Mechanisms of Neural Development and Plasticity Flashcards
Characteristics of Nervous System
- extensive
- massively complex
- billions of nerve cells
- trillions of connections
Neurogenesis
creating the right number of nerve cells
migration and differentiation
getting the right cells to the right place
axon guidance
growing an axon to the right target area
synaptogenesis
making connections with potentially useful partners
activity-dependent refinement
testing and perfecting the neural circuit
the origin of neural tissue
trilaminar germ disc (ectoderm, mesoderm, endoderm)
which germ layer gives rise to nervous system
ectoderm. infolds and then breaks away to form neural tube
how does the neural tube start?
as a single layer of replicating neuroepithelial cells
outer surface of neural tube?
pial cells
inner luminal surface?
ventricular surface
What if each neuroepithelial cell made one too many / few divisions?
can occur by mutation of microcephalin genes (involved in centrosome function, dysfunction –> too few divisions. small brain with normal organisation but reduced function
what are neuroepithelial cells progenitors of?
neurons and glia
how do neuroblasts know where to go?
they migrate away from place of birth through the use of right chemical signals
what tells the new born nerve cells what type of cell to become?
morphogens
what tells the new born nerve cells where to go?
guidance chemicals (reelin)
combo of morphogens switch on genes that insert receptors into outer membrane
these detect guidance chemicals they’ve been programmed for.
What do basal ganglia cells become?
inhibitory neurones
what do cells born in cerebral hemiphere do?
go towards reelin and become excitatory neurones
where do neuroblasts go?
towards the pia matter
how are cortical layers created?
from inside to outside. different types of cells are generated at different times in response to changing chemical signals
what do superificial layer of cortex send signals to?
other coritcal areas
middle layers of cortical layers
recieve subcortical and cortical inputs
deep layers
subcortical structures
inhibitiroy intermeurones
migrate to deep layers
astrocytes
born in cortex
when are neurones are born?
3 months into pregnancy
What will happen if reelin chemical is absent?
loss of reelin leads to lissencephaly- severe learning difficulties and seizures
What will happen if they have impneuroblastsaired motility?
Due to mutation of one copy of the X-linked DCX gene, which encodes a microtubule-associated protein. Without a functional protein, migration is severely disrupted.
What will happen if they have impneuroblastsaired motility?
loss of doublecortin protein in female leads to heterotopia. range from nomoral intellect to severse learning difficulty + epilespy
Due to mutation of one copy of the X-linked double cortical X gene, which encodes a microtubule-associated protein. Without a functional protein, migration is severely disrupted.
what are growing tips of neurites called?
growth cones
what are filopodia?
supported by actin bundles, they seek out chemical guidance signals. attractive guidance signals causes actin bundles to grow
what do repulsive guidance signals on filopedia do?
causes actin bundles to shrink
what do attractive guidance signals on filopedia do?
causes actin bundles to grow
how do dendrites grow?
follow guidance signals
what do growth cones follow?
a series of way points. eg. nociceptor relay cells in developing spinal cord.
what do floor plate signalling proteins do in spinal cord?
axons are attracted to the floor plate
Contact with floor plate alters gene expression
less attractive receptors, more repulsive receptors so axons repel from floor plate
where can growth cones grow?
through tissues they can stick to. filopodia needs to bind to the extracellular matrix for traction. there are matching binding molecules (.e.g integrin) that bind to the matrix proteins (e.g. laminin)
what do axons do when exploring target region?
make trail contacts with potentially useful cells
synaptogenesis
1) filopodia extend from dendrites, seeking contact from passing axons
2) complementary surface proteins bind
3) triggering formation of synaptic structures
e. g. muscle spindle la afferent + own muscle motor neurone
failed synaptogenesis
If surface molecules can’t bind to one another, the filopodium retracts
eg. muscle spindle Ia afferent + antagonist motor neurone
when is the glia birthed?
6 months of pregnancy
when does myelination occur?
from birth
when does synaptogenesis occur?
from 3 months
activity dependent refinement, how are trail contacts strengthened or weakened?
according to their usefulness
how do you identify usefulness of an excitatory synapse?
trial and error. when synapse activates, does the dendrite depolarise? if yes, its useful and works
long term potentiation of fast excitatory synpase
1) activation of a single synapse will produce little effect
2) NMDA receptors remain closed
3) if this happens a lot, then the synapse is probably not doing anything useful
what happens if synapse is part of an effective circuit?
1) . . then many synapses will activate simultaneously, depolarising the dendrite
2) NMDA receptors open and allow Ca++ entry- only at active the synapses
3) increased [Ca++]in triggers processes that strengthen these effective synapses
what happens to synapses that are often active when the post-synaptic cell depolarises
GROW
MAKE MORE TRANSMITTER
MAKE MORE AMPA RECEPTORS
when does synaptic plasticity decrease?
during development. effective in the foetus and still high in babies so they adapt to abnormal conditions. PLasticity fades with age and wiring in the major pathways become permanent. Critical period is where big changes can occur
why can young babies grow effective ciruits in abnormal situations?
high synaptic plasticity. eg this child lost half of his cerebral cortex, but the other half now controls both sides of his body.
what happens if young brain has a compromised eye?
Normally, inputs from the two eyes have an equal share of visual cortex.
But if one eye is compromised in early life, then its synapses will not be part of an effective circuit
and will make very few connections
why can plasticity be maladaptive?
if an eye is permanently compromised, it doesnt matter if there are few connections
when is best time to fix something like a cataract?
Within first year of life as otherwise plasticity decreases and wont be as adaptable.
when is best time to fix something like a cataract?
Within first year of life as otherwise plasticity decreases and wont be as adaptable. even if you fix cataract later on, they still wont be able to see properly
