Neural System - Glial Development - Revision history

Z8600021 at 00:40, 21 February 2020

2020-02-21T00:40:55Z

← Older revision		Revision as of 11:40, 21 February 2020
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	In human development, microglia are present in the extracerebral mesenchyme at 4.5 weeks, invade the parenchyma during week 5, and can then be identified at several different neural locations.{{#pmid:17483694\|PMID17483694}}{{#pmid:20557401\|PMID20557401}}		In human development, microglia are present in the extracerebral mesenchyme at 4.5 weeks, invade the parenchyma during week 5, and can then be identified at several different neural locations.{{#pmid:17483694\|PMID17483694}}{{#pmid:20557401\|PMID20557401}}

	'''Microglia Developmental Location'''{{#pmid:17029271\|PMID17029271}{{#pmid:17483694\|PMID17483694}		'''Microglia Developmental Location'''{{#pmid:17029271\|PMID17029271}}{{#pmid:17483694\|PMID17483694}}
	* Dorsal to the {{diencephalon}}–{{telencephalon}} fissure (behind cephalic flexure)		* Dorsal to the {{diencephalon}}–{{telencephalon}} fissure (behind cephalic flexure)
	* At the level of the eminentia thalami, near the {{choroid plexus}}		* At the level of the eminentia thalami, near the {{choroid plexus}}

Z8600021 at 23:16, 4 February 2020

2020-02-04T23:16:35Z

← Older revision		Revision as of 10:16, 5 February 2020
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	~~'''Glia Types:'''~~ {{~~radial glia}} \| {{astroglia}} \| {{oligodendroglia}} \| {{microglia}} \| {{Schwann cell~~}}		{{Glia Links}}

Z8600021 at 00:00, 23 Ocak 2020

2020-01-23T00:00:41Z

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 Glial cells that act within the central nervous system in the same role as macrophages (Mϕ) in other body tissues and act as an innate immune system. There other role is as the cellular mediators of neuroinflammatory processes{{#pmid:15285801|PMID15285801}} and cell death{{#pmid:17106878|PMID17106878}}. Microglia have also been suggested as having a role during brain developmental synaptogenesis.{{#pmid:25823474|PMID25823474}}
-In human development, microglia are present in the extracerebral mesenchyme at 4.5 weeks and invade the parenchyma at about 5 weeks.{{#pmid:17483694|PMID17483694}}{{#pmid:20557401|PMID20557401}}
+===Human===
 In {{mouse}} development, microglia derive only from you sac progenitor cells migrating and then proliferating within the CNS.{{#pmid:10567732|PMID10567732}}{{#pmid:21951310|PMID21951310}}{{#pmid:31818979|PMID31818979}} Microglia differentiation requires The hematopoietic transcription factor [https://www.omim.org/entry/165170 PU.1] and interferon regulatory factor [https://www.omim.org/entry/601565 IRF8] pathways.{{#pmid:23334579|PMID23334579}}

Z8600021 at 23:40, 22 Ocak 2020

2020-01-22T23:40:32Z

← Older revision		Revision as of 10:40, 23 Ocak 2020
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	== Microglia ==		== Microglia ==

	Glial cells that act within the central nervous system in the same role as macrophages (Mϕ) in other body tissues and act as an innate immune system. There other role is as the cellular mediators of neuroinflammatory processes{{#pmid:15285801\|PMID15285801}} and cell death{{#pmid:17106878\|PMID17106878}}. ~~In the {{mouse}} embryo, these cells derive only from you sac progenitor cells migrating and then proliferating within the CNS~~.{{#pmid:~~10567732\|PMID10567732}}{{#pmid:21951310\|PMID21951310}}{{#pmid:31818979~~\|~~PMID31818979~~}}		Glial cells that act within the central nervous system in the same role as macrophages (Mϕ) in other body tissues and act as an innate immune system. There other role is as the cellular mediators of neuroinflammatory processes{{#pmid:15285801\|PMID15285801}} and cell death{{#pmid:17106878\|PMID17106878}}. Microglia have also been suggested as having a role during brain developmental synaptogenesis.{{#pmid:25823474\|PMID25823474}}

