Chat with AIExam 10: Memory, Learning, and Synaptic Plasticity
What are some of the challenges in linking correlation of changes in synaptic strength in the hippocampus to causations of learning and memory? Briefly describe one experiment that has provided a better link between correlation and causation.
(42) 
VerifiedThere are many different answers to this question. It has been difficult to show causation between synaptic changes and learning in mammals. To show that changes in synaptic strength result in learning it is necessary to identify which neurons are activated and measure how their synaptic weight changes with a task. However, the neurons in the hippocampus that are activated during a task are distributed and therefore it is difficult to know exactly which neurons are involved. It is also difficult to show that blocking those specific synapses block learning, or that activating specific synapses trigger a memory. In addition, as discussed in the next section of the textbook, memories are not stored in the hippocampus for long periods of time and there are many ways to access those circuits. This makes tracing the memory even more difficult.
There are a couple of experiments discussed that link changes in synaptic strength to learning and memory. One experiment used multi-electrode arrays in the hippocampus to identify some of the CA1 neurons that were potentiated after training. After training, the input fibers to the CA1 neurons were activated with high frequency stimulation to induce LTP and it was found that LTP was occluded from these neurons. Therefore these synapses could no longer be potentiated after they had already been potentiated in one learning task. In a second experiment investigators artificially induced LTP in many synapses in the hippocampus. These rats did not perform well on the Morris water maze suggesting their synapses could not undergo further LTP and the rat could therefore not learn well.
Hebb's postulate from 1949 states "When an axon of cell A is near enough to excite cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A's efficiency, as one of the cells firing B, is increased." Give an example of how synaptic plasticity results in:
A. Growth processes
B. Metabolic changes
What Is the Relationship Between Learning and Synaptic Plasticity?
(35) VerifiedA.Synaptic plasticity results in the formation of new synapses. It has been shown in both Aplysia and mammals that long-term increases in synaptic strength result in the growth of dendrites and dendritic spines. The increase in synaptic contacts will increase the synaptic strength as there is now more neurotransmitter released onto more receptors.
B. Metabolic changes involve changes in synaptic strength, including changes in presynaptic transmitter release or postsynaptic receptors. For example, in spike-time dependent synaptic plasticity, when the presynaptic neuron fires an action potential within 50 ms of an action potential in the postsynaptic neuron the synapse will be potentiated. Silent synapses are also a good example of this idea. When there is activity in the presynaptic neuron that occurs with depolarization in the postsynaptic neuron, more AMPA receptors will be inserted into the membrane and the synapse will become 'visible'.
Figure Q10-29 shows short- and long-term memory in Aplysia using the gill withdrawal reflex. 
Figure Q10-29
A. What would happen to the 4 single shock response if cAMP was inhibited?
B. What would happen to the 4 single shock response if CREB was inhibited?
C. What would happen to the 4 days, 4 trains per day response if CREB was inhibited?
Figure Q10-29
A. What would happen to the 4 single shock response if cAMP was inhibited?
B. What would happen to the 4 single shock response if CREB was inhibited?
C. What would happen to the 4 days, 4 trains per day response if CREB was inhibited? (32) VerifiedA.If cAMP was inhibited there would not be an increase in the gill withdrawal. The response would look like that of the control. cAMP is required for short-term memory and so blocking it would block short-term memory.
B. Nothing would happen-that is, the response would look the same-as CREB is necessary for long-term memory, but not short-term memory.
C. The response would increase on the first day as short-term processes would still be intact, although the long-term changes would be blocked.
Figure Q10-15 illustrates the data from one of the original experiments that showed evidence for 'silent synapses'. CA3 axons were stimulated while the postsynaptic response when the CA1 neuron were voltage-clamped at -65 mV. 
Figure Q10-15
A. Why were the CA1 neurons held at -65 mV?
B. What happened when the CA3 axons were stimulated before pairing, in which the presynaptic CA3 neurons were stimulated while the CA1 neurons were depolarized and what are two reasons for the result?
C. What happened when the CA3 axons were stimulated after 'pairing' and what was the interpretation of the result?
D. Summarize the idea of 'silent synapses' as a form of synaptic plasticity. Include the basic conclusions drawn from the experiments outlined in this and the previous experiment.
Figure Q10-15
A. Why were the CA1 neurons held at -65 mV?
B. What happened when the CA3 axons were stimulated before pairing, in which the presynaptic CA3 neurons were stimulated while the CA1 neurons were depolarized and what are two reasons for the result?
C. What happened when the CA3 axons were stimulated after 'pairing' and what was the interpretation of the result?
D. Summarize the idea of 'silent synapses' as a form of synaptic plasticity. Include the basic conclusions drawn from the experiments outlined in this and the previous experiment. (35) H.M. could still learn a motor task. The following is a figure showing how H.M improved in his ability to trace an image over three days. If he was able to learn the motor task, but his long-term memory of learning the motor task was impaired, what do you think his performance on day 2 would look like? 
Figure Q10-3
Figure Q10-3 (39) Assume we can record spatially related neural activity from the entorhinal cortex and hippocampus of human. You are on vacation in London and have a map to find the Tower of London (you also do not have a smartphone).
A. What spatially related activity would you see in the entorhinal cortex as you are walking around London with your map with Cartesian coordinates?
B. What activity pattern would you see in the hippocampus as you were moving toward your destination?
C. Once you arrived at the Tower of London you find you need to move to the gate that is in the neighboring wall and so you have to walk along one wall of a building. What activity pattern would you see in the entorhinal cortex?
(34) Verified (39) In an experiment that showed that CaMKII was involved in synaptic plasticity, one input was stimulated at high frequency (S1), which induced LTP. LTP was not induced from a second input that was not stimulated at high frequency (S2). Later in the same experiment, constitutively CaMKII was injected into the cell body of the postsynaptic neuron and both inputs were stimulated. Stimulation of which input resulted in LTP and why? Choose all that apply.
(28) Why was the postsynaptic CA1 neuron voltage clamped to +30 mV? Select all that apply.
(40) In the sentence below, circle the correct terms.
LTD and LTP represent a continuum of modifications of synaptic strength. Low-frequency stimulation results in DEPHOSPHORYLATION/PHOSPHORYLATION of AMPA/NMDA receptors, which results in ENDOCYTOSIS/EXOCYTOSIS of the receptors. This results in synaptic DEPRESSION/POTENTIATION.
(43) In 2000, Eric Kandel received the Nobel Prize in Physiology and Medicine, along with two other people for their "discoveries concerning signal transduction in the nervous system." Most of Kandel's work uncovered the contributions of the cAMP signal transduction pathway in memory formation in Aplysia. Why are the discoveries in Aplysia so important for our molecular understanding of learning and memory?
Where Does Learning Occur, and Where Is Memory Stored in the Brain?
(34) According to the circuit diagram in Figure Q10-41, why does lesioning the amygdala disrupt contextual and fear conditioning whereas hippocampal lesions only disrupt contextual conditioning? 
Figure Q10-41
Figure Q10-41 (23) The neural circuitry underlying the gill-withdrawal reflex is known: A sensory neuron in the gill synapses onto a motor neuron that innervates the gill. What is a neural mechanism for habituation?
(25) The amnesic patient, H.M., could still learn motor tasks, like learning to draw while looking in a mirror. What kind of memory is this? Choose all that apply.
(39) Which is true for spike-timing-dependent plasticity? Select all that apply.
(27) Why does the NMDAR provide a good molecular mechanism for coincidence detection? Select the best answer.
(26) 
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