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Cerebral Hypoxia-Induced Molecular Alterations and Their Impact on the Physiology of Neurons and Dendritic Spines: A Comprehensive Review

Summary

This review explains how low oxygen levels in the brain damage nerve cells and their connection points (dendritic spines) through a cascade of molecular changes. The brain normally has protective mechanisms, but severe or prolonged hypoxia overwhelms these defenses, leading to memory loss and cognitive problems. Several molecular pathways and supporting cells called astrocytes and microglia can help protect neurons. Understanding these protective mechanisms may lead to new treatments for brain conditions caused by low oxygen, such as stroke.

Background

Cerebral hypoxia is a severe pathological condition that significantly alters the morphology and function of neurons and dendritic spines. Dendritic spines, critical structures for neuronal information reception, undergo structural changes including reduction in number and morphological abnormalities under hypoxic conditions. These alterations affect synaptic function and neurotransmission.

Objective

This review comprehensively examines how cerebral hypoxia impacts neurons and dendritic spines through molecular changes and explores the causal relationships between these alterations and neuronal functional impairment. The review delves into molecular pathways including MAPK, AMPA receptors, NMDA receptors, and BDNF in hypoxia-induced changes.

Results

The review identifies key molecular mechanisms including MAPK pathway regulation through lncRNAs, AMPA and NMDA receptor dysfunction, and BDNF-mediated neuroprotection. Dendritic spines show progressive morphological changes including swelling, fragmentation, and degeneration during different hypoxia stages. Astrocytes and microglia play crucial protective roles through glutamate clearance, neurotrophic factor secretion, and immune regulation.

Conclusion

Cerebral hypoxia triggers complex molecular cascades affecting neuronal survival, synaptic plasticity, and cognitive function through multiple interconnected pathways. Understanding these mechanisms is essential for developing novel therapeutic strategies targeting MAPK, glutamate receptors, and BDNF pathways. Future research should focus on dynamic changes in neurons and dendritic spines under hypoxic conditions and their connections to cognitive function recovery.
  • Published in:Cellular and Molecular Neurobiology,
  • Study Type:Review,
  • Source: PMID: 39105862, PMCID: PMC11303443, DOI: 10.1007/s10571-024-01491-4
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