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BIO 435
Synaptic Plasticity
Question | Answer | |
---|---|---|
Define plasticity | 1. changes in the structure and function of the nervous system due to experience 2. can strengthen or weaken synapses 3. can be short-term or long-term | |
What are ways that structure and function of nervous system can change (plasticity) | 1. number of receptors 2. number of synapses 3. amount of NTs released 4. number of neurons | |
Describe synaptic facilitation | - a short-term type of plasticity -the 2nd postsynaptic potential is larger than the first -only lasts for milliseconds -occurs when Ca2+ builds up in the presynaptic neuron builds up | |
Explain why the 2nd postsynaptic potential is greater in synaptic facilitation | If the second AP occurs soon enough after the first, there is still enough Ca2+ left. Therefore, there is a greater amount of calcium ions in the presynaptic neuron due to the creation of more for the second potential. | Therefore, with greater Ca2+, there is more glutamate released and there is a larger EPSP |
Describe synaptic depression | -a type of short-term plasticity -sustained activity causes NTs release to decrease -results from a depletion of pool of reserve vesicles (therefore there is no way to release NTs) | |
What did Eric Kandel's research with Aplysia study? | Habituation and sensitization; when more water was squirted on the siphon or it was touched, the gills would withdraw | |
Define habituation | The magnitude of withdrawal decreases over time (when siphon is continuously touched, the gill is withdrawn less and less | |
Why does habituation occur? | Each time the motor neuron is activated, the resulting EPSP becomes smaller (most likely due to synaptic depression and depletion of vesicles in sensory neuron) | |
What would occur if you unexpectedly shocked the head or tail of the aplysia? | The withdrawal response for the withdrawal reflex would be greater. This new sensitization would then last for about a hour | |
What is the name of the synapse involved in early sensitization? | the axo-axonal synapse (includes serotonin modulatory neuron and sensory neuron synapsing on the motor neuron) | |
Describe the sensitization pathway | 1.The sensitizing stimulus is received 2.Serotonin from a serotonin modulatory neuron that is part of axo-axonal synapse releases serotonin 3.Serotonin release decreases probability of K+ channels opening the axon terminal during the action potential | 4. Less K+ channels opening means a greater depolarization 5. More Ca2+ channels are able to open resulting in greater NTs release 6. More vesicles dock at the membrane |
What affects the duration of sensitization? | The number of shocks received | |
What is the PKA? | protein kinase A (cAMP dependent protein kinase) | |
What does repeated activation of PKA result in? | Long-term sensitization due to transcription of synaptic growth proteins | |
What happens when the presynaptic and postsynaptic neuron activate simultaneously? | The synapse between the two is strengthened and neurons (neurons that fire together wire together) | |
What happens when presynaptic neurons is active when postsynaptic neuron is not (or is only weakly active)? | The synapse between the two is weakened (neurons that fire out of sync lose their link) | |
In what part of the brain is long-term potentiation most extensively studied? | hippocampus | |
What does the high frequency stimulation (tetanus) of CA3 neurons result in? | An increase in the response from CA1 neurons | |
How long can tetanus of CA3 and CA1 neurons last? | days, weeks, months, or even a lifetime (this is a long-term potentiation that can occur naturally) | |
Does it matter where the synapse is placed for potentiation to occur? | Yes, potentiation is site specific (the closer synapse is to the terminals, the stronger it is) | |
Describe the process of early LTP | 1. Tetanus depolarizes presynaptic neurons enough to open NMDA (glutamate) receptors 2. Ca2+ activates protein kinases (PKC, CAMKII | 3. The released protein kinases phosphorylate AMPA receptors and add more AMPA receptors to the postsynaptic cell (receptor trafficking occurs during this period of potentiation) |
Describe the process of late LTP | 1. If enough Ca2+ enters, CREB (cAMP-response element binding protein that regulates the expression of genes is produced and gene transcription is modulated 2. This often results in the growth of new synapses | |
What does late LTP require? | Protein synthesis | |
What causes long-term depression (LTD)? | low frequency stimulation (levels of Ca2+ decrease and activates phosphatases; AMPA receptors then dephosphorylated and removed from the synapse) | |
When does long-term depression occur in the cerebellum? (not a life stage) | Cerebellum is in charge of movement feedback and if movement went as planned. If movement of was faulty, LTD occurs so body doesn't make wrong movement again | |
What type of cells receive input in the cerebellum? | Purkinje neurons | |
How are purkinje neurons involved in LTD? | 1. Purkinje cells receive many synapses from each climbing fiber. These climbing fibers are activated when there is an error signal. | 2. Purkinje cells receive one synapse from tons of parallel fibers (which release glutamate). Parallel fibers activated when plan is initiated |
What occurs when climbing fibers and parallel fibers are active simultaneously? | Subsequent EPSPs are induced by parallel fibers only (The error signal from the climbing fiber only affects the one parallel fibers | |
Why is there a decrease in EPSPs in purkinje cells when error signal is induced by the climbing fibers? | Because purkinje cells have decreases cell response to glutamate | |
Describe the cellular process of LTD | 1. Climbing fibers cause massive depolarization 2. Depolarization causes opening of the voltage-gated Ca2+ channels | 3. Parallel fibers release glutamate and activates AMPA receptors and mGluRs 4. Massive influx of Ca2+ causes reduction in AMPA receptors on purkinje cell dendrites (only on the part of the dendrite in contract with active parallel fiber) |
What causes the internalization (removal of receptors from membrane) of AMPA receptors? | Activation of PKC by Ca2+ | |
During what time during life does the total number of synapses and synapses per mm3 increase? | 3rd trimester and first year of childhood | |
What happens to synapses as you age? | The synapses are pruned and the brain gets ride of synapses you don't use | |
What is the formation of ocular dominance columns in layer 4 dependent on? | The early postnatal experience | |
Define arborization | The fine branching structure at the end of a nerve fiber | |
What happens to LGN axons in V1 as a result of deprivation? | Arborization | |
Why does capacity for change decrease as we age? | 1. decreases ability for axon growth 2. changes in receptor composition and function 3. changes in other pathways that constrain plasticity | |
What is neurogenesis? | the formation of new neurons | |
Where does neurogenesis occur? | hippocampus and olfactory bulb (but don't know purpose of these new neurons in the olfactory bulb) | |
Why is neurogenesis in the hippocampus important? | New neurons are essential for SSRIs (antidepressants) to function; exercise also impacts new neuron generation |