Term
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Definition
| the capacity of the nervous system to change; the brain's ability to rewire itself, alter synpatic signaling, and/or relocating information-processing functions to different brain regions |
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Term
| at what stage of development is plasticity obvious |
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Definition
| during the embryonic development of neurons and neural circuits |
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Term
| do adult brains posess plasticity? |
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Definition
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Term
| in what ways do adult brains possess plasticity |
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Definition
| adult brains can learn, establish new memories, and respond to injury |
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Term
| what is one form of neural plasticity |
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Definition
| changes in the strength of synapses |
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Term
| what organism has been studied to learn about neuronal plasticity |
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Definition
| Aplysia Californica - sea slug/mollusk |
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Term
| why are sea slugs studied to learn about neural plasticity rather than humans |
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Definition
| mammalian CNS is complex; sea slugs have simple nervous system |
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Term
| is it possible to monitor electric signals between identifiable nerves in sea slugs |
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Definition
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Term
| what happens if you touch Aplysia's siphon |
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Definition
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Term
| what happens if you touch Aplyisa's siphon repeatedly |
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Definition
| smaller gill contractions due to habituation until there are no gill contractions because of habituation |
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Term
| what happened to gill contractions when the siphon touch was paired with electrical stimulus to the tail |
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Definition
| once again, a vigorous gill withdrawal |
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Term
| what does the noxious stimulus to the tail do? |
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Definition
| sensitizes the gill withdrawal reflex to light touch |
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Term
| what is short-term sensitization in the sea slug |
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Definition
| after a single noxious stimuls to the tail, gill withdrawal remains enhanced for about an hour |
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Term
| what happens if you do repeated shocking of the tail with siphon touch |
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Definition
| short term sensitization increases in duration to long term sensitization: the behavior can be altered for weeks (sea slug will vigorously withdraw gill following light siphon touch without habituating.) |
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Term
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Definition
| enhancement of the strength of a reflex response that is produced by a noxious stimulus |
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Term
| what are the neural players in the sensitization of the sea slug |
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Definition
| mechanosensory afferents from the siphon, motor neurons that innervate the gill, internuerons that receive input from other neurons, modulatory interneurons |
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Term
| What is the path of the synaptic mechanisms in short-term sensitization in the sea slug |
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Definition
| 1. touching the siphon activates mechanosensory afferents; 2. mechanosensory neurons form excitatory synapses on both interneurons and motor neurons; 3. interneurons excite motor neurons, meaning that motro neurons receive exciatory synapses from both interneurons and mechanosensory neurons; 4. summed excitation increases likelihood of action potential in motor neuron |
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Term
| how is the synaptic circuit modified by pairing a noxious stimulus with touching the siphon |
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Definition
| additional sensory neurons are activated |
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Term
| what od the newly activated sensory neurons (from the noxious stimulus) do? |
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Definition
| these sensory neuronse excite modulatory interneurons that release serotonin onto presynaptic terminals of the siphon's sensory neurons (as they go to interneuron and motor neuron) |
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Term
| what is the result of the serotonin release |
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Definition
| serotonin produces a prolonged enhancement of transmitter release from siphon sensory neurons |
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Term
| what is the result of the prolonged enhancement of transmitter release from the siphon sensory neurons |
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Definition
| increased synaptic excitation of motor neurons and consequent enhanced gill withdrawal |
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Term
| what is it, bottom line, that causes the behavioral plasticity in sea slugs |
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Definition
| recruitment of additional synaptic elements that change synaptic transmission in the gill reflex |
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Term
| how does serotonin enhance synpatic transmission during short-term sensitization (what are the steps.) |
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Definition
| 1. serotonin is released from modulatory interneurons. 2. serotonin binds to G protein receptors on the presynaptic terminal of the siphon sensory neuron. 3. The G protein stimulates cAMP. 4. cAMP activates protein kinase A. 5. PKA inhibits potassium channels from opening. 6. because potassium channels are blocked, the action potential is prolonged and more calcium channels are opened. 7. the increased calcium (in the presynaptic terminal of this sensory neuron from the siphon) increases the amount of neurotransmitter release onto the motor neuron. 8. this cascade enhances synaptic transmission between sensory and motor neurons within the gill reflex |
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Term
| typically, when an action potential comes in and the synaptic cleft is depolarized, how does it become repolarized |
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Definition
|
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Term
| describe how serotonin enhances synaptic transmission during short-term sensitization without breaking it into specific steps |
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Definition
| Once an action potential comes in and I depolarize the synaptic cleft, I have to repolarize it. The way to repolarize it is to open the potassium channels so that potassium can leave. Protein Kinase A blocks potassium channels so that potassium stays in and the action potential persists in the terminal. The longer the action potential, the more calicum can enter. The more calcium that enters, the more neurotransmitter that's released. The more neurotransmitter that's released, the more likely we are of activating the motor neuron that causes the gill to react. |
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Term
