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Neurogenesis and Regeneration of Nervous Tissue

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In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...

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Derivation of Glial Restricted Precursors from E13 mice

Derivation of Glial Restricted Precursors from E13 mice

Published on: June 20, 2012

Astrocyte precursor response to embryonic brain injury.

Miriam S Domowicz¹, Judith G Henry, Natasha Wadlington

¹Department of Pediatrics, The University of Chicago Medical Center, 5841 S. Maryland Avenue, MC 5058, Chicago, IL 60637, USA. mdxx@uchicago.edu

|March 15, 2011

Summary

Traumatic brain injury in developing fetuses can cause lasting cognitive issues. This study reveals that early injury triggers precursor cell division, while later injury relies on differentiation to repair astrocytes, potentially hindering recovery.

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Three-dimensional Tissue Engineered Aligned Astrocyte Networks to Recapitulate Developmental Mechanisms and Facilitate Nervous System Regeneration

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Isolation and Culture of Mouse Cortical Astrocytes

Isolation and Culture of Mouse Cortical Astrocytes

Published on: January 19, 2013

Area of Science:

Neuroscience
Developmental Biology
Trauma Research

Background:

Perinatal brain injury is a significant cause of fetal demise and long-term cognitive deficits.
Understanding astrocyte development after injury is crucial but limited by marker and model availability.

Purpose of the Study:

To investigate astrocyte precursor responses to penetrating embryonic brain trauma at different developmental stages (E11 and E15) using an avian model.
To elucidate the mechanisms of astrogliogenesis following acute injury in the developing brain.

Main Methods:

Utilized an avian tectal model to simulate penetrating embryonic brain trauma.
Analyzed cellular and molecular responses, including glial marker expression (TUBB3, PLP, GFAP, NFIA, SOX9, GLAST), inflammation, apoptosis, and cell proliferation at E11 and E15.

Main Results:

Penetrating injury caused ventricular dilatation, necrosis, cysts, and hemorrhage.
Neuronal and oligodendrocyte precursor markers decreased, while mature astrocyte marker GFAP increased near injury sites.
Increased expression of astroglial precursor markers (NFIA, SOX9, GLAST) was observed.
Cell division in the ventricular zone increased only after early (E11) injury, not late (E15) injury.

Conclusions:

Astrogliogenesis post-injury relies on precursor proliferation in early development but shifts to differentiation in later stages.
The reduced capacity for precursor proliferation in later developmental stages may impair recovery and contribute to developmental abnormalities after traumatic brain injury.