Chapter 7: Life-Span Development of the Brain and Behavior

Neural Tube Formation

• The ectoderm (outermost layer) forms the nervous system.

• A neural groove develops and closes to form the neural tube.

• The anterior neural tube forms:

  • Forebrain

  • Midbrain

  • Hindbrain

The interior of the tube becomes the ventricular system and central canal of the spinal cord

Genotype

All genetic material (fixed throughout life)

Phenotype

Expressed traits (changes throughout life)

Cell Differentiation

Cells become specialized by expressing different genes

C. elegans (worm model)

Fixed neuronal development – predetermined fate

Vertebrates

More cell-cell interactions → more environmental influence

Hypoxia (low oxygen at birth)

brain damage

Maternal malnutrition

brain abnormalities

Viral infections & drugs

developmental disorders

Fetal Alcohol Syndrome (FAS)

Caused by maternal alcohol consumption.

Leads to physical, cognitive, and behavioral impairments

Autism Spectrum Disorder (ASD)

Social and language impairments.

Narrow range of interests.

Phenylketonuria (PKU)

Metabolic disorder – inability to break down phenylalanine.

Untreated → intellectual disability.

Controlled with diet.

Six Stages of Nervous System Development

1. Neurogenesis (Birth of Neurons)

2. Cell Migration

3. Differentiation

4. Synaptogenesis (Synapse Formation)

5. Neuronal Cell Death (Apoptosis)

6. Synapse Rearrangement (Pruning & Refinement)

Stage 1: Neurogenesis (Birth of Neurons)

Non-neural cells divide via mitosis in the ventricular zone.

Cells migrate out and become neurons or glia.

Most neurons are formed before birth, but some continue into adulthood (e.g., hippocampus, olfactory bulb).

Stage 2: Cell Migration

Neurons migrate from the ventricular layer using radial glial cells as guides.

• Cell Adhesion Molecules (CAMs):

  • Help neurons stick together and follow the correct path.

  • Cell-cell interactions guide development.

Stage 3: Differentiation

• Neurons specialize based on location and signals.

• Notochord (embryonic structure) releases proteins that induce motor neuron formation.

• Experimental Models:

  • Knockout (KO) studies: Remove a gene to study its effect.

Transgenic models: Add a gene to examine its function.

Stage 4: Synaptogenesis (Synapse Formation)

• Growth Cones & Filopodia:

  • Filopodia (tiny projections) reach out and follow CAMs.

  • Guide axons and dendrites to form connections.

• Chemical Signals:

  • Chemoattractants → attract growth cones.

  • Chemorepellents → repel incorrect connections.

Myelination

• Occurs after birth and continues into young adulthood.

• Oligodendrocytes (CNS) & Schwann Cells (PNS) form myelin.

• Increases speed and efficiency of neural transmission.

Stage 5: Neuronal Cell Death (Apoptosis)

• Apoptosis (programmed cell death) eliminates unnecessary neurons.

• Key Mechanism:

  • Caspases: Enzymes that break down proteins/DNA.

  • Diablo protein: Released by mitochondria → removes apoptosis inhibitors → triggers cell death.

  • Bcl-2 proteins: Prevent apoptosis by blocking Diablo.

• Neurons compete for survival factors:

  • Neurotrophic factors (e.g., NGF, BDNF) promote survival.

  • If a neuron doesn’t get enough, it dies.

Stage 6: Synapse Rearrangement & Refinement

• Synapses are overproduced, then pruned.

• Gray Matter Thinning:

  • Excess connections are lost in adolescence.

  • Prefrontal cortex is the last to mature (decision-making, impulse control).

• Hebbian Synapses ("Use it or lose it"):

  • Active synapses strengthen.

  • Inactive synapses weaken & disappear.

Binocular Deprivation

No light input → permanent vision loss

Monocular Deprivation

One eye blocked → cortical dominance shifts to the other eye

Hebbian Plasticity:

Strongly active synapses take over neurotrophic factors.

Weakly active synapses wither away.

Hebb (1947) Enrichment Study

• Rats in enriched environments had:

  • Larger synapses.

More astrocytes (support cells).

Epigenetics & Experience

Methylation can silence genes without changing DNA sequence.

Poor maternal care → lifelong stress response changes