	~~Developmental cell differentiation requires The hematopoietic transcription factor [https://www.omim.org/entry/165170 PU~~.1] and ~~interferon regulatory factor [https://www.omim.org/entry/601565 IRF8] pathways~~.{{#pmid:}~~23334579~~\|~~PMID}23334579~~}}		In human development, microglia are present in the extracerebral mesenchyme at 4.5 weeks and invade the parenchyma at about 5 weeks.{{#pmid:17483694\|PMID17483694}}{{#pmid:20557401\|PMID20557401}}

			In {{mouse}} development, microglia derive only from you sac progenitor cells migrating and then proliferating within the CNS.{{#pmid:10567732\|PMID10567732}}{{#pmid:21951310\|PMID21951310}}{{#pmid:31818979\|PMID31818979}} Microglia differentiation requires The hematopoietic transcription factor [https://www.omim.org/entry/165170 PU.1] and interferon regulatory factor [https://www.omim.org/entry/601565 IRF8] pathways.{{#pmid:23334579\|PMID23334579}}

Z8600021 at 22:11, 22 Ocak 2020

2020-01-22T22:11:57Z

← Older revision		Revision as of 09:11, 23 Ocak 2020
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			* '''Convergence between microglia and peripheral macrophages phenotype during development and neuroinflammation'''{{#pmid:31818979\|PMID31818979}} "Differently, from other myeloid cells, {{microglia}} derive exclusively from precursors originating within the {{yolk sac}} (YS) and migrating to the central nervous system ({{CNS}}) under development, without any contribution from fetal liver or postnatal hematopoiesis. Consistent with their unique ontology, microglia may express specific physiological markers, which have been partly described in recent years. Here we wondered whether profiles distinguishing microglia from peripheral macrophages vary with age and under pathology. To this goal, we profiled transcriptomes of microglia throughout the lifespan and included a parallel comparison with peripheral macrophages under physiological and neuroinflammatory settings using age and sex-matched wild type and bone marrow chimera mouse models. This comprehensive approach demonstrated that the phenotypic differentiation between microglia and peripheral macrophages is age-dependent and that peripheral macrophages do express some of the most commonly described microglia-specific markers early during development, such as Fcrls, P2ry12, Tmem119, and Trem2. Further, during chronic neuroinflammation CNS-infiltrating macrophages and not peripheral myeloid cells acquire microglial markers, indicating that the CNS niche may instruct peripheral myeloid cells to gain the phenotype and, presumably, the function of the microglia cell. In conclusion, our data provide further evidence about the plasticity of the myeloid cell and suggest caution in the strict definition and application of microglia-specific markers.Significant StatementUnderstanding the respective role of microglia and infiltrating monocytes in neuroinflammatory conditions has recently seemed possible by the identification of a specific microglia signature. Here instead we provide evidence that peripheral macrophages may express some of the most commonly described microglia markers at some developmental stages or pathological conditions, in particular during chronic neuroinflammation. Further, our data support the hypothesis about phenotypic plasticity and convergence among distinct myeloid cells so that they may act as a functional unit rather than as different entities, boosting their mutual functions in different phases of disease."

