Karteikarten
Seminar 5 - Developmental Synaptic Plasticity
Karten in diesem Stapel (61)
- 1at what age do you have the highest total number of synapses in the brain?1 year
hardly any before born - 2what stage of your life do you have the most synapses in the PFC and why?teenage years
personality and decision making - 3what is synaptic pruning?losing synapses you don't need based on previous experiences (selection processes) --> left with the synapses you do need and this remains stable for the rest of your life
- 4what is the neocortex?outer layer of cerebrum
? higher sensory processing - 5what is the sensory homunculus?distorted sensory map of body
more sensitive areas/ density of sensory receptors --> larger representation (size) - 6what are the names given to the vertical and horizontal structure?columnar (vertical)
laminar (horizontal) - 7how many cortical layers/laminar are there? what surrounds them?top/pia
lamina 1
lamina 2/3 - pyramidal cells
lamina 4 - stellate cells
lamina 5
lamina 6
white matter - 8do the columns relate to function?yes
cells recorded as he went down were different cells but all responded to a common stimulus
sensory information would come in an stay in a column - 9what is the significance of staining vibrissaw (whisker hairs)?get areas that are clusters of cells --> get an exact map of where the whiskers are
thus get an organisation within the cortex - 10who first stained golgi?santiago ramón y cajal
drew a section through the optic tectum - 11what did Hubel and Weisel do in 1962?looked at the cat visual cortex
wanted to know how the visual cortex encoded the info coming into the eye
found that there were diagonal ocular dominance columns (ODCs) that are found in layer 4 of the visual cortex (v1) - 12what is occular dominance?the dominance of one eye over another
- 13how did they determine the presence of ODCs?electrode was moved down and then across
down --> same dominance
across --> different dominance - 14what is the deprivation experiment?what happens if we deny sensory input to one or both eyes --> closing eye
- 15different between monocular and binocular deprivation?mono - close on eye
bi - close two eyes - 16what happens in this experiment?initially, have some cells that respond to the left and some to the right
when you close the left eye, all the cells will end up responding to the right eye
the system has shifted its responsiveness to the eye that was open because it wasn't getting useful information from the left eye
AN EXPERIENCE-DEPENDENT SHIFT IN CORTICAL RESPONSE INDUCED BY MONOCULAR DEPRIVATION - 17conclusions from monocular deprivation on the visual cortex?a period of monocular deprivation causes changes in the response properties of the cortex
- 18what is the barrel cortex?the somatotopic representation map of whiskers in a rodent- also found in layer 4
- 19in a normal whisker map, what happens if you tweak D1?tend to get cells responding in the D1 barrel and occasionally a small amount of overlap
- 20all but D1 removed?let whiskers grow back --> a lot more cells will respond to that D1 tweak
spatial responsiveness to D1increases --> rewiring and undergone plasticity (adapted)
- 21what happens as you gain experience?discrimination improves and become able to differentiate between different sensory stimuli
- 22what are critical periods?a defined period within early postnatal development with a heightened or exclusive capacity for plasticity
i.e. brain very plastic when young - 23what is the opposite to plasticity?stability
- 24why do we want a CP?don't want to have to constantly re-learn things
environment, generally speaking, is stable and so you want that stability
you want to retain what you have already learnt to aid evolutionary survival - 25problems with CPs?once CP is shut, becomes much harder to learn
- 26are there different critical periods for different things?yes
you can define a CP for a specific synapse - 27human language?0-12 years
- 28Whisker RF (receptive field and tuning)p14 - p16
- 29occular dominance?p3
weeks - months - 30whisker barrel map formation< p7
- 31name 2 real life examples of CP pathology1) amblyopia and vision
2) cleft palate and speech - 32what is amblyopia?lazy eye
one eye is dominant over the other
a loss of visual acuity because brain is only using one eye (depth/discriminative/resolution)
walleyes (strabismus) - caused by having one dominant eye early in life/cataracs --> one eye can't follow the other very well - 33how do you treat amblyopia?first fix the eye problem, then patch/ eye drops over the good eye
forces the brain to use the UNDERDEVELOPED EYE - 34prognosis of amblyopia?depends critically on how old the person is when you start the treatment - due to CP of monocular deprivation
treatment before 5 years old usually have full recovery of vision - 35leave amblyopia for 10 years?after the CP of monocular deprivation --> never fully recover vision
- 36what is the link between synaptic plasticity and experience?experience drives synaptic change
experience can induce plasticity that is similar to in vitro synaptic plasticity (pairing/spike-timing)
temporal correlation between experience-dependent and synaptic plasticity induction
molecular requirements overlap between experience-dependent and synaptic plasticity induction - 37characteristics of rapid, Hebbian plasticity?use and correlation-dependent potentiation (NMDA-LTP) --> timing-dependent plasticity
training-dependent potentiation in adults
