Transcript The Developing Brain

Brain Development
Good book:
Johnson, M. H. (2011).
Developmental Cognitive
Neuroscience: An Introduction,
Oxford: Blackwell. (3rd edition)
In Education library (x1)
Arts & Social Sci library (x11)
Development – the reduced version:
Development is interaction of genes and environment
PHENOTYPE = GENOTYPE * ENVIRONMENTAL HISTORY
Phenotype (the organism you get, inc. traits, behaviour in any context)
BEHAVIOUR = PHENOTYPE * PRESENT CONTEXT
In theory, every action taken could be explained in this way……?!
i.e. ACTIONS = (Genes * environmental history) * present context
Cells multiply and
differentiate
Inner cells cluster to
leave a cavity
The outer cells “hatch”/implant
into uterine wall
Two new types of tissue form (a bilaminar disc ) from inner and outer cells
(according to bird/reptile or mammal).
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Between the top (ectoderm) and bottom layer (endoderm),
the mesoderm forms (whose cells create the notocord). On
the ectoderm layer, opposite the primitive streak (if
symmetric), the neural plate forms.
Primitive streak
Neural plate forming
Ectoderm
Notocord
(releases
proteins that
drive neurulation
Mesoderm
Endoderm
Ectoderm will become the outer layer of the embryo and
later skin and, via the neural tube, the brain
Mesoderm will become muscle, bone connective tissue
Endoderm will become internal organs
Embryonic folding/neurulation then occurs
Neurulation
Cells from the
neural crest
become the
Peripheral Nervous
System (PNS)
The neural tube
becomes the
Central Nervous
System (CNS)
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The Central Nervous System
develops….
The neural tube generates neuroblasts and glioblasts - cells that
produce neurons and glial cells
One end becomes a series of repeated units -> spinal cord
The other end becomes a series of bulges ….becoming the
forebrain, midbrain and hindbrain….and finer structures…
Chick embryo
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Cells on the move...
Precursor cells (neuroblasts and glioblasts) produce:
- neurons and
- glial cells (poss. structure rather than cognition)
The bulges in the tube grow larger as cells:
- proliferate (are born)
- migrate (travel)
- differentiate into types
These either:
* migrate past older ones, e.g. cortex, from inside to out
•displace older ones pushing them further away – passive
cell displacement – e.g. thalamus
The laminate structure of the cortex forms….
Laminate (layered) structure of cortex
Three drawings by Santiago Ramon y Cajal, taken from the book "Comparative study of the sensory areas of
the human cortex", pages 314, 361, and 363. By User:Looie496 created file, Santiago Ramon y Cajal created
artwork [Public domain], via Wikimedia Commons
Can you spot the layers?
Visual cortex (stained pink).
Subcortical white matter (blue)
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What are the key changes?
Weight, neurons, synapses, myelin
Prior to birth: neurons are generated at around
250,000 per minute, most of your life’s stock
arrives in the first 3 months after your
conception.
Postnatal:
Additive changes:
- 4 x increase in weight
- increase in synaptic density – peaks
(e.g. in visual cortex) after 10 months, then
pruned back.
- myelination (insulation) increases
NB: Some changes continue into teens:
Synaptic pruning in Prefrontal Cortex is postpubertal. Over-production related to plasticity?
PFC myelination also increases in teens.
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Commons
By SCA Svenska Cellulosa Aktiebolaget (Flickr: Teens
sharing a song) [CC-BY-2.0
(http://creativecommons.org/licenses/by/2.0)], via
Wikimedia Commons
Three drawings by Santiago Ramon y Cajal, taken from the book "Comparative study of the sensory areas of
the human cortex", pages 314, 361, and 363. By User:Looie496 created file, Santiago Ramon y Cajal created
artwork [Public domain], via Wikimedia Commons
Q: What sort of interaction is responsible
for cortical laminate structure?
How do different
neurons know
where to go?!
