synaptic plasticity Flashcards
define activity dependent plasticity
Activity-dependent plasticity refers to the ability of neural circuits in the brain to change and adapt in response to patterns of activity or stimulation. In simpler terms, it means that the connections between neurons can be strengthened or weakened based on how often they are used or stimulated. This process is essential for learning and memory formation.
which stages of neuronal development are hard wiring and which are activity-dependent
hard wired: patterning, proliferation, migration, differentiation and maturation is not dependent on activity
activity dependent: synapse formation and maturation
Apoptosis is both
synapse pruning is activity dependent- Synapse pruning when synapses that are present get removed due to lack of activity
what two types of apoptosis is there
hard wired and activity dependent
experience about synaptic connections
Experiments that use genetics to abolish synaptic connections.
2 main ways: 1: By removing the ability to have synaptic transmission, synaptic vesicles cannot be released to stimulate the neurons.
Or you can do it by removing the receptors on the other side of the synapse.
Anything that is not related to activity will progress.
Phenotype of mice: they are able to be born but they cannot thrive unless you feed them and keep them warm, They are weak and have well-established anatomy. You can see the structure of neurons is fairly stable. There is surprisingly good evidence, which suggests that activity-dependent mechanism are important for refining but not that important in the beginning
what is neurotrophic factor hypothesis
involved in neurogenesis
Neurotrophic growth factor such as nerve growth factor is important for the growth of neurons.
How this takes place:
A cell will release this growth factor which will be taken up by the neuron.
A molecule called trka in the neurone will bind to the growth factor, phosphorylating and this will lead to the synthesis of bcl2 which is an inhibitor of appptosis. Therefore this synapse will not undergo apoptosis.
Other cells that are not able to take up this growth factor won’t be able to make the bcl2 and therefore will undergo apoptosis
how does apoptosis regulate cell numbers in the cerebral cortex
in neurological research or treatment where transplanted inhibitory interneurons are introduced into a brain region exhibiting increased excitatory activity.
neuronal netowrks in the brian are balanced by systems of excitation and inhibition. excitsatory neurones increase liklihood of AP firing while inhbitory neuroens decrease that liklihood. this is important for normal cellular brain fucntion and prevention of damage by excessive neuronal activity.
areas of increased excitation in brain that cuases an imbalalce leaning towards excessive excitation. this is where there is greater release of glutmamte (Primary excitatory neurotransmitter) or overstimulation of its receptors, this can lead to increased calcuium influx an cause cellular damage in excess or even undergo apoptosis.
the transplanted inhibitory interneurones are introduced to regions where there is excessive excitation and integrate into existing neuronal circulatory inorder to counterbalance this excitation via the release of the inhbitiory neurotransmitter GABA, this dampense down this excitation, to restore balance ibetween excitation and inhbition, reducing risk of excitotoxicity which could lead to cell death.
what is sensory-driven neuronal plasticity and what changes are seen
Sensory-driven neuronal plasticity refers to the ability of neurons in the brain to undergo structural and functional changes in response to sensory input.
ie ocular dominance collumns
-formation of new synapses
-dendritic growth and branching (indirect routes to the same area)
-upregulation/increases in ion channel conductance/integration allowing for greater response from the neuron.
describe the ocular dominance collumns (and what happens if there’s compromise- shot eye and no compromise within critical period), what happens eyes open during/after critical period
Ocular dominance columns are clusters of neurons in the primary visual cortex (V1) that respond preferentially to input from one eye or the other.
stucturein brains visual cortex that respond to visual info from eye and each collumn prefr visual info from one eye or the other, comparing the dfferent views and creating a clear 3D picture of world.
In normal visual development, each eye sends input to both hemispheres of the brain, but initially, there is some degree of overlap in the inputs from the two eyes.
During a critical period early in development, typically in infancy and early childhood, the visual system is highly plastic and responsive to sensory input.
If there is balanced input from both eyes, ODCs representing each eye will develop relatively evenly.
There is also equal access to territory resources from each eye.
However, if one eye receives significantly more stimulation than the other, the ODCs representing that eye will expand at the expense of the less stimulated eye taking over that territory to compensate.
In this experiment, one eye of an animal (e.g., a kitten or a mouse) is temporarily deprived of visual input by suturing it shut for a period of time during the critical period.
As a result of monocular deprivation, the ocular dominance of the non-deprived eye is strengthened, and the ODCs representing the deprived eye become weaker or fail to develop fully.
Following monocular deprivation, the deprived eye’s representation in the visual cortex is reduced, and the non-deprived eye’s representation expands.
This shift in ocular dominance is a result of synaptic plasticity, including changes in the strength and number of synaptic connections between neurons representing each eye in the visual cortex.
Importantly, sensory-driven plasticity during the critical period is reversible to some extent. If monocular deprivation is lifted before the critical period ends, some recovery of visual function and ODC organization can occur.
However, beyond the critical period, the ability of the visual system to undergo large-scale reorganization diminishes, and ODCs become more stable.
what is critical period for development of balanced ocular dominance columns in V1
birth- 10 weeks of age/ infacy to early childhood (7 or 8)
refers to the timeframe in which an organism is most sensitive to the environmental stimuli or experiences, from which an absence or presence of this will have long-lasting impact on the organism’s development and functioning.
explain is long-term potentiation
Glutamate activates AMPA receptors, with Na+ flowing into the post-synaptic neuron and causing depolarisation
NMDA receptors open due to depolarization, removing the voltage-gated Mg2+ ion block
Ca2+ ions enter the cell activate post-synaptic protein kinases such as calmodulin kinase II (CaMKII) and protein kinase C (PKC)
CaMKII and PKC trigger a series of reactions that lead to the insertion of new AMPA receptors into the post-synaptic membrane
AMPA receptors increase the post-synaptic membranes sensitivity to glutamate and increase ion channel conductance
This underlies the initial phase of long-term potentiation (LTP)
how does plasticity changes over time
There is a concept that all the plasticity mechanisms that occur during learning have a critical period.
If you plot plasticity over time of age, any mechanism, there would be region where the brain is most susceptible/plastic to these changes.
This is called the critical period. The development of new language for example.
You have a period where it is easier to learning language.
Experimental manipulation has shown you can shift this critical period from different abilities, by shifting the maturation of inhibitory systems. This is important in modulating the amount of plasticity you have
example of the plasticity of adulthood
One of the aspects of LTP is the growth of synapses, you can measure this growth using MRI.
They looked at London cabdrivers that have gone through the knowledge test, they have an enlarged hippocampus.
They measured a number of brains from medical students. Measurements before and after the exam.
They have growth in different areas of the brain.
long term potentiation and chronic pain
Clinical implications on this.
Some areas with chronic pain have increased in size such as the anterior cingulate cortex and the insula.
ACC: people have looked at this area and have shown that both ltp and ltd can be studied in these areas and are shown to be larger in mouse models of pain.
LTD (long term depression): is the opposite, where synapses decrease in size.
There are some clinical trials that are looking at mechanism of ltp, in particular one of the downstream targets of calcium adenylate cyclase, One sub form of this is particularly highly expressed in the ACC.
By developing a drug that is specific to this adenylate cyclase isoform, you can block chronic pain.
By blocking the formation of ltp by acute pain, you can suppress the formation of chronic pain