| what does serotonin activate in long term sensitization resulting from repeated noxious stimulation |
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Definition
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Term
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Definition
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Term
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Definition
| binds to DNA and increases transcription rate of genes |
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Term
| what is the result of CREB binding to DNA |
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Definition
| new proteins are synthesized in the neuron |
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Term
| what can the newly synthesized proteins do |
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Definition
| modify synaptic functions |
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Term
| what does behavioral plasticity arise from |
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Definition
| changes in the efficacy/efficiency/strength of synaptic transmission |
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Term
| what do short term effects of neural plasiticity arise from |
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Definition
| post-translational modifications of existing synapses and synapse proteins (by touching the siphon and and electrocuting the tail) to affect chnnels |
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Term
| what do long term neural plasticity effects require |
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Definition
| change in gene expression, new proteins, or new synapses |
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Term
| where in mammals has short-term synaptic plasticity been studied most extensively |
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Definition
| peripheral neuromuscular synapses (NMJ) |
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Term
| what happens when a series of action potentials invades the NMJ in close succession |
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Definition
| triggers several changes: synaptic facilitation, synaptic depression, post-tetanic potentiation |
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Term
| define synaptic facilitation |
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Definition
| transient increase in synaptic strength |
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Term
| when does synaptic facilitation occur |
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Definition
| when 2 or more action potentials invade the presynaptic terminal in close succession |
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Term
| what does synaptic facilitation result in |
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Definition
| progressive increase in post synaptic endplate potential |
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Term
| what does facilitation result from |
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Definition
| prolonged elevation of presynaptic calcium levels |
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Term
| what is the bottom line of facilitation |
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Definition
| when action potentials arrive in close succession, calcium builds up in terminal and allows more transmitter release with each action potential |
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Term
| when does synaptic depression occur |
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Definition
| following rapid succession of many action potentials |
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Term
| what causes synaptic depression |
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Definition
| depletion of the pool of synaptic vesicles following repeated action potentials |
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Term
| in synaptic depression, how long will the strength of synapses be diminished |
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Definition
| until vesicles can be replenished |
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Term
| in other words, if you keep bombing a motor neuron with action potentials, what will happen |
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Definition
| you'll run out of neurotransmitters and the synaptic strength will eventually start to decline (short-term) |
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Term
| when does post-tetanic potentiation occur |
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Definition
| following a high frequency burst of presynaptic action potentials |
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Term
| what is the immediate result of post-tetanic potentiation |
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Definition
| yieds even more prolonged elevation of presynaptic calcium and therefore enhanced neurotransmitter release |
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Term
| describe the timing of post-tetanic potentiation |
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Definition
| delayed in onset and lasts several minutes following the burst of action potentials |
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Term
| when would you get a post-tetanic reaction? (does it happen in real life) |
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Definition
| arises in the odd/experimental scenario when you send a train of action potentials |
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Term
| what happens with calcium in the post-synaptic potentiation |
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Definition
| the train of action potentials causes so much calcium to be released into the synaptic terminal that there is a large concentration of it sitting there a few minutes later when another action potential comes, there's another surge because the calcium causes you to dump a lot of neurotransmitters |
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Term
| for how long does facilitation, depression, and potentiation modify synaptic transmission |
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Definition
| briefly: seconds or minutes |
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Term
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Definition
| ultimate changes occur in synaptic strength that lasts for a long time |
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Term
| what are the 2 forms of long term synaptic plasticity |
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Definition
| long term potentiation, long term depression |
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Term
| what is long term potentiation (what does it do) |
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Definition
| produces long lasting increase in synaptic strength |
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Term
| what is long term depression (what does it do) |
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Definition
| produces long lasting decrease in synaptic strength |
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Term
| what mediates long term potentiation and long term depression |
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Definition
| different intercellular signaling pathways |
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Term
| where in the mammalian brain has long term potentiation been aggressively studied |
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Definition
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Term
| what part of the brain is activated during memory tasks (we know this from functional MRIs) |
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Definition
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Term
| what is the result on memory of damage to the hippocamups |
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Definition
| inability to form certain types of new memories such as spatial memories |
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Term
| in the rat/pool study, what happened to the poor little rats with a damaged hippocampus |