Q: What sort of interaction is responsible
for cortical laminate structure?
Neuronal migration appears aided by radial glioblasts that act as “training stalks” or “guides”
- appears regulated by local intrinsic cellular and
molecular interactions - i.e., to some extent innate.
On a petri dish Molnar & Blakemore (1991) placed visual thalamus
with
a) visual cortex - thalamus afferents invaded, stopped at layer 4
b) Hippocampal tissue - they grew unconstrained
c) Cerebellum - just simply turned away
Levels of genetic/biological
interaction with environment
Johnson and Morton (1991):
Interaction Level
Term
1.Mollecular
Internal Environment
(e.g. blood oxygenation )
2. Cellular
Internal Environment – innate
(e.g. embryonic neurogenesis)
3. Whole Organism
a) Species-typical environment – primal
-external environment
(e.g. light and visual cortext)
b) Individual-specific environment - learning
(e.g. language)
Q: What sort of interaction is
responsible for areal structure?
Areal structure = areas of the
brain can be differentiated by
microstructure - Brodmann
Areas (BA) - strongly
associated with function
2 theories for areal structure
* due to a protomap: early differentiation into cortical
regions according to intrinsic factors. No activity required.
* due to protocortex: later differentiation depending on
external factors e.g. input from thalamus and other areas
of the cortex
2 theories for areal structure
- evidence
* protomap (early differentiation due to intrinsic factors. No
activity required)
- “knockout” rodents without the thalamic connections
still have well-defined boundaries due to gene expression
* protocortex (later differentiation due to external factors e.g.
i/p from thalamus other areas of the cortex
- spontaneous pre-natal activity in the brain appears
important for differentiation(Shatz, 2002)
- Later plasticity and lack of “neat”
regionalisation/function relationships - even primary sensory
areas can shift according to later experience
- known gene expressions (above) can still give rise to
“graded maps” through overlay and different combinations
Cortical Plasticity:
role of thalamic (sensory) inputs
* Reducing thalamic input to a cortical region
reduces its size
* rewiring of thalamic inputs causes new target
region to take on properties of the normal target
tissue, and transplanted cortex takes on
characteristics of new location
So: Neural activity (external environment)
appears a critical factor in areal development not just innate.
The answer maybe protomap AND protocortex
Development is about
Interaction of Nature + Nurture
Biological structures emerge from a complex interaction
between genes and the environment
- Piaget (amongst others)
PHENOTYPE = GENOTYPE * ENVIRONMENTAL HISTORY
Phenotype (the organism you get, inc. traits, + behaviour in specific
context)
GENOTYPE = genes – heritable part but….also see epigenetics
Our genetic background is very important for our
educational outcomes
For example, amongst UK 9 year-olds , most of the
variance in UK English , Science and Maths achievement
is genetic (Plomin et al. 2007)
We can assume (?) the rest is the environment
But life is probabilistic. Biology is not destiny, but there may
be a progressive restriction of fate……
The probabilistic developmental
landscape
Large perturbations influence selection of predefined routes,
or smaller perturbations if close to a decision….
(Waddington, 1975 - influenced Piaget)
Beyond “simple” genetics…
DNA→RNA→protein (->structures, e.g. brain structure)
Waddington referred to this as an “epigenetic” landscape
– meaning all environmental influences on development
epi- (Greek: επί- over, outside of, around) -genetics.
These days, “epigentics” refers to heritable changes
not caused by DNA changes
Epigenetics
epi- (Greek: επί- over, outside of, around) -genetics.
Generally = Heritable changes not caused by DNA
changes
But be aware that some use this term to mean all
environmental influences on development
DNA→RNA→protein (->structures, e.g. brain structure)
Epigenetic factors influencing DNA expression may be inherited
Epigenetics Example
“Methylation”
Areas where many methyl groups attach to DNA become
less “transcriptionally” active
This can be heritable – although the mechanisms are not
well understood
May help tune an anticipated environment over 1-3
generations 
May produce negative looping patterns  if anticipated
environment mismatches the experienced. E.g. deficient
licking and grooming of rat pups by mother -> altered
pattern of methylation in pups -> heightened stress
response in a normal environment.
