The migrational patterns and developmental fates of glial precursors in the rat subventricular zone are temporally regulated

Development ◽  
1993 ◽  
Vol 119 (3) ◽  
pp. 611-622 ◽  
Author(s):  
S.W. Levison ◽  
C. Chuang ◽  
B.J. Abramson ◽  
J.E. Goldman
Keyword(s):  
White Matter ◽  
Subventricular Zone ◽  
Subcortical White Matter ◽  
Contralateral Hemisphere ◽  
Environmental Signals ◽  
Germinal Zone ◽  
Glial Progenitors ◽  
Migratory Patterns

Postnatal gliogenesis in the rodent forebrain was studied by infecting subventricular zone cells of either neonates or juvenile rats with replication-deficient retroviruses that encode reporter enzymes, enabling the migration and fate of these germinal zone cells to be traced over the ensuing several weeks. Neither neonatal nor juvenile subventricular zone cells migrated substantially along the rostral-caudal axis. Neonatal subventricular zone cells migrated dorsally and laterally into hemispheric gray and white matter and became both astrocytes and oligodendrocytes. Juvenile subventricular zone cells migrated into more medial areas of the subcortical white matter and on occasion appeared in the white matter of the contralateral hemisphere, but rarely migrated into the neocortex. Juvenile subventricular zone cells almost exclusively differentiated into oligodendrocytes. Thus, the migratory patterns and the developmental fates of subventricular zone cells change during the first 2 weeks of life. When either neonatal or juvenile subventricular zone cells were labeled in vivo and then removed and cultured, some generated homogeneous clones that contained either astrocytes with a ‘type 1′ phenotype or oligodendrocytes, but some generated heterogeneous clones that contained both glial types. These results provide additional evidence for a common progenitor for astrocytes and oligodendrocytes and strongly suggest that temporally and spatially regulated environmental signals control the destiny of glial progenitors during postnatal development.

What Has Direct Cortical and Subcortical Electrostimulation Taught Us about Neurolinguistics?

2019 ◽  
pp. 185-211
Author(s):  
Hugues Duffau
Keyword(s):  
White Matter ◽  
Large Scale ◽  
Functional Neuroimaging ◽  
Great Accuracy ◽  
Subcortical White Matter ◽  
Cerebral Lesions ◽  
Physiological Basis ◽  
Postoperative Mri ◽  
The Brain

Investigating the neural and physiological basis of language is one of the most important challenges in neurosciences. Direct electrical stimulation (DES), usually performed in awake patients during surgery for cerebral lesions, is a reliable tool for detecting both cortical and subcortical (white matter and deep grey nuclei) regions crucial for cognitive functions, especially language. DES transiently interacts locally with a small cortical or axonal site, but also nonlocally, as the focal perturbation will disrupt the entire subnetwork sustaining a given function. Thus, in contrast to functional neuroimaging, DES represents a unique opportunity to identify with great accuracy and reproducibility, in vivo in humans, the structures that are actually indispensable to the function, by inducing a transient virtual lesion based on the inhibition of a subcircuit lasting a few seconds. Currently, this is the sole technique that is able to directly investigate the functional role of white matter tracts in humans. Thus, combining transient disturbances elicited by DES with the anatomical data provided by pre- and postoperative MRI enables to achieve reliable anatomo-functional correlations, supporting a network organization of the brain, and leading to the reappraisal of models of language representation. Finally, combining serial peri-operative functional neuroimaging and online intraoperative DES allows the study of mechanisms underlying neuroplasticity. This chapter critically reviews the basic principles of DES, its advantages and limitations, and what DES can reveal about the neural foundations of language, that is, the large-scale distribution of language areas in the brain, their connectivity, and their ability to reorganize.

scholarly journals The Lipid Peroxidation By-product 4-Hydroxynonenal is Toxic to Axons and Oligodendrocytes

