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Immature Neurons in the Postnatal Brain: Markers, Modulation, and Involvement in Normal and Aberrant Plasticity
Viacheslav Riga1, Victor Aniol1, Natalia Gulyaeva1
1Department of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, RAS, Butlerov Street 5A, Moscow 117485, Russia.
Cortical immature neurons (cINs) are adult neurons born before birth that don't divide. This review explores their unique biology, role in brain plasticity, and implications for neurological disorders.
Area of Science:
- Neuroscience
- Developmental Biology
- Cellular Plasticity
Background:
- Cortical immature neurons (cINs) are a unique population of prenatally generated, non-dividing neurons.
- They maintain an immature phenotype, marked by doublecortin (DCX) and polysialylated neural cell adhesion molecule (PSA-NCAM) expression, into adulthood.
- cINs represent a form of structural plasticity termed "neurogenesis without division," distinct from canonical adult neurogenesis.
Purpose of the Study:
- To comprehensively review the molecular markers, morphology, origins, and maturation of cINs across species.
- To examine factors influencing cIN phenotype and their clinical relevance in neurological conditions.
- To identify knowledge gaps and potential therapeutic applications of cIN biology.
Main Methods:
- Literature review of studies on cortical immature neurons.
- Comparative analysis of cIN abundance and canonical adult neurogenesis across mammalian lineages.
- Evaluation of clinical evidence linking cIN alterations to neurological disorders.
Main Results:
- An inverse relationship exists between cIN abundance and canonical adult neurogenesis across species.
- Factors like neurotransmitters, stress, sensory experience, and aging modulate cIN phenotype.
- cIN alterations are implicated in temporal lobe epilepsy, traumatic brain injury, and stroke.
Conclusions:
- Understanding cIN biology provides new perspectives on cortical plasticity.
- cINs may play roles in pathological remodeling and endogenous repair mechanisms.
- Further research into cINs could inform therapeutic strategies for brain repair targeting endogenous cellular reserves.
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