L33-36

Question 1

Explain the concept of fear conditioning.

Answer 1

Vairant of classical conditioning:
- associating UC (e.g., electric shock) and CS (sound signal)

Question 2

Describe the dual pathways from stimulus perception to emotional response: “the high road”.

Answer 2

Retina –> thalamus –> cortex –> amygdala

Question 3

Describe experiments demonstrating the importance of amygdala in implicit learning.

Answer 3

Lesion studies:
- one group of patients with bilateral amygdala damage and another group with bilateral hippocampus damage
- handshake with small shock
- bilateral amygdala damage: patients are missing implicit memory (the patients does not shun the handshake, and no skin conductance response occur)
- explicit memory are intact (they know the handshake may hurt a bit)

Question 4

Explain the concept of explicit emotional learning.

Answer 4

Being afraid of something, because it is tought, not because of experience, “instructed fear”

Question 5

Describe some effects of amygdala in explicit learning.

Answer 5

Response in left amygdala was seen in response to “threat” vs “safe” conditions, which correlated with the expression of the fear response (skin conductance)

Question 6

Describe the dual pathways: “the low road” from stimulus perception to emotional response.

Answer 6

Retina –> thalamus –> amygdala

Question 7

Describe how the dual pathways differ in speed and depth of cognitive evaluation.

Answer 7

Low:
- crude info
- fast, app. 15 ms

High:
- detailed info
- slow, app. 300 ms

Question 8

How does explicit emotional learning differ from fear conditioning?

Answer 8

In explicit: only a threat of e.g., a shock

Question 9

Are different memory systems associated or dissociated in the brain? Explain how we know.

Answer 9

Dissociated
Lesion studies (working vs. declarative memory):
- patients with bilateral damage to the temporal lobe cannot form new memories for events (declarative memory), but working memory is spared (can uphold a conversation)
- patients with lesions in the left temporoparietal cortex, vice versa - declarative memory intact, deficits in working memory

Nondeclarative vs declarative:
- patient with the right occipital regions removed (patient M.S.) had impaired nondeclarative, but intact declarative

Question 10

Describe the cellular mechanism responsible for long-term potentiation in the hippocampus

Answer 10

• can be induced by a single high-frequency train of stimulation (may explain how some memories can be formed by a single experience)
• can last for days/weeks (may explain the persistence of memory over these sorts of time intervals)
• has a degree of specificity that fits well with the specificity of memories (only synapses activated during stimulation are enhanced)
• has a prooerty of associativity (Hebbian learning)

Question 11

Are long-term potentiation synapse specific?

Answer 11

Yes.

Question 12

Explain the role of NMDA receptors in synaptic plasticity.

Answer 12

Mice lacking NMDA-R showed littel or no LTP.

Question 13

Explain the concept of place cells and their role in spatial navigation.

Answer 13

Hippocampal neurons that are only activated when an animal is in a particular spatial location in its local enviornment, has also been identified in humans.

Question 14

Explain the Hebb principle.

Answer 14

Neurons that fire together wire together:
- spike-timing-dependent plasticity
- synapses are either potentiated or depressed according to the casual order of pre- and postsynaptic activation within a narrow ms-long time window

Question 15

Explain non-Hebbian forms of learning.

Answer 15

• emergence of local dendritic NMDA spikes that preceded place field formation and were tuned to its future spatial location
• CA1 pyrimidal neurons
  (formation of place cells)
• important in engrams supporting spatial/contextual memories
• stable in the same context, but remapping in a new context