2000 ◽  
Vol 20 (11) ◽  
pp. 1529-1536 ◽  
Author(s):  
Eileen McCracken ◽  
V. Valeriani ◽  
C. Simpson ◽  
T. Jover ◽  
James McCulloch ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
White Matter ◽  
Injection Site ◽  
Subcortical White Matter ◽  
Intracerebral Injection ◽  
Dependent Manner ◽  
Concentration Dependent Manner

Lipid peroxidation and the cytotoxic by-product 4-hydroxynonenal (4-HNE) have been implicated in neuronal perikaryal damage. This study sought to determine whether 4-HNE was involved in white matter damage in vivo and in vitro. Immunohistochemical studies detected an increase in cellular and axonal 4-HNE within the ischemic region in the rat after a 24-hour period of permanent middle cerebral artery occlusion. Exogenous 4-HNE (3.2 nmol) was stereotaxically injected into the subcortical white matter of rats that were killed 24 hours later. Damaged axons detected by accumulation of β-amyloid precursor protein (β-APP) were observed transversing medially and laterally away from the injection site after intracerebral injection of 4-HNE. In contrast, in the vehicle-treated animals, axonal damage was restricted to an area immediately surrounding the injection site. Exogenous 4-HNE produced oligodendrocyte cell death in culture in a time-dependent and a concentration-dependent manner. After 4 hours, the highest concentration of 4-HNE (50 μmol/L) produced 100% oligodendrocyte cell death. Data indicate that lipid peroxidation and production of 4-HNE occurs in white matter after cerebral ischemia and the lipid peroxidation by-product 4-HNE is toxic to axons and oligodendrocytes.

Patient-derived glial enriched progenitors repair functional deficits due to white matter stroke and vascular dementia in rodents

2021 ◽  
Vol 13 (590) ◽  
pp. eaaz6747
Author(s):  
Irene L. Llorente ◽  
Yuan Xie ◽  
Jose A. Mazzitelli ◽  
Emily A. Hatanaka ◽  
Jessica Cinkornpumin ◽  
...  
Keyword(s):  
White Matter ◽  
Neural Progenitor Cells ◽  
Scale Up ◽  
Hypoxia Inducible Factor ◽  
Cell Types ◽  
Experimental Manipulation ◽  
Subcortical White Matter ◽  
Repair Activity ◽  
Induced Pluripotent

Subcortical white matter stroke (WMS) accounts for up to 30% of all stroke events. WMS damages primarily astrocytes, axons, oligodendrocytes, and myelin. We hypothesized that a therapeutic intervention targeting astrocytes would be ideally suited for brain repair after WMS. We characterize the cellular properties and in vivo tissue repair activity of glial enriched progenitor (GEP) cells differentiated from human-induced pluripotent stem cells, termed hiPSC-derived GEPs (hiPSC-GEPs). hiPSC-GEPs are derived from hiPSC–neural progenitor cells via an experimental manipulation of hypoxia inducible factor activity by brief treatment with a prolyl hydroxylase inhibitor, deferoxamine. This treatment permanently biases these cells to further differentiate toward an astrocyte fate. hiPSC-GEPs transplanted into the brain in the subacute period after WMS in mice migrated widely, matured into astrocytes with a prorepair phenotype, induced endogenous oligodendrocyte precursor proliferation and remyelination, and promoted axonal sprouting. hiPSC-GEPs enhanced motor and cognitive recovery compared to other hiPSC-differentiated cell types. This approach establishes an hiPSC-derived product with easy scale-up capabilities that might be effective for treating WMS.

scholarly journals Adenosine in Relation to Calcium Homeostasis: Comparison between Gray and White Matter Ischemia

2001 ◽  
Vol 21 (5) ◽  
pp. 503-510 ◽  
Author(s):  
Christian Dohmen ◽  
Eiji Kumura ◽  
Gerd Rosner ◽  
Wolf-Dieter Heiss ◽  
Rudolf Graf
Keyword(s):  
White Matter ◽  
Gray Matter ◽  
Calcium Influx ◽  
Subcortical White Matter ◽  
Extracellular Calcium ◽  
Protective Agent ◽  
Gamma Aminobutyric Acid ◽  
Global Brain Ischemia

