cortical progenitor
Recently Published Documents


TOTAL DOCUMENTS

60
(FIVE YEARS 13)

H-INDEX

24
(FIVE YEARS 3)

2022 ◽  
Vol 8 (2) ◽  
Author(s):  
Kaviya Chinnappa ◽  
Adrián Cárdenas ◽  
Anna Prieto-Colomina ◽  
Ana Villalba ◽  
Ángel Márquez-Galera ◽  
...  

Expression of miR-3607 in embryonic mammalian cerebral cortex was lost in rodents, limiting progenitor cell proliferation.


2021 ◽  
Author(s):  
◽  
Timothy John Sargeant

<p>Opiate drugs, such as codeine, morphine and heroin are powerful analgesics and drugs of abuse. The unborn child is invariably exposed to opiate drugs as a consequence of maternal use. Studies that have investigated the impact of opiate drugs demonstrated opioid system expression in proliferating regions of the developing brain, as well as on proliferative astroglia taken from the developing central nervous system. The effects of opiates on astroglial proliferation (largely mediated by the mu opioid receptor) are predominantly inhibitory, but are extremely context dependent. This context dependency exists because of the complexity resident within the opioid signalling system. However, since this previous research was conducted, there has been impressive progress made in the field of developmental neurobiology with the demonstration that cells of astrocytic lineage are responsible for the generation of the central nervous system. It was therefore the aim of the current research project to investigate the developmental impact of opiate exposure in the context of the foetal mouse cerebral cortex. This aim was divided into 3 separate aims that comprised of; determining the cellular localisation of the mu opioid receptor, the effects of opiate exposure on cortical progenitor cells, and to determine the effect of opiate exposure on the development of the cerebral cortex itself. The mu opioid receptor was expressed on proliferative radial glia of both the embryonic day 15.5 (neurogenic) and embryonic day 18.5 (gliogenic) ventricular zone of the dorsal forebrain. Interestingly and significantly, the mu opioid receptor-positive glia observed in the embryonic day 18.5 mouse forebrain were also observed at a comparable developmental stage in the foetal human forebrain. Morphine exposure slowed down G2 phase of the cell cycle at embryonic day 15.5 in the neurogenic murine cortical ventricular zone. This opiate-induced slowing in cell cycle progression was shown not to impact on proliferation in the ventricular zone, although future research should address whether this perturbation altered differentiation or developmental maturation of the radial glia. Morphine exposure throughout corticogenesis decreased levels of doublecortin expression (a migratory neuronal marker) at the end of gestation. Postnatally, mice exposed to morphine during corticogenesis also showed decreased numbers of neurons in layer V of the cerebral cortex. Collectively, this thesis presents the first evidence that shows morphine affects cortical progenitor cells in vivo. This research supports the possibility that the opioid system plays an endogenous role in corticogenesis. The clinical significance is morphine has the potential to perturb normal development of the cerebral cortex.</p>


2021 ◽  
Author(s):  
◽  
Timothy John Sargeant

<p>Opiate drugs, such as codeine, morphine and heroin are powerful analgesics and drugs of abuse. The unborn child is invariably exposed to opiate drugs as a consequence of maternal use. Studies that have investigated the impact of opiate drugs demonstrated opioid system expression in proliferating regions of the developing brain, as well as on proliferative astroglia taken from the developing central nervous system. The effects of opiates on astroglial proliferation (largely mediated by the mu opioid receptor) are predominantly inhibitory, but are extremely context dependent. This context dependency exists because of the complexity resident within the opioid signalling system. However, since this previous research was conducted, there has been impressive progress made in the field of developmental neurobiology with the demonstration that cells of astrocytic lineage are responsible for the generation of the central nervous system. It was therefore the aim of the current research project to investigate the developmental impact of opiate exposure in the context of the foetal mouse cerebral cortex. This aim was divided into 3 separate aims that comprised of; determining the cellular localisation of the mu opioid receptor, the effects of opiate exposure on cortical progenitor cells, and to determine the effect of opiate exposure on the development of the cerebral cortex itself. The mu opioid receptor was expressed on proliferative radial glia of both the embryonic day 15.5 (neurogenic) and embryonic day 18.5 (gliogenic) ventricular zone of the dorsal forebrain. Interestingly and significantly, the mu opioid receptor-positive glia observed in the embryonic day 18.5 mouse forebrain were also observed at a comparable developmental stage in the foetal human forebrain. Morphine exposure slowed down G2 phase of the cell cycle at embryonic day 15.5 in the neurogenic murine cortical ventricular zone. This opiate-induced slowing in cell cycle progression was shown not to impact on proliferation in the ventricular zone, although future research should address whether this perturbation altered differentiation or developmental maturation of the radial glia. Morphine exposure throughout corticogenesis decreased levels of doublecortin expression (a migratory neuronal marker) at the end of gestation. Postnatally, mice exposed to morphine during corticogenesis also showed decreased numbers of neurons in layer V of the cerebral cortex. Collectively, this thesis presents the first evidence that shows morphine affects cortical progenitor cells in vivo. This research supports the possibility that the opioid system plays an endogenous role in corticogenesis. The clinical significance is morphine has the potential to perturb normal development of the cerebral cortex.</p>


2021 ◽  
pp. JN-RM-0226-21
Author(s):  
Suranjana Pal ◽  
Deepanjali Dwivedi ◽  
Tuli Pramanik ◽  
Geeta Godbole ◽  
Takuji Iwasato ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1209
Author(s):  
Michael Heide ◽  
Wieland B. Huttner

