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Developmental plasticity:
Developmental plasticity
Critical periods
Article studies
Developmental plasticity
Plasticity - the adaptive changes in functional brain organization
adolescent brain copes with one’s environment
immediately -> years
lots of connections and high plasticity in child’s brain
skills, sensory input
room for development vs. not that much skill
development by pruning connections
apoptosis (programmed cell death)
reflects competition for trophic factors (neurotrophins) and produces the proper match in the number of
presynaptic and postsynaptic neurons
synaptic capacity declines as the neurons mature
synaptic rearrengement (Hebbian modifications)
1. neurons that fire together wire together
2. neurons that fire out of sync lose their link
NMDA & AMPA receptors
Neurons that fire together wire together
● But why?
NMDA receptors open only with synaptic coactivation
AMPA receptors do not require coactivation
NMDA activation changes the amount of AMPA receptors
● the more activation the more receptors
Long term potentiation: results from lots of coactivation
Long term depression: results from little coactivation
Critical period
a property of brain development is more sensitive during a fixed period of time
examples of critical periods
certain skills are easier to learn during critical periods
certain development also occurs during critical periods
intercellular communications and synaptic activity alter cell’s fate
language during the first few years (Friederici 2002, Snow 1978)
vision during postnatal development
ocular dominance (first six weeks for macaque)
why critical periods end
plasticity diminishes when axon growth stops
plasticity diminishes when properties of synaptic receptors change
plasticity diminishes when cortical activation is constrained
■ activity doesn’t activate receptors anymore
Loss in Gray Matter (GM) density over time
(Gogtay et al., 2004)
The GM density on MRI is an indirect measure of a complex architecture of glia,
vasculature, and neurons with dendritic and synaptic processes.
Studies of GM maturation show a loss in cortical GM density over time, which
temporally correlates with postmortem findings of increased synaptic pruning
during adolescence and early adulthood.
The primary cause for loss of GM density is unknown. It may be driven at least
partially by the process of synaptic pruning, together with trophic glial and vascular
changes and or cell shrinkage.
Brain maturation
Higher-order association cortices mature only after lower-order somatosensory
and visual cortices, the functions of which they integrate, are developed.
Phylogenetically older brain areas mature earlier than newer ones.
Alterations either in degree or timing of basic maturational pattern may at least
partially be underlying these neurodevelopmental disorders such as
childhood-onset schizophrenia or autism.
Glial Control of Neuronal Development
(Freeman et al.,2006)
Glial cells function as important regulators of nervous system development.
They provide trophic support to neurons, modulate axon pathfinding, and
drive nerve fasciculation.
They regulate the number of neurons at early developmental stages by
dynamically influencing neural precursor divisions, and at later stages by
promoting neuronal cell death through engulfment.
Glia also participate in the fine sculpting of neuronal connections by pruning
excess axonal projections, shaping dendritic spines, and secreting multiple
factors that promote synapse formation and functional maturation.
Though glial cells are emerging as essential participants in nervous system
morphogenesis, it remains unclear whether glial cells act instructively, or simply
respond to neuronal developmental programs.
Do glia influence which axons will be pruned?
Could glial cells promote neurodegenerative disease by inappropriately pruning