Neuroepithelial cell

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Neuroepithelial cells, or neuroectodermal cells, form the wall of the closed

embryonic development. The neuroepithelial cells span the thickness of the tube's wall, connecting with the pial surface and with the ventricular or lumenal surface. They are joined at the lumen of the tube by junctional complexes, where they form a pseudostratified layer of epithelium called neuroepithelium.[1]

Neuroepithelial cells are the stem cells of the central nervous system, known as neural stem cells, and generate the intermediate progenitor cells known as radial glial cells, that differentiate into neurons and glia in the process of neurogenesis.[1]

Embryonic neural development

Brain development

Development of the neural tube

During the third week of

tight junctions to maintain the cell polarity.[4] Integrin alpha 6 anchors the neuroepithelial cells to the basal lamina.[4] The neural tube begins as a single layer of pseudostratified epithelial cells, but rapid proliferation of neuroepithelial cells creates additional layers and eventually three distinct regions of growth.[2][4] As these additional layers form the apical-basal polarity must be downregulated.[3] Further proliferation of the cells in these regions gives rise to three distinct areas of the brain: the forebrain, midbrain, and hindbrain. The neural tube also gives rise to the spinal cord.[2]

Neuroepithelial cell proliferation

Stem cell division and differentiation
Neuroepithelial cells symmetrically divide or differentiate into progenitor cells called radial glial cells in asymmetric cell division. These can further differentiate into neurons or glial cells.

Neuroepithelial cells are a class of stem cell and have the ability to self-renew. During the formation of the neural tube, neuroepithelial cells undergo symmetric proliferative divisions that give rise to two new neuroepithelial cells. At a later stage of brain development, neuroepithelial cells begin to self renew and give rise to non-stem cell progenitors, such as

actin filaments.[4]

Radial glial cell transition

Neuroepithelial cells give rise to radial glial progenitor cells in early embryonic development. To make this change, neuroepithelial cells begin to downregulate their epithelial features, by stopping the expression of

N-cadherin and keeps the apical face of the neuroepithelial cell intact.[4] In the absence of occludin some polarity is still lost and the neuroepithelial cell gives rise to the radial glial cell.[4]

Adult neurogenesis

Genesis of neuroepithelial cells in the adult CNS

cytokines or neuregulin 1 (NRG1) - that can determine whether the cells will differentiate into either neurons or glia.[5] On a whole, neurogenesis is regulated both by many varied regulatory pathways in the CNS as well as several other factors, from genes to external stimuli such as the individual behavior of a person. The large interconnected web of regulatory responses acts to fine-tune the responses provided by newly formed neurons.[6]

Neurogenesis in neural repair

Neurogenesis in the adult brain is often associated with diseases that deteriorate the CNS, like

presenilin 1, MAPT (microtubule associated protein tau) and huntingtin are also often associated with plasticity in the brain and its modification.[8] Neuroplasticity is associated with neurogenesis in a complementary fashion. The new neurons generated by the neuroepithelial cells, progenitors and radial glial cells will not survive unless they are able to integrate into the system by making connections with new neighbors. This also leads to many controversial concepts, like neurogenic therapy involving the transplant of local progenitor cells to a damaged area.[7]

Associated diseases

Dysembryoplastic neuroepithelial tumor (DNT)

Dysembryoplastic neuroepithelial tumor

A

invasive surgery and the patients are usually capable of recovering fully, with little to no long-term effects.[9]

Neuroepithelial cysts

Neuroepithelial cysts, also known as colloid cysts, develop in individuals between the ages of 20 and 50 and is relatively rare in individuals under the age of twenty. The cysts are benign tumors that usually appear in the anterior third ventricle. The cysts occur in the epithelium putting their patients at risk for obstructive hydrocephalus, increased intracranial pressure, and rarely intracystic hemorrhage. This results from the cysts enlarging by causing the epithelium to secrete additional mucinous fluid. The cysts are usually found incidentally or if patients become symptomatic presenting with the symptoms of hydrocephalus. The larger cysts are operated on while smaller cysts that are not obstructive can be left alone.[10]

Oligodendroglial tumors

cerebral spinal fluid resulting in swelling around the tumor. The location of the tumor may also affect the symptoms since frontal lobe tumors can cause gradual mood or personality changes while temporal lobe tumors result in coordination and speech problems.[11]

Ongoing research

Neural chimeras

Researchers have been able to create neural

embryonic stem cells. These neural chimeras give researchers a comprehensive way of studying the molecular mechanisms behind cell repair and regeneration via neuroepithelial precursor cells and will hopefully shed light on possible nervous system repair in a clinical setting. In an attempt to identify the key features that differentiate neuroepithelial cells from their progenitor cells, researchers identified an intermediate filament that was expressed by 98% of the neuroepithelial cells of the neural tube, but none of their progenitor cells. After this discovery it became clear that all three cell types in the nervous system resulted from a homogenous population of stem cells. In order make clinical neural repair possible researchers needed to further characterize regional determination of stem cells during brain development by determining what factors commit a precursor to becoming one or the other. While the exact factors that lead to differentiation are unknown, researchers have taken advantage of human-rat neural chimeras to explore the development of human neurons and glial cells in an animal model. These neural chimeras have permitted researchers to look at neurological diseases in an animal model where traumatic and reactive changes can be controlled. Eventually researchers hope to be able to use the information taken from these neural chimera experiments to repair regions of the brain affected by central nervous system disorders. The problem of delivery, however, has still not been resolved as neural chimeras have been shown to circulate throughout the ventricles and incorporate into all parts of the CNS. By finding environmental cues of differentiation, neuroepithelial precursor transplantation could be used in the treatment of many diseases including multiple sclerosis, Huntington's disease, and Parkinson's disease. Further exploration of neural chimera cells and chimeric brains will provide evidence for manipulating the correct genes and increasing the efficacy of neural transplant repair.[12]

Depression

Research on depression indicates that one of the major causal factors of depression, stress, also influences neurogenesis. This connection led researches to postulate that depression could be the result of changes in levels of neurogenesis in the adult brain, specifically in the dentate gyrus. Studies indicate that stress affects neurogenesis by increasing Glucocorticoids and decreasing neurotransmitters such as serotonin. These effects were further verified by inducing stress in lab animals, which resulted in decreased levels of neurogenesis. Additionally, modern therapies that treat depression also promote neurogenesis. Ongoing research is looking to further verify this connection and define the mechanism by which it occurs. This could potentially lead to a better understanding of the development of depression as well as future methods of treatment.[13]

See also

References

  1. ^ .
  2. ^ . Retrieved 7 December 2011.
  3. ^ .
  4. ^ .
  5. .
  6. .
  7. ^ .
  8. . Retrieved 2011-11-28.
  9. ^ "Dysembryoplastic Neuroepithelial Tumor". Children's Hospital Boston. Archived from the original on 26 September 2011. Retrieved 1 November 2011.
  10. ^ Chin, L. S.; Jayarao, M. "Colloid Cysts". Medscape. Retrieved 7 December 2011.
  11. ^ "Oligodendroglioma". Macmillan. Retrieved 7 December 2011.
  12. S2CID 14847541
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  13. .

External links