Lecture: postnatal brain development

24 important questions on Lecture: postnatal brain development

Tell something about the formation of the synapse. The first ocntact is mediated by recognition of .....
Explain this term

Cell adhesion molecules on the membrane. Adhesion molecules are proteins that help cells stick to each other or to the extracellular matrix.

  • Nectins, ephrins, (proto)cadherins form temporary connections between pre- and postsynaptic partners → immature synapse. All these proteins are called cell adhesion molecules.

Example dscam 1: Drosophila homologue of mammalian protocadherin.
  • If you have 2 different types of neurons, if you follow the axon there is a difference between a mutant and a wild type of mushroom.

Explain the function of Dscam 1 (adhesion molecule) in drosphelia. Explain also protocadherins

Dscam1 helps Drosophila neurons avoid each other when growing. It does this at branch points and by making sure their dendritic fields are separate.

Protocadherin is more complex: mathing and not matching. In mammals, including humans, things are a bit more complex. Protocadherins can do both: help neurons match up correctly and also avoid each other.


Which dendrite shows normal synaptic maturation?

The right one shows that mature type, the left one shows the immature.
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Induction of synapse maturation

Changes in the DNA sequence of .... Associated with autism and schizophrenia.

Adhesion molecules.

Adhesion molecules (neurexin, neuroligin, neuregulin 1) provide:  (2)

  1. Stability
  2. clustering of pre- and postsynaptic proteins involved in neurotransmission

Tell something about neurologin and presynaptic maturation.

Use HEK-293 in your answer













By putting Neuroligin into non-neuronal cells (HEK-293), the researchers tricked these cells into behaving like neurons. This made the neurons believe they could form synapses with these "neuron-like" HEK-293 cells. It demonstrates the crucial role of Neuroligin in influencing cellular behavior and promoting the formation of connections between cells.

The factors that regulate the process (which is the winner) are called neurotrophins (growth factors).
Explain the neuronal survival.

(Where they are secreted? )

They are secreted by target cells.
The neuronal survival is all about the neurotrophins. There is a competition for the availibiliy of them. If they receive this there will be axon growth and retraction. This will lead to synapse maturation/elimination.

Nerve cell elimination
Example chick embryo.
Normally neurons in the spinal cord synapse onto muscle cells in the limb bud.
Explain what the removal or addiontional of the synpatic target (limb bud) leads to. .

  • Removal of synaptic target (limb bud) → motor neurons fail to interact and are eliminated.
  • Additional synaptic target (limb bud) → less elimination and more motor neurons survive.

Synapse elimination is accompanied by reduction in

Gray matter volume

Timing varies per brain region depending on critical period.

How can we look at ocular dominance colums in the visual cortex?

By inserting a tracer in the eye. This is taken up by the cells in the retina. The tracer is a transporter to axons in the cell where it jumps to the next neuron.

Which factors determine closure of a critical period?

The extracellular matrix (ECM) and the perineuronal nets (PNNs).
The ECM limits ocular dominance plasticity.
PNN density peaks at the end of the critical period in the visual cortex.

.... The ECM restores ocular dominance plasticity in the adult cortex

Degrading.

Other examples of experience-dependent plasticity during childhood?

  • language
  • memory
  • walking/other motoric skills

Explain the activity dependent modulation of the eCM In three steps.

When it’s locally degraded it creates more space.
there are several things happening:
  1. Activity dependent release anditor activation of ECM-degrading enzymes
  2. Local degradation of the ECM\Increased lateral diffusion of receptors
  3. ECM signaling via integrins

Critical periods of memory systems: learning to learn and remember
Infantile amnesia:
Episodic memory

Infantile amnesia: Early (0-3 years) episodic memories are rapidly forgotten
Episodic memory= who, what, where and when.

Is infantile amnesia caused by a deficit in learning or memory retrieval?

Memory

What happens in the critical period of the amygdala?

The ECM protects against memory erasure.

Infantile amnesia influences:

Hippocampal neurogenesis.  Neurogeneis in the subgranular zone remains high during first postnatal years, but sharply declines during childhood. In mice, neurogenesis declines after 3 weeks of age. Reducing neurogenesis in subgranular zones prolonged memory retention in young mice.

Why would neurogenesis disrupt acquired memories?

Memory formation requires strengthening of synaptic connections. New neurons integrate in existing networks → disrupt established synaptic connections that were strengthened by learning.

What happens in the critical period of the hippocampus?

There is a switch in NDMA-type glutamate receptors. Infantile amnesia coincides with maturation of the hippocampus.

Learning experiences during critical period ---> switch in NMDA -receptor subunits: NR2B → NR2A.
Explain NDMA
Explain NRB2
Explain NR2A

NMDA receptors are a type of glutamate receptors:
NR2b sbununit containing receptors: immature synapse
NR2A subunit containing receptors: lower threshold for synaptic flasticity.

Infantile amnesia:
Inability to learn? Retrieve memories?

  • Infantile amnesia is thought to be a failure of memory retrieval
  • Infants and young animals learn well, but forget faster
  • Reminders during early years can reinstate and prolong memory

When is the critical period of the perfrontal cortex and what are the functions of the PFC?

Adolescence?
Maturation of the PFC continues till age 25.
PFC functions:
  • Planning
  • Decision making
  • Attention
  • Impulse control

Which psychiatric disorders parallel maturation of the PFC?

  • ADHD
  • Schizophrenia
  • Addiction
  • Disorders emerge during adolescence.

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