In vitro studies suggest that adenosine may attenuate anoxic white matter damage as an intrinsic protective substance. The authors investigated ischemic alterations of purines in relation to tissue depolarization and extracellular calcium and amino acid concentrations in vivo using microdialysis and ion-selective electrodes in cortical gray and subcortical white matter of 10 cats during 120 minutes of global brain ischemia. Immediately on induction of ischemia, regional cerebral blood flow ceased in all cats in both gray and white matter. The direct current potential rapidly decreased, the decline being slower and shallower in white matter. Extracellular calcium levels decreased in gray matter. In contrast, they first increased in white matter and started to decrease below control levels only after approximately 30 minutes. Adenosine levels transiently increased in both tissue compartments; the peak was delayed by 30 minutes in white matter. Thereafter, levels declined faster in gray than in white matter and remained elevated in the latter tissue compartment. Inosine and hypoxanthine elevations were progressive in both regions but smaller in white matter. Levels of gamma-aminobutyric acid, another putatively protective agent, steadily increased, starting immediately in gray matter and delayed by almost 1 hour in white matter. The delayed and prolonged accumulation of adenosine correlates with a slower adenosine triphosphate breakdown in white matter ischemia and may result in protection of white matter by suspending cellular calcium influx.

scholarly journals Restricted Migration of Transplanted Oligodendrocytes or their Progenitors, Revealed by Transgenic Marker MβP

1993 ◽  
Vol 4 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Victor L. Friedrich, Jr. ◽  
Robert A. Lazzarini
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Transgenic Mice ◽  
Subventricular Zone ◽  
Normal Development ◽  
Subcortical White Matter ◽  
Host Tissue ◽  
Marker Enzyme ◽  
Wild Type ◽  
Transplantation Experiments

Transgenic mice of line MβP3 express bacterial β-galactosidase in oligodendrocytes but not other cells of the CNS. The marker enzyme, demonstrated histochemically or by immunostaining in oligodendrocyte cell bodies and along myelin internodes, appears at the time of myelination and persists thereafter; in transplantation experiments, the marker may serve to indicate both the source of particular cells and their state of differentiation. The subventricular zone of the lateral ventricle, grafted from transgenic to wild-type perinatal recipient mice, yields histochemically labeled oligodendrocytes in surrounding host tissue. When grafts are placed in cerebral cortex near callosal radiations, graft-derived oligodendrocytes are found in cerebral cortex and subcortical white matter as far as 1.5 mm from the site of implant but not in nearby caudoputamen. This study is the first to document differentiation of transplant-derived oligodendrocytes in normal developing CNS. Our results are consistent with the well- established notion that oligodendrocyte progenitors migrate during normal development and suggest that such migration might be guided or restricted by mechanisms yet to be identified.

scholarly journals Glial cells in the rat optic nerve and some thoughts on remyelination in the mammalian CNS

1987 ◽  
Vol 132 (1) ◽  
pp. 35-41
Author(s):  
M. C. Raff ◽  
C. Ffrench-Constant ◽  
R. H. Miller
Keyword(s):  
White Matter ◽  
Optic Nerve ◽  
Progenitor Cells ◽  
White Matter Tracts ◽  
Optic Stalk ◽  
Environmental Signals ◽  
The Past ◽  
Neuroepithelial Cells

Studies on the rat optic nerve in the past 5 years have produced two surprises. First, they demonstrated that there are two biochemically, developmentally and functionally distinct types of astrocytes in the optic nerve, and probably in white matter tracts throughout the CNS: one seems to be responsible for inducing endothelial cells to form the blood-brain barrier while the other seems to service nodes of Ranvier. Second, they showed that oligodendrocytes and type-2 astrocytes develop from a common bipotential (O-2A) progenitor cell that seems to migrate into the developing optic nerve, and may well migrate all over the CNS to wherever myelination is required; this implies that the neuroepithelial cells of the optic stalk are restricted to forming type-1 astrocytes. Some of the findings in the optic nerve may be relevant to the problem of CNS regeneration after injury. These include the following. (1) Reactive gliosis in white matter tracts seems to be mainly a function of type-1 astrocytes. (2) Proliferating O-2A progenitor cells are present in the adult CNS, raising the possibility that they may be able to produce new oligodendrocytes and type-2 astrocytes following injury and thereby aid regeneration. (3) Type-1 astrocytes seem to be able to respond to environmental signals and form localized barriers that block the migration of O-2A progenitor cells; it is conceivable that the same barriers block the migration of regenerating axonal growth cones.