	* '''Maternal {{viral infection}} causes global alterations in porcine fetal {{microglia}}'''{{#pmid:31527230\|PMID31527230}}} "Maternal infections during pregnancy are associated with increased risk of neurodevelopmental disorders, although the precise mechanisms remain to be elucidated. Previously, we established a maternal immune activation (MIA) model using swine, which results in altered social behaviors of {{pig}}let offspring. These behavioral abnormalities occurred in the absence of microglia priming. Thus, we examined fetal microglial activity during prenatal development in response to maternal infection with live porcine reproductive and respiratory syndrome virus. Fetuses were obtained by cesarean sections performed 7 and 21 d postinoculation (dpi). MIA fetuses had reduced brain weights at 21 dpi compared to controls. Furthermore, MIA microglia increased expression of major histocompatibility complex class II that was coupled with reduced phagocytic and chemotactic activity compared to controls. High-throughput gene-expression analysis of microglial-enriched genes involved in neurodevelopment, the microglia sensome, and inflammation revealed differential regulation in primary microglia and in whole amygdala tissue. Microglia density was increased in the fetal amygdala at 7 dpi. Our data also reveal widespread sexual dimorphisms in microglial gene expression and demonstrate that the consequences of MIA are sex dependent. Overall, these results indicate that fetal microglia are significantly altered by maternal viral infection, presenting a potential mechanism through which MIA impacts prenatal brain development and function."		* '''Maternal {{viral infection}} causes global alterations in porcine fetal {{microglia}}'''{{#pmid:31527230\|PMID31527230}}} "Maternal infections during pregnancy are associated with increased risk of neurodevelopmental disorders, although the precise mechanisms remain to be elucidated. Previously, we established a maternal immune activation (MIA) model using swine, which results in altered social behaviors of {{pig}}let offspring. These behavioral abnormalities occurred in the absence of microglia priming. Thus, we examined fetal microglial activity during prenatal development in response to maternal infection with live porcine reproductive and respiratory syndrome virus. Fetuses were obtained by cesarean sections performed 7 and 21 d postinoculation (dpi). MIA fetuses had reduced brain weights at 21 dpi compared to controls. Furthermore, MIA microglia increased expression of major histocompatibility complex class II that was coupled with reduced phagocytic and chemotactic activity compared to controls. High-throughput gene-expression analysis of microglial-enriched genes involved in neurodevelopment, the microglia sensome, and inflammation revealed differential regulation in primary microglia and in whole amygdala tissue. Microglia density was increased in the fetal amygdala at 7 dpi. Our data also reveal widespread sexual dimorphisms in microglial gene expression and demonstrate that the consequences of MIA are sex dependent. Overall, these results indicate that fetal microglia are significantly altered by maternal viral infection, presenting a potential mechanism through which MIA impacts prenatal brain development and function."

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	== Microglia ==		== Microglia ==

	Glial cells that act within the central nervous system in the same role as macrophages in other body tissues and act as an innate immune system. There other role is as the cellular mediators of neuroinflammatory processes{{#pmid:15285801\|PMID15285801}} and cell death{{#pmid:17106878\|PMID17106878}}. In the mouse embryo, these cells derive from you sac progenitor cells migrating and then proliferating within the CNS.{{#pmid:10567732\|PMID10567732}}{{#pmid:21951310\|PMID21951310}}		Glial cells that act within the central nervous system in the same role as macrophages (Mϕ) in other body tissues and act as an innate immune system. There other role is as the cellular mediators of neuroinflammatory processes{{#pmid:15285801\|PMID15285801}} and cell death{{#pmid:17106878\|PMID17106878}}. In the {{mouse}} embryo, these cells derive only from you sac progenitor cells migrating and then proliferating within the CNS.{{#pmid:10567732\|PMID10567732}}{{#pmid:21951310\|PMID21951310}}{{#pmid:31818979\|PMID31818979}}

			Developmental cell differentiation requires The hematopoietic transcription factor [https://www.omim.org/entry/165170 PU.1] and interferon regulatory factor [https://www.omim.org/entry/601565 IRF8] pathways.{{#pmid:}23334579\|PMID}23334579}}



			:Search PubMed: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Microglia+Development ''Microglia Development''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Microglia+Differentiation ''Microglia Differentiation'']
	== Schwann cells ==		== Schwann cells ==
	[[File:Schwann_cell_myelination_and_dedifferentiation.jpg\|thumb\|Schwann cell myelination and dedifferentiation{{#pmid:18490509\|PMID18490509}}]]		[[File:Schwann_cell_myelination_and_dedifferentiation.jpg\|thumb\|Schwann cell myelination and dedifferentiation{{#pmid:18490509\|PMID18490509}}]]

Z8600021 at 22:42, 19 November 2019

2019-11-19T22:42:41Z

← Older revision		Revision as of 09:42, 20 November 2019
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			* '''Maternal {{viral infection}} causes global alterations in porcine fetal {{microglia}}'''{{#pmid:31527230\|PMID31527230}}} "Maternal infections during pregnancy are associated with increased risk of neurodevelopmental disorders, although the precise mechanisms remain to be elucidated. Previously, we established a maternal immune activation (MIA) model using swine, which results in altered social behaviors of {{pig}}let offspring. These behavioral abnormalities occurred in the absence of microglia priming. Thus, we examined fetal microglial activity during prenatal development in response to maternal infection with live porcine reproductive and respiratory syndrome virus. Fetuses were obtained by cesarean sections performed 7 and 21 d postinoculation (dpi). MIA fetuses had reduced brain weights at 21 dpi compared to controls. Furthermore, MIA microglia increased expression of major histocompatibility complex class II that was coupled with reduced phagocytic and chemotactic activity compared to controls. High-throughput gene-expression analysis of microglial-enriched genes involved in neurodevelopment, the microglia sensome, and inflammation revealed differential regulation in primary microglia and in whole amygdala tissue. Microglia density was increased in the fetal amygdala at 7 dpi. Our data also reveal widespread sexual dimorphisms in microglial gene expression and demonstrate that the consequences of MIA are sex dependent. Overall, these results indicate that fetal microglia are significantly altered by maternal viral infection, presenting a potential mechanism through which MIA impacts prenatal brain development and function."

