure, is associated with milder neurodevelopmental deficits, which have been partly attributed to dysregulated TH action in utero secondary to reduced circulating fetal TH concentrations and decreased cerebral TH receptor expression. We postulate that altered MCT8 expression is implicated in this pathophysiology and sought to quantify changes in cortical MCT8 expression with IUGR. Firstly, MCT8 immunohistochemistry was performed on occipital and parietal cerebral cortex sections from appropriately grown for gestational age (AGA) human fetuses between 19 weeks gestation and term. Secondly, MCT8 immunostaining in the occipital cortex of stillborn IUGR human fetuses at 24-28 weeks gestation were objectively compared with gestationally-matched AGA fetuses. Fetuses demonstrated widespread MCT8 expression in neurons within the cortical plate and subplate, in the ventricular and subventricular zones, epithelium of the choroid plexus and ependyma, and microvessel wall. When complicated by IUGR, fetuses showed a significant 5-fold reduction in the percentage area of cortical plate immunostained with MCT8 compared with AGA fetuses (p<0.05) but there was no significant difference in the proportion of subplate microvessels immunostained. Cortical MCT8 expression negatively correlated with the severity of IUGR indicated by brain:liver weight ratios (r2=0.28, p<0.05) at post-mortem. Our results support the hypothesis that a reduction in MCT8 expression in the IUGR fetal brain could further compromise TH-dependent brain development.
The Journal of endocrinology.J Endocrinol.2013 Nov 7. [Epub ahead of print]
The importance of the thyroid hormone (TH) transporter, monocarboxylate transporter (MCT8), to human neurodevelopment is highlighted by findings of severe global neurological impairment in subjects with MCT8 mutations. Intrauterine growth restriction (IUGR), usually due to uteroplacental failure, is
PMID 24204008

Distribution of MT1 Melatonin Receptor Promoter-Driven RFP Expression in the Brains of BAC C3H/HeN Transgenic Mice.

Adamah-Biassi E, Zhang Y, Jung H, Vissapragada S, Miller R, Dubocovich M.Author information Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo NY (EBAB, YZ, SV, MLD).AbstractThe pineal hormone melatonin activates two G-protein coupled receptors (MT1 and MT2) to regulate in part biological functions. The MT1 and MT2 melatonin receptors are heterogeneously distributed in the mammalian brain including humans. In the mouse, only a few reports have assessed the expression of the MT1 melatonin receptor expression using 2-iodomelatonin binding, in situ hybridization and/or polymerase chain reaction (PCR). Here, we described a transgenic mouse in which red fluorescence protein (RFP) is expressed under the control of the endogenous MT1 promoter, by inserting RFP cDNA at the start codon of MTNR1a gene within a bacterial artificial chromosome (BAC) and expressing this construct as a transgene. The expression of RFP in the brain of this mouse was examined either directly under a fluorescent microscope or immunohistochemically using an antibody against RFP (RFP-MT1). RFP-MT1 expression was observed in many brain regions including the subcommissural organ, parts of the ependyma lining the lateral and third ventricles, the aqueduct, the hippocampus, the cerebellum, the pars tuberalis, the habenula and the habenula commissure. This RFP-MT1 transgenic model provides a unique tool for studying the distribution of the MT1 receptor in the brain of mice, its cell-specific expression and its function in vivo.
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.J Histochem Cytochem.2013 Oct 23. [Epub ahead of print]
The pineal hormone melatonin activates two G-protein coupled receptors (MT1 and MT2) to regulate in part biological functions. The MT1 and MT2 melatonin receptors are heterogeneously distributed in the mammalian brain including humans. In the mouse, only a few reports have assessed the expression of
PMID 24051358

Neurogenesis in the lamprey CNS following spinal cord transection.

Zhang G, Pizarro IV, Swain GP, Kang SH, Selzer ME.Author information Shriners Hospitals Pediatric Research Center, Temple University School of Medicine, Philadelphia, PA, 19140; Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, 19104.AbstractAfter spinal cord transection, lampreys recover functionally and axons regenerate. It is not known whether this is accompanied by neurogenesis. Previous studies suggested a baseline level of non-neuronal cell proliferation in the spinal cord and rhombencephalon (where most supraspinal projecting neurons are located). To determine whether cell proliferation increases after injury and whether this includes neurogenesis, larval lampreys were spinally transected and injected with BrdU at 0-3 weeks post-transection. Labeled cells were counted in the lesion site, within 0.5 mm rostral and caudal to the lesion, and in the rhombencephalon. One group of animals was processed in the winter, and a second group was processed in the summer. The number of labeled cells was greater in winter than in summer. The lesion site had the most BrdU labeling at all times, correlating with an increase in the number of cells. In the adjacent spinal cord the percentage of BrdU labeling was higher in the ependymal than in non-ependymal regions. This was also true in the rhombencephalon but only in summer. In winter, BrdU labeling was seen primarily in the subventricular and peripheral zones. Some BrdU-labeled cells were also double-labeled by antibodies to glial-specific (anti-keratin) as well as to neuron-specific (anti-Hu) antigens, indicating that both gliogenesis and neurogenesis occurred after spinal cord transection. However, the new neurons were restricted to the ependymal zone, were never labeled by anti-neurofilament antibodies, and never migrated away from the ependyma, even at 5 weeks after BrdU injection. They would appear to be CSF-contacting neurons. J. Comp. Neurol., 2013. © 2013 Wiley Periodicals, Inc.
The Journal of comparative neurology.J Comp Neurol.2013 Oct 22. doi: 10.1002/cne.23485. [Epub ahead of print]
After spinal cord transection, lampreys recover functionally and axons regenerate. It is not known whether this is accompanied by neurogenesis. Previous studies suggested a baseline level of non-neuronal cell proliferation in the spinal cord and rhombencephalon (where most supraspinal projecting neu
PMID 24151158

Japanese Journal

Anatomy: Constitution of the ependyma in the chicken telencephalon

Uchida Shinsuke,Imagawa Tomohiro,Furue Masato [他]
日本獣醫學会会誌 73(3), 319-323, 2011-03
NAID 40018785953

Constitution of the Ependyma in the Chicken Telencephalon

UCHIDA Shinsuke,IMAGAWA Tomohiro,FURUE Masato,ALI Safwat Ali Mohamed,HOSAKA Yoshinao Z.,UEHARA Masato
Journal of Veterinary Medical Science advpub(0), 1010190366, 2010
… The constitution of ependyma derived from the ventricular zone is different from that derived from other regions of the central nervous system. … In the mammalian cerebrum, the ependyma is varied by the regions to cortex or basal ganglia (BG). … In the avian telencephalon (Tc), previous studies about the constitution of the ependyma have not revealed clear findings. …
NAID 130000444302

Related Pictures

★リンクテーブル★

リンク元	「上衣」「ependymal」「脳室上皮」「髄腔上皮」
拡張検索	「subependymal giant cell astrocytoma」「subependymal glioma」

「上衣」

Ependyma
	Section of central canal of medulla spinalis, showing ependymal and neuroglial cells.
	Photomicrograph of hematoxylin stained section of normal ependymal cells at 400x magnification. Human autopsy tissue
Gray's	subject #189 829
MeSH	Ependyma
Code	TA A14.1.00.022