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five phases of neurodevelopment

induction of the neural plate
neural proliferation
axon growth and synapse formation
neuron death and synapse rearrangement


potency after zygote

A fertilised egg is totipotent- develops into any cell
After specialisation they become pluripotent- can develop into many but nit all classes
Eventually they become multipotent- can develop into different cells of only one class
Most developing cells eventually become unipotent- can only develop into one type of cell


induction of the neural plate

3 weeks post conception in all vertebrates
Induced by chemical signals from the organiser (in mesoderm layer)
Tissue taken from the dorsal mesoderm of one embryo (the donor) and implanted beneath the ventral ectoderm of another embryo (the host) induces the development of an extra neural plate on the ventral surface of the host
Neural plate folds to form neural groove, and then lips of the groove fuse to form the neural tube (neural tube defects happen here)
Inside of the neural tube eventually becomes the cerebral ventricles and spinal canal


40 days post conception

3 swellings visible at the anterior end of the human neural tube; develop into fore, mid and hindbrain


stem cells

unlimited capacity for self renewal, can be totipotent, pluripotent or multipoint
Neurons develop from glial cells
When a stem cell divides into two, one becomes a type of body cell and the other is another stem cell which keeps dividing until error happens to stop it


3 layers of embryonic cells

ectoderm, mesoderm, endoderm


neural plate

tissue for NS
a small patch of ectodermal tissue on the dorsal surface of the developing embryo


neural proliferation

After neural tube is formed
Most occurs in ventricular zone, adjacent to ventricle
gives brain its swelling and folding
controlled by chemical signals from two organiser areas in neural tube- floor plate (along midline of the ventral surface of the tube) and roof plate (midline of dorsal surface of tube)



Immature neuron cells (No dendrites or axons) migrate to target location governed by two major factors- specific time and location


cell migration within neural tube

radial and tangential
can use both


radial migration

proceeds from the ventricular zone in a straight line outward toward the outer wall of the tube


tangential migration

at a right angle to radial migration; parallel to the tube’s walls


cell migration out of neural tube

Somal translocation and glia-mediated migration


somal translocation

extension grows from cell in migration direction, explores for attractive and repulsive cues, then cell body moves along extension and removes old ones as it passes


glia mediated migration

radal glia cells appear in neural tube, cells move along this network
Because each wave of cortical cells migrates through the already formed lower layers of cortex before reaching its destination, this radial pattern of cortical development is referred to as an inside-out pattern


neural crest

dorsal to neural tube, formed from cells that break off developing neural tube, develop into neurons and glial cells of PNS



mediated by CAMs on the surface of cells
Gap junctions using connexins
Migrated neurons align themselves with others to form structures


axon growth

Axons and dendrites grow
Growth cone at tip of both structures extends and retracts fingerlike cytoplasmic extensions called filopodia, which grow towards target


retinal ganglion cells

compose the optic nerve (Sperry’s experiment on frogs)


chemoaffinity hypothesis of axonal development

hypothesised that each postsynaptic surface in the NS releases a specific chemical label which attracts growing axon during neural development and regeneration
Fails to account for the discovery that some growing axons follow the same circuitous route to reach their target in ever member of a species rather than growing directly to it
According to this discovery, growth cones are influenced by a series of chemical and physical signs along the route


pioneer growth cones

first to travel along a particular route; presumed to follow the correct trail by interacting with guidance molecules along the route
Then subsequent growth cones follow these routes



tendency of developing axons to grow along the paths established by preceding axons


topographic gradient hypothesis

explains accurate axonal growth involving topographic mapping; axons growing from one topographic surface (retina) to another (optic tectum) are guided to targets that are arranged on the terminal surface in the same way as the axons’ cell bodies are arranged on the original surface
The growing axons are guided to their destinations by two intersecting signal gradients (an anterior- posterior and medial-lateral gradient)


synapse formation

Synaptogenesis: formation of new synapses
Astrocytes (a type of glial cell) aid by processing, transferring and sorting information supplied by neurons
More research needs to be done
Any type of neuron will form synapses with another type, those that do not function afterwards are eliminated


neuron death

50% more neurons than required are produced
apoptosis or necrosis



active process
DNA and other internal structures are cleaved apart and packaged before cell breaks
Apoptosis could result in cancer if genetic programs for cell death are blocked
If over activated, neurodegenerative disease



passive cell death
cell breaks and spill content into extracellular fluid, causing harmful inflammation


triggers for apoptosis

ome developing neurons are genetically programmed for an early death without an obvious external stimulus
Some die because they do not get life-preserving chemicals that are supplied by targets


evidence that life preserving chemicals are supplied to developing neurons by their post synaptic targets

