CEREBRAL DEVELOPMENT
Development of the human Brain
By the 14th day of human development, the embryo consists of several sheets of cells which
are raised in the middle to form the primitive body.
3 weeks later it possesses a primitive brain which is essentially sheet of cells at one end of
the embryo. This sheet of cells rolls into a cylinder to form the neural tube.
After about 100 days the brain starts to look human but has not forms any gyri or sulci until
about 7 months.
By the end of 9 months, the brain has the gross appearance of an adult human organ, but
cellular structure is still different.
Research has shown that changes in the developing brain happen in a fixed sequence
Cell birth Cell migration Cell differentiation Cell maturation Synaptogenesis
Cell death and synaptic pruning Myogenesis
This has two distinct features:
1. Nervous system subcomponents form from cells whose destination and function are
predetermined.
2. Development is initiated with an abundance of cells, branches and connections, and is
followed by a maturation process consisting of apoptosis – genetically programmed cell
death or pruning.
Genetic deficits, trauma occurring within the womb, toxic agents or other errors in
development leads to severe or subtle deformities and disabilities.
Neuron Generation
The multipotential stem cells in the neural tube have extensive capacity for self-renewal. In
adults, stems cells line the ventricles, forming the subventricular zone.
Stem cells give rise to the progenitor cells produce nondividing cells called; neuroblasts and
glioblasts that mature into neurons and glial cells respectfully.
This continues in aging brain (in olfactory bulb & hippocampus).
Neurogenesis is important in adulthood because it means that when injury or disease
causes neurons to die, the brain may be induced to replace them.
But usually injury to the CNS is permanent.
Cell Migration and Differentiation
At 20 weeks (mid) gestation the production of neuroblasts destined for the cerebral cortex is
complete.
Migration continues until 8 months after birth.
In the 2nd half of gestation the fetal brain is vulnerable to injury/trauma
The brain is coping better with injury during neurogenesis than during cell migration &
differentiation.
Following migration, cells begin to differentiate into specialized neurons and glial cells
Differentiation is essentially complete at birth, but neuron maturation incl. growth of
dendrites, axons & synapses continues in some parts of brain to adulthood.
, Cells originating in various regions of the subventricular zone migrate to specific cortical
locations – e.g. to the visual cortex or frontal lobes
Mostly by following “mapped roads” of glial cells (radial glial fibers), but some cortical
neurons follow chemical signals.
Incorrect, failed or incomplete migration result in atypical consequences e.g. dyslexia &
epilepsy.
Neural Maturation
After migrating, neurons begin to grow dendrites through
Arborization (complex branching)
Dendritic spine growth
to provide surface area for synapses with other cells and extend axon to appropriate targets
to initiate the formation of other synapses.
Although growth starts prenatally, it continues after birth into adulthood.
Demonstrate slow rate of growth when compared to axons.
Axons extend to initiate the formation of other synapses.
Growing as fast as 1mm/day to make contact with specific target cells before the dendrite is
completely formed in order to influence differentiation
Specific axons develop uniquely, for example:
Grow by being pulled from their body by a structure (e.g. muscle) that is growing
away from a region (e.g. spinal cord) in early development.
Others grow over extensive distances with targets moved or cell bodies rotated
Some follow electrical, chemical or physical “road map”
Send out branches, which once the target is reached others follow
Normal neural pathway development can be disrupted:
Pathways can be blocked – e.g. scaring from early head trauma
Axon development can be disturbed – e.g. malnutrition, toxins
Abnormalities in development can be of genetic cause
If axons target is damaged it may connect with inappropriate targets
Atypical behaviour and/or outcomes:
• Axons are able, to some extent, overcome some obstacles to reach their targets, for
example:
–Crossing and re-crossing over spinal cord
–Axons may substitute for other axons
Synapse Formation and Pruning
Neurons cannot be assigned exact location destination.
Only general outlines of neural connections are pre-determined
Cues & signals guide cells to their specific synaptic contacts
Synapse formation is divided into 5 phases:
– 1st two phases occur during early embryonic development & are characterized by areas
that generate low density synapse. They are both independent of experience.
– Phase 3 (before birth until 2 yrs): rapid synapses growth (40 000/sec)
– Phase 4 (2 yrs – puberty): initial plateau in synapses followed by rapid elimination through
puberty. (50% fall from age 2) massive organizational changes in adolescence → moody?