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Definition
| couldn't make spatial memories to remember how to find the platform in the pool and/or enjoyed swimming too much to get on the platform |
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Term
| what did Tim Bliss and colleagues discover would happen to synaptic activity in rodent hippocampi following a few seconds of high frequency stimulation |
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Definition
| enhanced synaptic activity |
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Term
| what are the 2 cells whose synaptic connections are important in long term potentiation |
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Definition
| Schaffer collateral, CA1 Pyramidal cells |
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Term
| of Schaffer collateral cells and CA1 Pyramidal cells, which cells synapse on which? |
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Definition
| Schaffer collaterals synapse on CA1 Pyramidals |
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Term
| If you stick an electrode in a Schaffer collateral cell and send 2/3 action potentials/minute, what is the synaptic strength felt at the CA1 Pyramidal cell? |
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Definition
| the end plate synaptic potential at the CA1 pyramidal cell remains the same. |
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Term
| if you stick an electrode in a Schaffer collateral cell and send a train of action potentials, what is the synaptic strength felt at the CA1 Pyramidal cell? |
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Definition
| you'll get an increase in synaptic strength that can last for hours |
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Term
| what do we call the high frequency train of stimuli |
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Definition
|
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Term
| if you apply the same stimulus to the Schaffer collateral cell before tetanus and one hour after tetanus, how will the endplate post synaptic potential recorded in the CA1 pyramidal cell be different for the 2 stimuli |
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Definition
| tetanus will increase the size of the EPSP in the CA1 neuron |
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Term
| what do we call the change in the synaptic strength that lasts for an hour |
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Definition
|
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Term
| to recap, high frequency stimulation/tetanus will cause what in the EPSP? |
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Definition
| prolonged enhancement that lasts hours = LTP |
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Term
| if you don't send a train of action potentials through the Schaffer cells, will the CA1 pyramidal cells EPSP change |
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Definition
|
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Term
| what mechanisms do neurons use to produce LTP |
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Definition
|
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Term
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Definition
| antagonists of NMDA receptors |
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Term
| where is glutamate released from in LTP |
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Definition
| Schaffer collateral cells |
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Term
| what does the glutamate released by schaffer cells bind to |
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Definition
| AMPA receptors, NMDA receptors |
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Term
| what do AMPA receptors do |
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Definition
|
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Term
| what do NMDA receptors do |
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Definition
| allow calcium entry, though the channel is usually blocked by magnesium |
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Term
| on what cells are the AMPA and NMDA repecptors |
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Definition
|
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Term
| when is magnesium expelled from the NMDA receptor |
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Definition
| only during high frequency stimulation when the postsynaptic cell is sufficiently depolarized |
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Term
| what can happen when magnesium is expelled from the NMDA receptor |
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Definition
| calcium can enter the postsynaptic neuron (the CA1 pyramidal neuron) |
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Term
| what does the entry of calcium into the postsynaptic neuron through the NMDA receptor following removal of magnesium trigger? |
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Definition
|
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Term
| recap: what 2 things must happen for the NMDA receptor to open and allow calcium entr |
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Definition
| glutamate binds to NMDA receptor, postsynaptic membrane is sufficiently depolarized to expel magnesium |
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Term
| what do protein kinase C and CaMKII do once they have been stimulated by calcium |
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Definition
| stimulate the production of additional receptors or increase the current flow through the existing receptors => allow more ions to enter the cell, making it easier to change synaptic strength AND/OR phosphorylat transcription factors like CREB |
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Term
| what can alter transmitter release from the presynaptic neuron |
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Definition
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Term
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Definition
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Term
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Definition
| increases protein synthesis |
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Term
| what is long term synaptic depression |
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Definition
| plasticity that results in long-lasting depression of synaptic activity |
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Term
| does LTP require simulation of high or low frequency and for short or long periods of time? |
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Definition
|
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Term
| does LTD require simulation of high or low frequency and for short or long periods of time? |
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Definition
| low frequency for long periods |
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Term
| at what frequency of stimulation to Schaffer collaterals does LTD occur and for how long |
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Definition
|
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Term
| how long does LTD depress end plate post synaptic potentials |
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Definition
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Term
| how does LTD affect the increased EPSPs that arise from LTP |
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Definition
|
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Term
| what do LTP and LTD do as complements to each other |
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Definition
| control synaptic plasticity |
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Term
| what key elements of Schaffer-CA1 synapses do both LTP and LTD share |
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Definition
| both are involved in activation of NMDA-type glutamate receptors resulting in calcium entry into postsynaptic cells. |