scholarly journals Breakdown of Calcium Homeostasis in Relation to Tissue Depolarization: Comparison between Gray and White Matter Ischemia

1999 ◽  
Vol 19 (7) ◽  
pp. 788-793 ◽  
Author(s):  
E. Kumura ◽  
R. Graf ◽  
C. Dohmen ◽  
G. Rosner ◽  
W. D. Heiss
Keyword(s):  
White Matter ◽  
Gray Matter ◽  
Direct Current ◽  
Subcortical White Matter ◽  
Global Cerebral Ischemia ◽  
Cerebral White Matter ◽  
Cellular Mechanisms ◽  
Current Potential

In vitro studies suggest that ischemic injury of cerebral white matter is mediated by nonsynaptic cellular mechanisms, such as Ca2+ entry into axons through reversal of the Na+-Ca2+ exchanger. The authors investigated extracellular Ca2+ concentration in relation to tissue depolarization (direct current potential) in vivo using ion-selective electrodes in cortical gray and subcortical white matter of α-chloralose-anesthetized cats during 120 minutes of global cerebral ischemia. On induction of ischemia, regional CBF, as measured by hydrogen clearance, ceased. The direct current potential decreased rapidly within minutes in gray matter and with little time delay in white matter. Extracellular Ca2+ concentration decreased just as quickly in gray matter. In white matter, in contrast, extracellular Ca2+ increased in the first 20 to 30 minutes, and a delayed and much slower decline, compared with gray matter, was observed thereafter, reaching a minimal level only about 60 minutes after occlusion. Our results suggest that smaller and delayed transmembrane shifts of Ca2+ are correlates of delayed ischemic membrane dysfunction in central white matter tracts, which may be explained by a lack of synaptic mechanisms.

scholarly journals MiR-137 and miR-122, two outer subventricular zone-enriched non-coding RNAs, regulate basal progenitor expansion and neuronal differentiation

2021 ◽  
Author(s):  
Ugo Tomasello ◽  
Esther Klingler ◽  
Mathieu Niquille ◽  
Nandkishor Mule ◽  
Laura de Vevey ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Subventricular Zone ◽  
Ventricular Zone ◽  
Superficial Layer ◽  
Basal Progenitor ◽  
Germinal Zone ◽  
Layer Neuron ◽  
A Cell ◽  
Non Coding Rnas

Cortical expansion in the primate brain relies on the presence and the spatial enlargement of multiple germinal zones during development and on a prolonged developmental period. In contrast to other mammals, which have two cortical germinal zones, the ventricular zone (VZ) and subventricular zone (SVZ), gyrencephalic species display an additional germinal zone, the outer subventricular zone (OSVZ), which role is to increase the number and types of neurons generated during corticogenesis. How the OSVZ emerged during evolution is poorly understood but recent studies suggest a role for non-coding RNAs, which allow tight regulations of transcriptional programs in time and space during development (Dehay et al. 2015; Arcila et al., 2014). Here, using in vivo functional genetics, single-cell RNA sequencing, live imaging and electrophysiology to assess progenitor and neuronal properties in mice, we identify two ferret and human OSVZ-enriched microRNAs (miR), miR-137 and miR-122, which regulate key cellular features associated with cortical expansion. MiR-137 promotes basal progenitor self-replication and superficial layer neuron fate, while miR-122 slows down neuronal differentiation pace. Together, these findings support a cell-type specific role for miR-mediated transcriptional regulation in cortical expansion.

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