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Published on: November 6, 2017
Postnatal neuronal apoptosis in the cerebral cortex: physiological and pathophysiological mechanisms
M Nikolić1, H A R Gardner, K L Tucker
1Interdisciplinary Center for Neurosciences, Department of Anatomy and Cell Biology, University of Heidelberg, 69120 Heidelberg, Germany.
Postnatal cerebral cortex development involves programmed cell death, or apoptosis, eliminating up to 30% of neurons. This review explores the link between active neuronal networks and this crucial developmental process.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- A significant wave of apoptosis occurs in the mammalian cerebral cortex during the first week of postnatal life.
- This process can lead to a substantial loss of neurons, up to 30% from birth to adulthood.
Purpose of the Study:
- To review recent advances in understanding the phenomenon of developmental apoptosis in the cerebral cortex.
- To explore the relationship between active neuronal network formation and selective neuronal apoptosis.
- To discuss the molecular mechanisms and pathophysiological implications of this apoptotic wave.
Main Methods:
- Literature review of phenomenological and molecular studies on postnatal cerebral cortex apoptosis.
- Analysis of the roles of insulin-like growth factor I (IGF-1) and Rho GTPases (RhoA, RhoB).
- Discussion of drug-induced and N-methyl-d-aspartate receptor (NMDAR) antagonist-induced apoptosis.
Main Results:
- A putative relationship is proposed between the formation of active neuronal networks and the elimination of non-participatory neurons.
- Molecular mechanisms involving IGF-1 and Rho GTPases are being elucidated.
- Certain drugs and NMDAR blockade can induce significant apoptosis during this critical developmental window.
Conclusions:
- Developmental apoptosis in the postnatal cerebral cortex is a complex process with emerging molecular explanations.
- Understanding these mechanisms is crucial, as external factors like drugs can disrupt normal apoptotic processes.
- Further research is needed to fully link molecular causes of developmental and pathophysiological apoptosis.
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