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Related Experiment Video

Updated: Nov 16, 2025

Ex utero Electroporation and Whole Hemisphere Explants: A Simple Experimental Method for Studies of Early Cortical Development

Ex utero Electroporation and Whole Hemisphere Explants: A Simple Experimental Method for Studies of Early Cortical Development

Published on: April 3, 2013

Creative Destruction: A Basic Computational Model of Cortical Layer Formation.

Roman Bauer¹, Gavin J Clowry², Marcus Kaiser^3,4,5

¹Department of Computer Science, University of Surrey, Guildford, GU2 7XH, UK.

Cerebral Cortex (New York, N.Y. : 1991)

|February 24, 2021

Summary

This summary is machine-generated.

This study presents a computational model for cortical layer formation, demonstrating how apoptosis influences neuronal numbers and layer thickness. The model also simulates neurodevelopmental diseases by altering gene regulatory dynamics.

Keywords:

agent-based model apoptosis cell migration cell proliferation cortical layer formation neural development

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Last Updated: Nov 16, 2025

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Published on: April 3, 2013

Differentiation and Characterization of Neural Progenitors and Neurons from Mouse Embryonic Stem Cells

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Published on: May 15, 2020

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

Published on: March 18, 2021

Area of Science:

Neuroscience
Computational Biology
Developmental Biology

Background:

Vertebrate neural systems exhibit characteristic layered organization in structures like the cortex and retina.
Understanding the developmental mechanisms of neural layer formation is crucial for neuroscience research.

Purpose of the Study:

To develop a general computational model for cortical layer formation in 3D physical space.
To investigate the role of apoptosis in regulating neuronal numbers and layer architecture.
To explore how gene regulatory dynamics influence normal and pathological cortical development.

Main Methods:

A multiscale, agent-based computational model was developed.
The model incorporates two distinct stages of apoptosis.
Gene regulatory dynamics were modulated to simulate disease conditions.

Main Results:

The model successfully accounts for variations in neuronal numbers across different cortical areas and species.
Apoptosis was shown to enable independent changes in layer thickness, increasing architectural flexibility.
Altered gene regulatory dynamics recapitulated key features of neurodevelopmental diseases.

Conclusions:

The proposed computational model provides insights into normal and pathological cortical development.
Apoptosis plays a significant role in the evolutionary adaptability of neural layer architecture.
The model offers a framework for studying gene-type rules in neurodevelopment.