response depression to deprived inputs (CB1 - LTD, NMDA - LTD and potentiation of inhibition) - 38slower, non-Hebbian, heterosynaptic plasticity?response potentiation to spared inputs
substantial overuse or deprivation - 39what is homeostatic synaptic scaling?decrease all activity in a system, originally identified in culture neurons, e.g. blocking APs (TTX)
put in an incubator and leave for a few days
synaptic responses become STRONGER --> not hebbian (opposite)
chronic decrease in activity cause the system to try and get back to where it was (SCALES BACK) - 40why is homeostatic synaptic scaling necessary?you can't get LTP in a single synapse forever
brings the level back down so there is still capacity for LTP - 41give an example of how experience can change synaptic propertiesshort-term plasticity in barrel cortex
Finnerly (1999) and Cheetham (2007) - 42what did Finnerty do?visualise the barrel cortex --> can see without staining because they are so prominent recorded from 2 layer 2/3 pyramidal cells
stimulate 1 and get a response in the other
if you give a train of high frequency stimuli (8 APs) may vary along the time course - 43what happens to the spared uEPSP amplitude compared to the control amplitude?short-term LTD --> amplitude decreases as you go along the train --> run out of vesicles --> depleted pool --> less vesicles --> Pr decreases
SPARED - not only is the EPSP amplitude much larger but also stronger initial depression - 44what does this study show us?there has been a change in the synaptic strength
size of responses is larger in the spared mouse
changes in the presynaptic release dynamics
SHOWS US THAT EXPERIENCE CAN INDEED CHANGE SYNAPTIC PROPERTIES - 45what did Meliza and Dan show in 1996?induction of STDP by sensory stimulus
can induce plasticity by altering external stimulus - 46how did they do this?instead of an electrode, they drive it with a visual stimulus to young rat
simultaneously measure and record postsynaptic response
pair visual stimulus with an AP in that postsynaptic cell by injecting current --> have a form of spike-timing dependent plasticity
spike after visual stimulation - LTP
spike before stimulation - LTD - 47problem with this experiment?not entirely physiological as you are injecting current to stimulate an AP
- 48if we know SP is important for experience-dependent plasticity (in mice) --> there is a particular developmental time course for it would you expect SP to share this time course?yes
- 49what did cheetham and fox compare (2010)?BC and VC at p12 compared to at p28
- 50—less depression is seen at VC p28, the synapses have matured and changed their properties --> probably more synaptic vesicles --> less prone to depression
in the VC, it reaches maturity much later at p42 --> eyes are still developing at a time where we know the whiskers are mature
STP MATURES EARLIER IN THE BARREL CORTEX THAN VISUAL CORTEX
- 51what is the consequences, with regards to synaptic plasticity, of a CaMK2 mutant?LTP is blocked
receptive field plasticity is also blocked - 52what was the sparing experiment Hardingham carried out?D2 and D1 stimulation and recorded responses
'deprived WT' - deprive all but the D1 input
control shows potentiation of D1 response as you would expect --> rises up and becomes same size as D2
mutant blocks the potentiation of the D1 response - 53what is the thalamo-cortical pathway and what information does it carry?thalamus to layer 4 and barrel cortex
brings whisker info into the cortex
brain slice preparation where you stimulate the thalamus and measure the response in the barrel cortex - 54how can we tell if LTP is involved in circuit assembly?after a pairing stimulus, LTP is induced and unsilences silent synapses
decrease in failure rate
interpreted to be new AMPA-R into the synapse - 55does the number of silent synapses correlate with the age of the animal?yes, negative correlation
as it gets older --> less silent synapses and more AMPA-Rs and more responses at -70mV - 56what experiment could be carried out to show experience drives AMPA-R into synapses?take an animal an infect into its barrel cortex AMPA-R subunits GluA1 tagged to GFP
then allow animals 2 days of experience. one group with whiskers and another group without (only one side of face)
take brain slices from these animals and can compare green and non-green cells - 57conclusion of the study?presence of experience-dependent increase in rectification suggests that AMPA-Rs driven into synapse during development
homomeric recombinant GluA1- GluA1 show a characterisitc increase ins rectification and subsequent decrease in the passing of current at positive voltages compared to the normal GluA2 containing AMPA-Rs - 58what happens to AMPA-R expression when you trim?spines are still there but lack AMPA-Rs
MORE EVIDENCE FOR SENSORY EXPERIENCE BEING RESPONSIBLE FOR TRAFFICKING OF AMPA-R TO THE SYNAPSE - 593 ways to control opening and closing of critical periods1) NMDA-R subunit - metaplasticity
2) interneuron plasticity
3) astrocytes and astrocyte transplant - 60explain changes in AMPA-R subunitduring development, have a change in the type of NMDA-R in the synapse
during CP have slow NR2B receptors that will allow plasticity
NR2A will close it - 61LOOK AT INHIBITORY NEURON TRANSPLANTATION EXPERIMENT PLASTICITY OUTSIDE THE CRITICAL PERIOD
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- 3rd Year Synaptic Plasticity Karteikarten am Seminar 5 - Developmental Synaptic Plasticity, erstellt von William Chapman am 01/05/2017.
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- William Chapman
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