Wiring the brain Flashcards
Neural progenitor
dividing cell, give rise to all neurons
Radial glial cells
astrocytes of the cerebral cortex
Symmetrical cell division
multipotent stem cells divide to expand the population of neural progenitors(vanhempi, edeltäjä, kantaisä)
Asymmetrical cell division:
Later the daughter cell migrates away to take up its position in the cortex and never divides again.
Fate of the migrating daughter cell is determined by
age of the precursor cell, position within ventricular zone, environment at the time of division.
Cell Migration, Inside out development of cortex
-First cells to migrate form the subplate (disappear in the end)
-Cortical plate: Neural precursor cells that are destined to come adult cortex migrate form the second cell layer cortical plate
-This process repeats until all layers have differentiated
(This are formed between marginal zone and ventricular zone)
Cell differentiation
a cell takes on appearance and characteristic of a neuron
Neuronal structure develops in three major stages
cell proliferation, cell migration, cell differentiation
Cell proliferation
Develop from the walls of five fluid-filled vesicles
->vesicles consist of only two layers: ventricular zone (inside) and marginal zone (outside)
Gradients of transcription factors that control the size of cortical areas
Pax6:expansionof anterior cortex
Emx2: expansion of posterior cortex
Three phases of pathway formation:
1.Durind pathway selection, axon must choose correct path 2. During target selection, must choose correct structure to innervate 3. During address selection, must choose correct cells to synapse with in the target structure
Growth cone
Growing tip of a neurite. The filopodia probe the environment and direct the growth of the neurite towards attractive cues.
extracellular matrix and the appropriate proteins
space between cells, and the needed proteins laminin and integrins, that bind laminin
fasciculation and specific surface molecules why it is due
a mechanism that causes axons growing together to stick together
-cell-adhesion molecules CAMs, in the membrane of neighboring axons bind tightly to one another causing axons to grow in unison.
chemoattractant, netrin
a diffusible molecule that acts over distance to attract growing axons toward their targets
-netrin:secreted by neurons in the ventral midline of the spinal cord->axons with appropriate netrin receptors are atrracted to the region of highest netrin consentration
(grows toward the source of netrin)
chemorepellent, slit
Is an diffusible molecule that chases axons away
slit:another protein secreted by midline cells->axons with these receptors go away from the highest concentration of slit
chemoaffinity hypothesis
the idea of chemical markers on growing axons are matched with complementary chemical markers on their targets to establish precise connections
steps in forming neuromuscular synapse
- The growing motor neuron secretes the protein agrin into the basal ganglia 2. Agrin interacts with MuSK in the muscle membrane 3.This interaction leads to the clustering of ACh receptors in the postsynaptic membrane via actions of rapsyn.
steps in forming CNS synapse
1.A dendritic filopodium contacts an axon 2. Contact leads to the recruitment of synaptic vesicles and active zone proteins to the presynaptic membrane 3. Neurotransmitter receptors accumulate postsynaptically
programmed cell death
Entire population of neurons are eliminated during pathway formation
trophic factor
life sustaining substance provided in limited quantities by the target cells-> proper match in the number of presynaptic and postsynaptic neurons
->cell death reflects competition for them
nerve growth factor (NGF)
first tropic factor found, produced and released by the target tissue, is taken up by sympathetic axons and transported retrogradely, where it acts to promote neuronal survival.
apoptosis
The systematic disassembly of neuron, caused the expression of cell death genes ->causes neurons to die
Synaptic rearrangement
The target cell can receive inputs from several synapses, mut when first two neurons each provide three synapses on the target tissue but the pattern changes such that other one provides 5 and other one 1.
->occurs as a consequence of neural activity and synaptic transmission.
Three ways Ca2+ is thought to contribute to the processes of synapse formation and rearrangement?
- Ca2+ entry in a action when forming synapse, triggers changes in the cytoskeleton that cause it to assume the appearance of a presynaptic terminal and to stick tightly to its postsynaptic partner
- Ca2+ enters the cell through NMDA receptors when glutamate is present and triggers enchanced synaptic effectiveness.
Hebb synapses
Synapses that can be modified by retinal terminals that are active at the same tie as their postsynaptic LGN target neuron -> are retained (säilyttää).
synaptic arrangements of this sort are called Hebbian modification.
monocular deprivation
One eyelid is sealed to close->open eye columns expand, closed eye columns shrink
ocular dominance shift
Neurons that normally have binocular receptive fields response only to stimulation of nondeprived eye.
binocular conpetition
inputs from the two eyes actively sompete for synaptic control of the postsynaptic neuron.
strabismus
a condition which the eyes are not perfectly aligned->causes in cortical binocularity: cells in visual cortex are driven by either the right or left eye but not both.
can result in the permanent loss of stereoscopic vision and depth perception. The disconnection of inputs in one eye results from competition rather than disuse(“winner takes it all”).
two simple rules for synaptic modification:
- Postsynaptic axon active and postsynaptic neuron is STRONGLY activated by other inputs->the synapse is strengthened. Hebb’s hypothesis : neurons that fire together wire together
- When presynaptic axon is active and the same time the post synaptic neuron is WEAKLY activated by other inputs-> presynaptic axon is weakened-> neurons that fire out of sync lose their link.
NMDA activate by simultaneus presynaptic and postsynaptic activity
When the postsynaptic membrane is depolarized and glutamate active-> NDMA receptors allow Ca2+ to pass.-> stronger synapse. (depolarization caused by other active synapses)More AMPA receptors
long-term potentiation LTP
consequence of strong NMDA receptor activation is strengthening of synaptic transmission
long term depression LTD
The active synapses are decreased in effectiviness, loss of AMPA receptors
Why do critical periods end?
- Plasticity diminishes when axon growth stops
- loss of capability for changes in axon length - When synaptic transmission matures
- properties of LTP and LTD varywith age, they sem to disapper with some synapses - cortical activation is constrained (hillitä)
- decline in the effectiveness of neurotransmitters or the change in conditions they are released may contribute to the decline