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Term
| what determines LTP vs LTD |
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Definition
|
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Term
| how does calcium determine LTP vs LTD |
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Definition
| small amounts of calcium lead to LTD. Large amounts of calcium leads to LTP |
|
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Term
| what type of proteins does LTP depend on |
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Definition
| LTP results from the activation of calcium dependent kinase proteins which phosphorylate target proteins, turning them on |
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Term
| what type of proteins does LTD depend on |
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Definition
| LTD results from the activation of calcium dependent phosphatase proteins which dephosphorylate target proteins, turning them off |
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Term
| to review, what (in general) do kinases do |
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Definition
| phosphate a protein and turn it on |
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Term
| to review, what (in general) do phosphatases do |
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Definition
| remove a phosphate from a protein to turn it off |
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Term
| do we know everything there is to know about how changes in synaptic strength encodes memory and complex learning functions |
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Definition
|
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Term
| can plasticity/reorganization occur in the cerebral cortex |
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Definition
|
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Term
| what are the 4 areas of the primary sensory cortex |
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Definition
|
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Term
| what does each of the 4 areas of the primary sensory cortex contain |
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Definition
| a complete somatotopic map of the body's surface |
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Term
| what animals did researchers Kaas and Merzenich use to map out somatotpic organization, particularly the hand representation in the cortex |
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Definition
|
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Term
| what did Kaas and Merzenich do to the poor little owl monkeys to show plasticity |
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Definition
| they mapped the location of each digit in the sensory cortex (1-5), cut off owl monkey's 3rd digit, re-examined somatotopic map of mokey's cortex 2 months later => cortical neurons that formerly responded to stimulation of digit 3 now responded to digits 2 and 4 |
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Term
| what happened in the cortex when the owl monkey's finger was cut off |
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Definition
| remaining digits expanded to take over the cortical territory that had lots its sensory input |
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Term
| what do we call the change in neurons in the cortex following losses in nearby areas |
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Definition
| functional reorganization |
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Term
| other than the sensory cortex, where else has functional organization/plasticity been demonstrated |
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Definition
| visual, auditory, and motor cortices |
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Term
| Is functional plasticity a general property of the adult cortex |
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Definition
|
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Term
| if you train a monkey to utilize digits 2-4 to perform a task, how will the cortex change after several months |
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Definition
| digits 2-4 will have a greater representation in the cortex |
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Term
| do we know what the mechanism and significance of reorganization of the sensory and motor maps are? |
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Definition
|
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Term
| are the changes in cortical circuitry limited |
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Definition
| yes. Otherwise, recovery from brain injurie would be greater than we se clinically. |
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Term
| can peripheral nerves regenerate |
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Definition
| when peripheral nerves are injured, damaged axons can regenerate over several centimeters and often re-establish synaptic connections |
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Term
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Definition
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Term
| what happens when PNS axons are injured |
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Definition
| injured axons in the PNS reactivate expression of growth-related genes that supports axon elongation; macrophages remove damaged cells; schwann cells increase the production of neurotrophic factors |
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Term
| what do neurotrophic factors do |
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Definition
| promote axon growth and regeneration |
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Term
| what happens when CNS axons are injured |
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Definition
| myelin sheaths are not efficiently removed following injury, consequently impeding regeneration. Oligodendrocytes produce a protein called Nogo which blocks axonal extension, astrocytes express additional inhibitors of axon growth, cell bodies fail to activate growth-associated genes |
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Term
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Definition
| protein produced by oligodendrocytes following CNS axon injury that blocks axonal extension |
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Term
| is production of new neurons in the adult brain possible |
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Definition
|
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Term
| where in the mammalian brain have new nerve cells been identified |
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Definition
| olfactory bulb, hippocampus |
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Term
| what types of nerves are the new nerve cells that have been found in the olfactory bulb and hippocampus in the mammalian brain |
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Definition
|
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Term
| have new neurons with long distance projections/axons been located in the mammalian brain |
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Definition
|
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Term
| where do the new neurons found in the mammalian brain arise from |
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Definition
| subventricular zone of the developing neural tube |
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Term
| how are new neurons able to arise from the subventricular zone of the developing neural tube |
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Definition
| the subventricular zone retains some neural stem cells that can divide and give rise to new neurons. |
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Term
| what is the subventricular zone of the neural tube |
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Definition
| the part of the neural tube that encircles the ventricles |
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