	* '''Strong sonic hedgehog signaling in the mouse ventral spinal cord is not required for oligodendrocyte precursor cell (OPC) generation but is necessary for correct timing of its generation'''{{#pmid:29122585\|PMID29122585}} "In the mouse neural tube, {{sonic hedgehog}} (Shh) secreted from the floor plate (FP) and the {{notochord}} (NC) regulates ventral patterning of the neural tube, and later is essential for the generation of oligodendrocyte precursor cells (OPCs). During early development, the NC is adjacent to the neural tube and induces ventral domains in it, including the FP. In the later stage of development, during gliogenesis in the spinal cord, the pMN domain receives strong Shh signaling input. While this is considered to be essential for the generation of OPCs, the actual role of this strong input in OPC generation remains unclear. Here we studied OPC generation in bromi mutant mice which show abnormal ciliary structure. ...The number of OPCs was also significantly decreased in the {{ME12.5}} and {{ME14.5}} bromi mutant spinal cord. In contrast, motor neuron (MN) production, detected by HB9 expression, significantly increased. It is likely that the transition from MN production to OPC generation in the pMN domain is impaired in bromi mutant mice. These results suggest that strong Shh input to the pMN domain is not required for OPC generation but is essential for producing a sufficient number of OPCs."		* '''Strong sonic hedgehog signaling in the mouse ventral spinal cord is not required for oligodendrocyte precursor cell (OPC) generation but is necessary for correct timing of its generation'''{{#pmid:29122585\|PMID29122585}} "In the mouse neural tube, {{sonic hedgehog}} (Shh) secreted from the floor plate (FP) and the {{notochord}} (NC) regulates ventral patterning of the neural tube, and later is essential for the generation of oligodendrocyte precursor cells (OPCs). During early development, the NC is adjacent to the neural tube and induces ventral domains in it, including the FP. In the later stage of development, during gliogenesis in the spinal cord, the pMN domain receives strong Shh signaling input. While this is considered to be essential for the generation of OPCs, the actual role of this strong input in OPC generation remains unclear. Here we studied OPC generation in bromi mutant mice which show abnormal ciliary structure. ...The number of OPCs was also significantly decreased in the {{ME12.5}} and {{ME14.5}} bromi mutant spinal cord. In contrast, motor neuron (MN) production, detected by HB9 expression, significantly increased. It is likely that the transition from MN production to OPC generation in the pMN domain is impaired in bromi mutant mice. These results suggest that strong Shh input to the pMN domain is not required for OPC generation but is essential for producing a sufficient number of OPCs."

Z8600021 at 21:55, 25 Mayıs 2019

2019-05-25T21:55:39Z

← Older revision		Revision as of 08:55, 26 Mayıs 2019
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	Myelination is the process of close wrapping around a neural axon by a glial cell. This second process occurs as a late feature of glial and nervous system development in both the central and peripheral nervous system and has mainly been studied in relation to demyelinating diseases, such as multiple sclerosis.		Myelination is the process of close wrapping around a neural axon by a glial cell. This second process occurs as a late feature of glial and nervous system development in both the central and peripheral nervous system and has mainly been studied in relation to demyelinating diseases, such as {{multiple sclerosis}}.


