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Lecture: postnatal brain development - Postnatal brain development learning goals

8 important questions on Lecture: postnatal brain development - Postnatal brain development learning goals

What factors determine synapse formation, maturation, and persistence?

Initial contact between pre- and postsynaptic cells is mediated by cell adhesion molecules (CAMs) such as nectins, ephrins, and (proto)cadherins. These CAMs form temporary connections, creating an immature synapse. The chemo-affinity hypothesis suggests that molecular markers on axons and dendrites define synapse specificity, contributing to the formation of synapses at specific locations.

How do protocadherins contribute to synapse specificity?

Protocadherins serve as molecular codes for synapse specificity. For example, in dendrites of hippocampal neurons, different variants of protocadherins are found in subsets of synaptic sites. While some instances, like Dscam1 in Drosophila, show repulsive guidance cues controlling non-matching, the protocadherin system is more complex, involving both matching and non-matching interactions.

How do cell adhesion molecules (neurexin, neuroligin, neuregulin 1) contribute to synapse maturation?

Adhesion molecules provide stability and contribute to the clustering of pre- and postsynaptic proteins involved in neurotransmission. Mutations in these molecules can lead to disturbed synapse maturation, resulting in altered wiring of neural networks. For example, neuroligin alone is sufficient to induce presynaptic maturation.
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What factors regulate synaptic refinement?

Neurotrophins, which are growth factors, play a crucial role. Secreted by target cells, they influence axon growth, retraction, synapse maturation, elimination, and neuronal survival. Factors like competition for innervation lead to the refinement of synaptic connections, with neurotrophins determining the winners and losers.

What is a critical period, and how does it relate to synaptic plasticity?

A critical period is a time-window during development when the nervous system exhibits heightened plasticity in response to experience. This period influences various brain regions, including the visual cortex, amygdala, hippocampus, and prefrontal cortex, shaping their functional development.

How does the extracellular matrix (ECM) contribute to critical periods and synaptic plasticity?

The ECM, specifically perineuronal nets (PNNs), plays a role in limiting plasticity. During postnatal development, the increase in the number of PNNs coincides with the end of critical periods, contributing to a reduction in neural plasticity. Degrading the ECM has been shown to restore plasticity in the adult cortex.

What is the role of neurogenesis in infantile amnesia?

Neurogenesis in the subgranular zone remains high during the first postnatal years and sharply declines during childhood. Reduction in neurogenesis prolongs memory retention in young animals. The decline in neurogenesis is thought to contribute to the phenomenon of infantile amnesia, where early episodic memories are rapidly forgotten.

How does the maturation of the prefrontal cortex (PFC) relate to "adolescent disorders"?

  • The PFC continues to mature until age 25, contributing to functions such as planning, decision-making, attention, and impulse control. The delayed maturation of the PFC may contribute to "adolescent disorders" such as schizophrenia, ADHD, and drug abuse. These disorders often emerge during adolescence, a period when the PFC is still undergoing maturation.

The question on the page originate from the summary of the following study material:

Developing brain

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