- Phase 5 (middle age →): plateau through middle age, followed by slow, steady decline with
a final rapid drop prior death
Development of the human Brain
By the 14th day of human development, the embryo consists of several sheets of cells which
are raised in the middle to form the primitive body.
3 weeks later it possesses a primitive brain which is essentially sheet of cells at one end of
the embryo. This sheet of cells rolls into a cylinder to form the neural tube.
After about 100 days the brain starts to look human but has not forms any gyri or sulci until
about 7 months.
By the end of 9 months, the brain has the gross appearance of an adult human organ, but
cellular structure is still different.
Research has shown that changes in the developing brain happen in a fixed sequence
Cell birth Cell migration Cell differentiation Cell maturation Synaptogenesis
Cell death and synaptic pruning Myogenesis
This has two distinct features:
1. Nervous system subcomponents form from cells whose destination and function are
predetermined.
2. Development is initiated with an abundance of cells, branches and connections, and is
followed by a maturation process consisting of apoptosis – genetically programmed cell
death or pruning.
Genetic deficits, trauma occurring within the womb, toxic agents or other errors in
development leads to severe or subtle deformities and disabilities.
Neuron Generation
The multipotential stem cells in the neural tube have extensive capacity for self-renewal. In
adults, stems cells line the ventricles, forming the subventricular zone.
Stem cells give rise to the progenitor cells produce nondividing cells called; neuroblasts and
glioblasts that mature into neurons and glial cells respectfully.
This continues in aging brain (in olfactory bulb & hippocampus).
Neurogenesis is important in adulthood because it means that when injury or disease
causes neurons to die, the brain may be induced to replace them.
But usually injury to the CNS is permanent.
Cell Migration and Differentiation
At 20 weeks (mid) gestation the production of neuroblasts destined for the cerebral cortex is
complete.
Migration continues until 8 months after birth.
In the 2nd half of gestation the fetal brain is vulnerable to injury/trauma
The brain is coping better with injury during neurogenesis than during cell migration &
differentiation.
Following migration, cells begin to differentiate into specialized neurons and glial cells
Differentiation is essentially complete at birth, but neuron maturation incl. growth of
dendrites, axons & synapses continues in some parts of brain to adulthood.
, Cells originating in various regions of the subventricular zone migrate to specific cortical
locations – e.g. to the visual cortex or frontal lobes
Mostly by following “mapped roads” of glial cells (radial glial fibers), but some cortical
neurons follow chemical signals.
Incorrect, failed or incomplete migration result in atypical consequences e.g. dyslexia &
epilepsy.
Neural Maturation
After migrating, neurons begin to grow dendrites through
Arborization (complex branching)
Dendritic spine growth
to provide surface area for synapses with other cells and extend axon to appropriate targets
to initiate the formation of other synapses.
Although growth starts prenatally, it continues after birth into adulthood.
Demonstrate slow rate of growth when compared to axons.
Axons extend to initiate the formation of other synapses.
Growing as fast as 1mm/day to make contact with specific target cells before the dendrite is
completely formed in order to influence differentiation
Specific axons develop uniquely, for example:
Grow by being pulled from their body by a structure (e.g. muscle) that is growing
away from a region (e.g. spinal cord) in early development.
Others grow over extensive distances with targets moved or cell bodies rotated
Some follow electrical, chemical or physical “road map”
Send out branches, which once the target is reached others follow
Normal neural pathway development can be disrupted:
Pathways can be blocked – e.g. scaring from early head trauma
Axon development can be disturbed – e.g. malnutrition, toxins
Abnormalities in development can be of genetic cause
If axons target is damaged it may connect with inappropriate targets
Atypical behaviour and/or outcomes:
• Axons are able, to some extent, overcome some obstacles to reach their targets, for
example:
–Crossing and re-crossing over spinal cord
–Axons may substitute for other axons
Synapse Formation and Pruning
Neurons cannot be assigned exact location destination.
Only general outlines of neural connections are pre-determined
Cues & signals guide cells to their specific synaptic contacts
Synapse formation is divided into 5 phases:
– 1st two phases occur during early embryonic development & are characterized by areas
that generate low density synapse. They are both independent of experience.
– Phase 3 (before birth until 2 yrs): rapid synapses growth (40 000/sec)
– Phase 4 (2 yrs – puberty): initial plateau in synapses followed by rapid elimination through
puberty. (50% fall from age 2) massive organizational changes in adolescence → moody?
- Phase 5 (middle age →): plateau through middle age, followed by slow, steady decline with
a final rapid drop prior death