Over the past few years, human-specific genes have received increasing attention as potential major contributors responsible for the 3-fold difference in brain size between human and chimpanzee. Accordingly, mutations affecting these genes may lead to a reduction in human brain size and therefore, may cause or contribute to microcephaly. In this review, we will concentrate, within the brain, on the cerebral cortex, the seat of our higher cognitive abilities, and focus on the human-specific gene ARHGAP11B and on the gene family comprising the three human-specific genes NOTCH2NLA, -B, and -C. These genes are thought to have significantly contributed to the expansion of the cerebral cortex during human evolution. We will summarize the evolution of these genes, as well as their expression and functional role during human cortical development, and discuss their potential relevance for microcephaly. Furthermore, we will give an overview of other human-specific genes that are expressed during fetal human cortical development. We will discuss the potential involvement of these genes in microcephaly and how these genes could be studied functionally to identify a possible role in microcephaly.


2020 ◽  
Author(s):  
Suranjana Pal ◽  
Deepanjali Dwivedi ◽  
Tuli Pramanik ◽  
Geeta Godbole ◽  
Takuji Iwasato ◽  
...  

AbstractThe cortical subplate is critical in regulating the entry of thalamocortical sensory afferents into the cortex. These afferents reach the subplate at embryonic day (E)15.5 in the mouse, but “wait” for several days, entering the cortical plate postnatally. We report that when transcription factor Lhx2 is lost in E11.5 cortical progenitors, which give rise to subplate neurons, thalamocortical afferents display premature, exuberant innervation of the E15.5 cortex. Embryonic mutant subplate neurons are correctly positioned below the cortical plate, but they display an altered transcriptome and immature electrophysiological properties during the waiting period. The sensory thalamus in these cortex-specific Lhx2 mutants displays atrophy, eventually leading to severe deficits in thalamocortical innervation. Strikingly, these phenotypes do not manifest if Lhx2 is lost in postmitotic subplate neurons. These results demonstrate a mechanism operating in subplate progenitors that has profound consequences on the growth of thalamocortical axons into the cortex.


2020 ◽  
Author(s):  
Sisu Han ◽  
Grey A Wilkinson ◽  
Satoshi Okawa ◽  
Lata Adnani ◽  
Rajiv Dixit ◽  
...  

SUMMARYTransition from smooth, lissencephalic brains to highly-folded, gyrencephalic structures is associated with neuronal expansion and breaks in neurogenic symmetry. Here we show that Neurog2 and Ascl1 proneural genes regulate cortical progenitor cell differentiation through cross-repressive interactions to sustain neurogenic continuity in a lissencephalic rodent brain. Using in vivo lineage tracing, we found that Neurog2 and Ascl1 expression defines a lineage continuum of four progenitor pools, with ‘double+ progenitors’ displaying several unique features (least lineage-restricted, complex gene regulatory network, G2 pausing). Strikingly, selective killing of double+ progenitors using split-Cre;Rosa-DTA transgenics breaks neurogenic symmetry by locally disrupting Notch signaling, leading to cortical folding. Finally, consistent with NEUROG2 and ASCL1 driving discontinuous neurogenesis and folding in gyrencephalic species, their transcripts are modular in folded macaque cortices and pseudo-folded human cerebral organoids. Neurog2/Ascl1 double+ progenitors are thus Notch-ligand expressing ‘niche’ cells that control neurogenic periodicity to determine cortical gyrification.HIGHLIGHTSNeurog2 and Ascl1 expression defines four distinct transitional progenitor statesDouble+ NPCs are transcriptionally complex and mark a lineage branch pointDouble+ NPCs control neurogenic patterning and cortical folding via Notch signalingNeurog2 and Ascl1 expression is modular in folded and not lissencephalic corticeseTOC BLURBEmergence of a gyrencephalic cortex is associated with a break in neurogenic continuity across the cortical germinal zone. Han et al. identify a pool of unbiased neural progenitors at a lineage bifurcation point that co-express Neurog2 and Ascl1 and produce Notch ligands to control neurogenic periodicity and cortical folding.


2020 ◽  
Vol 117 (26) ◽  
pp. 15221-15229 ◽  
Author(s):  
Setsuko Sahara ◽  
Takashi Kodama ◽  
Charles F. Stevens

The balance between proliferation and differentiation of stem cells and progenitors determines the size of an adult brain region. While the molecular mechanisms regulating proliferation and differentiation of cortical progenitors have been intensively studied, an analysis of the kinetics of progenitor choice between self-renewal and differentiation in vivo is, due to the technical difficulties, still unknown. Here we established a descriptive mathematical model to estimate the probability of self-renewal or differentiation of cortical progenitor behaviors in vivo, a variable we have termed the expansion coefficient. We have applied the model, one which depends only on experimentally measured parameters, to the developing mouse cortex where the expansive neuroepithelial cells and neurogenic radial glial progenitors are coexisting. Surprisingly, we found that the expansion coefficients of both neuroepithelium cells and radial glial progenitors follow the same developmental trajectory during cortical development, suggesting a common rule governing self-renewal/differentiation behaviors in mouse cortical progenitor differentiation.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Daniel W. Hagey ◽  
Danijal Topcic ◽  
Nigel Kee ◽  
Florie Reynaud ◽  
Maria Bergsland ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document