Grafting an extra target to an embryo reduces neuronal death
Destroying some neurons in an area increases survival rate of the remaining


Most prominent life-preserving chemicals are neurotrophins

Nerve growth factors (NGF) first to be isolated
Promote the growth and survival of neurons, function as axon guidance molecules and stimulate synaptogenesis


synapse rearrangement

As a neuron with incorrect synapse dies, this vacant space is filled by the sprouting axon terminals of remaining neurons
Tends to focus the output of each neuron on a smaller number of postsynaptic cells, so increasing the selectivity of transmission


postnatal growth of human brain

Brain volume grows x4 between birth and adulthood
Results from synaptogenesis, myelination of axons and increased branching of dendrites, NOT from additional neurons
sensory and motor areas reach functional maturity before association areas


development of prefrontal cortex

most prolonged period of development


prefrontal cortex cognitive functions

Working memory: keeping relevant info accessible for short periods of time while a task is being completed
Planning and carrying out sequences of actions
Inhibiting responses that are inappropriate in the current context but not in others
Following rules for social behaviour


prefrontal cortex: preservation

tendency to continue making a formerly correct response when it is currently incorrect, preservative error common between 7-12 MO


permissive experiences

permit the information in genetic programs of brain development to be expressed and maintained


instructive experiences

contribute tot he information in genetic programs and influence the course of development


critical period

it is absolutely essential for an experience to occur within a particular interval to influence development


sensitive period

an experience has a great effect on development when it occurs during a particular interval but can still have weak effects outside the interval
The vast majority of experiential effects on development have been shown to be sensitive periods


experience fine tunes neurodevelopment

Long before the NS is fully developed, neurons begin to interact with the environment
Resulting patterns of neural activity fine tune subsequent stages of neurodevelopment
It is the critical, final phase of typical development


neurogenesis in adult mammals

New neurons are added to the hippo campuses of primates, including humans, and the number of new neurones in the adult human hippocampus is approx. 700 per day per hippocampus
In most nonhuman adult mammals, substantial neurogenesis seems to be restricted to the olfactory bulb and hippocampus, and low levels in hypothalamus and cortex
In adult humans, it occurs in striatum and hippocampus, but not in the olfactory bulbs
New olfactory bulb and striatal neurons are created from adult neural stem cells at certain sites in the subventricular zone of the lateral ventricles and then migrate to the olfactory bulbs or stratum in nonhuman mammals and human mammals respectively
New hippocampal cells are created near their final location in the dentate gyrus of the hippocampus
Neurons generated during adulthood survive, become integrated into neural circuits and begin to conduct neural signals
Adult-generated olfactory bulb and striatal neurons become interneurons
Adult-generated hippocampus neurons become granule cells in the dentate gyrus


effects of experience on the reorganisation of the adult cortex

Experience in adulthood can lead to reorganisation of sensory and motor cortical maps
Tinnitus produces a major reorganisation of primary auditory cortex
Thus once the brain has adapted to abnormal environmental conditions, it acquires the ability to adapt more effectively if it encounters the same conditions again


ASD age

Almost always apparent before the age of 3 and does not typically increase in severity after


asd core symptoms required for diagnosis

Reduced capacity for social interaction and communication
Restricted and repetitive patterns of behaviour, interests or activities



repeating almost everything one hears
in asd


asd causes of concern

decline in eye contact between 2-6MO, no smiles or happy expressions by 9 MO, no communicative gestures such as pointing or waving by 12 MO


savant abilities in asd

persons with developmental disabilities who display amazing and specific cognitive or artistic abilities

Savant abilities emerge spontaneously not through learning or practice
Savant abilities can sometimes appear in otherwise healthy people after brain damage or transcranial magnetic stimulation to the left anterior temporal lobe- suggests that this is caused by compensatory responses in parts that are not damaged


williams syndrome characteristics

Heterogenous and intellectual like ASD
sociable, empathetic and talkative
Although they have a delay in language development and language deficits in adulthood, their language skills are good
Often musically gifted, perfect or near perfect pitch and rhythm
Near typical ability to recognise faces
Attentional problems, spatial inability
Health problems, including heart


williams syndrome biological

Missing chromosome 7 gene for elastin, causing heart disorder
Decreased basal ganglia volume
General thinning of the cortex and underlying white matter, greatest at the boundary of the parietal and occipital lobes and in the orbitofrontal cortex
These brain differences may be related to spatial impairment and hyper sociability respectively
Thickness at superior temporal gyrus is typical- high levels of language and music processing