Views on the role of
genetics 1
The instructions encoded in DNA have acquired “a unique
causal status in developmental outcomes due to their
unidirectional influence” (Plomin et al., 2007)
- specialist genes, e.g. linked to reading disability
(Paracchini et al., 2007)
- ‘generalist genes’ largely responsible for genetic
influence across domains of academic achievement and
cognitive ability (Plomin et al., 2007)
- possibility of tailoring education to genetic profile
Views on the role of
genetics 2
•Genetics provides probable not certain outcomes-Why?
•Microbiologists often assume (their central dogma)
DNA→RNA→protein (->structures, e.g. brain)
•Neuroconstructivists reject a maturational unfolding of
pre-existing information in the genes (Johnson, 2004)
•Epigenetic and protein synthesis processes that are
bidirectional (proteins can act on RNA and DNA
processes and, in exceptional cases, RNA can even
transform DNA in a process called reverse transcription
(Gottlieb, 2004)).
•These processes influenced by (normal) environments
BIOLOGY IS NOT DESTINY
Neuroconstructivism
Cognitive and neural outcomes emerge from a
complex bi-directional interaction between inputs including genetic, environmental, both sensory and
cortical activity from other regions
“Evolution is argued to have selected for adaptive
outcomes and a strong capacity to learn, rather than
prior knowledge. Within such a perspective, it is more
plausible to think in terms of what we might call
domain-relevant mechanisms that might gradually
become domain specific [during our development] as
a result of processing of different kinds of input”
Annette Karmiloff-Smith
Neuroconstructivism:
consequences
Neuroconstructivist approaches:
* probabilistic Waddington landscape and epigenetics
* considers external environmental effects and
emphasises importance of common stimuli (e.g. faces)
* if neural pathway construction influenced by neural
inputs from other areas, then “atypicality” in one area will
produce “atypicality” elsewhere.
* damage to brain systems more devasting in
development terms than damage to cortical areas
* different types of initial atypicality can result in same
outcomes - if the same one brain system affected.
The Developing Brain
(Morton and Frith, 1995)
Examples of
environmental factors
Examples of
Intra-individual factors
Oxygen
Nutrition
Toxins
Synaptogenesis
Synaptic pruning
Neuronal connections
BRAIN
Teaching
Cultural institutions
Social factors
Learning
Memory
Emotion
MIND
Temporary restrictions
e.g. teaching tools
Performance
Errors
Improvement
BEHAVIOUR
Factor affected
The Learning Brain
ENVIRONMENT
ENVIRONMENT
(Howard-Jones, 2010)
(see HJ(2010)
Intro NeuroEd
Res
And …. not forgetting experiential/insider perspectives!!
In summary – you can assume it’s as
below – but know it’s not that simple:
Development is interaction of genes and environment
PHENOTYPE = GENOTYPE * ENVIRONMENTAL HISTORY
Phenotype (the organism you get, inc. traits, behaviour in any context)
BEHAVIOUR = PHENOTYPE * PRESENT CONTEXT
In theory, every action taken could be explained in this way……?!
i.e. ACTIONS = (Genes * environmental history) * present context
Next Time - Language and Development
What would a Neuroconstructivist say?
• Areal structure, e.g. Wernicke’s and Brocke’s –
protomap/protocortex - left lateralisation but this
effected by environmental factors – e.g. position in
womb
• Critical/sensitive periods for very early language, e.g.
effects of hearing sounds before 12 months – early
language specificity – highly social activity.
Probabilistic landscape: Progressive restriction of
fate? But later environmental effects on plastic brain:
2nd language effects on basic cognition
• Language itself not innate but brain is not a blank
slate either: built in start-up mechanisms for highly
complex task of communication