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	Only humans spontaneously develop multiple sclerosis (MS){{#pmid:29492266\|PMID29492266}}, a chronic demyelinating immune-mediated disease. This disease has an onset generally coinciding with the end of the long-term myelination process{{#pmid:28817797\|PMID28817797}} and incidence has been recently increasing in female/male (F/M) ratio and occurring in women of childbearing age. {{#pmid:23133550\|PMID23133550}}		Only humans spontaneously develop multiple sclerosis (MS){{#pmid:29492266\|PMID29492266}}, a chronic demyelinating immune-mediated disease. This disease has an onset generally coinciding with the end of the long-term myelination process{{#pmid:28817797\|PMID28817797}} and incidence has been recently increasing in female/male (F/M) ratio and occurring in women of childbearing age. {{#pmid:23133550\|PMID23133550}}

			Search Pubmed: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Multiple+Sclerosis ''Multiple Sclerosis'']

	===Experimental Autoimmune Encephalomyelitis===		===Experimental Autoimmune Encephalomyelitis===

Z8600021 at 21:51, 25 Mayıs 2019

2019-05-25T21:51:43Z

← Older revision		Revision as of 08:51, 26 Mayıs 2019
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	== Abnormalities==		== Abnormalities==
	===Multiple Sclerosis===		===Multiple Sclerosis===
	* '''Activation of the subventricular zone in multiple sclerosis~~: evidence for early glial progenitors.'''~~{{#pmid:~~17360586~~\|~~PMID17360586~~}}~~"In multiple sclerosis (MS)~~, ~~oligodendrocyte and myelin destruction lead to demyelination with subsequent axonal loss~~. ~~Experimental demyelination in rodents~~ has ~~highlighted~~ the ~~activation~~ of the ~~subventricular zone~~ (~~SVZ~~) and ~~the involvement of progenitor cells expressing the polysialylated form~~ of ~~neural cell adhesion molecule (PSA-NCAM) in the repair process~~."
			Only humans spontaneously develop multiple sclerosis (MS){{#pmid:29492266\|PMID29492266}}, a chronic demyelinating immune-mediated disease. This disease has an onset generally coinciding with the end of the long-term myelination process{{#pmid:28817797\|PMID28817797}} and incidence has been recently increasing in female/male (F/M) ratio and occurring in women of childbearing age. {{#pmid:23133550\|PMID23133550}}



	===Experimental Autoimmune Encephalomyelitis===		===Experimental Autoimmune Encephalomyelitis===

Z8600021 at 21:37, 25 Mayıs 2019

2019-05-25T21:37:03Z

← Older revision		Revision as of 08:37, 26 Mayıs 2019
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	==Introduction==		==Introduction==
	[[File:Neural-development.jpg\|thumb\|300px\|alt=Neural Development timeline\|Neural Development]]		[[File:Neural-development.jpg\|thumb\|300px\|alt=Neural Development timeline\|Neural Development]]
	The term {{gliogenesis}} refers to the development of the many different types of glial cells within the developing and adult nervous ~~system~~ (CNS and PNS) including: radial glia, astrocytes, oligodendrocytes, Schwann cells, and microglia. Within the neural ~~tube~~ stem cells generate ~~the 2 major classes of cells that make the majority of the nervous system: neurons~~ and most ~~CNS glia. Both these classes~~ of cells ~~differentiate into many~~ different ~~types generated with highly specialized functions and shapes~~.		The term {{gliogenesis}} refers to the development of the many different types of glial cells within the developing and adult central and peripheral nervous systems (CNS and PNS) including: radial glia, astrocytes, oligodendrocytes, Schwann cells, and microglia. Within the CNS the neural stem cells generate firstly neutrons and then most of the central gila cells. Note that PNS {{Schwann cell}}s have a different embryonic origin ({{neural crest}}).


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	'''Glia Types:''' {{radial glia}} \| {{astroglia}} \| {{oligodendroglia}} \| {{microglia}} \| {{Schwann cell}} ~~[[#Radial Glia\|radial glia]], [[#Astroglia\|astroglia]], [[#Oligodendroglia\|oligodendroglia]], [[#Microglia\|microglia]] and [[#Schwann cell\|Schwann cells]].~~		'''Glia Types:''' {{radial glia}} \| {{astroglia}} \| {{oligodendroglia}} \| {{microglia}} \| {{Schwann cell}}

Z8600021 at 11:47, 29 Ocak 2019

2019-01-29T11:47:00Z

← Older revision		Revision as of 22:47, 29 Ocak 2019
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	===Reviews===		===Reviews===
	{{#pmid:30309946}}		{{#pmid:30309946}}

			{{#pmid:30309945}}

	{{#pmid:16314867}}		{{#pmid:16314867}}