Chapter 14: Remembering Relationships Flashcards

1
Q

Procedural learning

A

physical type of learning that facilitates the phenomenon of muscle memory ex/ memory of riding a bike

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2
Q

episodic memory

A

memory of a specific event, part of declarative memory

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3
Q

semantic memory

A

aka declarative memory (along with episodic memory), memory of facts

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4
Q

Describe HM’s amnesia.

A

he suffered from severe epilepsy and got a bilateral temporal lobe ressection that took out the hippocampus and amygdala. seizures stopped but he faced severe anterograde amnesia that extended across all sensory modalities and affected memories for faces, places, events, facts and words. he did not suffer from retrograde amnesia; he remembered old facts and childhood events. points to the fact that the hippocampus is probably not as involved in long term storage.

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5
Q

T/F people with superior autobiographical memory have enhanced forms of other types of learning such as procedual memory and learning

A

false. they remember a lot about their own experiences but have relatively normal other forms of memories and learning. ex/ they perform average in school and in number remembering tasks.

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6
Q

seizures themselves are thought to arise from an imbalance of ___ and ___. Explain this mechanism.

A

excitation and inhibition. the imabalnce is created by the DEATH of tonically active neurons that normally excite inhibitory neurons in the DENTATE GYRUS. without this tonix excitation of inhibition, the inhibitory neurons fall silent, causing the rest of the hippocampus to become overly excitable.

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7
Q

evidence that hippocampus is involved with medio-temporal epilepsy

A

1) hippocampus is overly excitable because of the death of neurons that normally excite inhibitory neurons in the hippocampal regions 2) initial trauma causes dentate granule cells in the HC to sprout abnormal connections that create an excitatory intrahippocampal FEEDBACK LOOP. LEADS TO EXCITOTOXICITY. medial temporal epilepy is a progressive, degenerative disease.

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8
Q

treatment for medio-temporal epilepsy

A

remobing the hippocampus and adjacent cortices on the side of the brain where the seizure begins. eliminates seizures in 80% of cases.

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9
Q

genetic component of developing epilepsy

A

if your twin has epilepsy, there is a 40-50% chance you’ll have it. this is a result of a genetic mutation that affects the voltage gated Na+ and K+ channels. Other mutations may affect GABA receptors.

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10
Q

hippocampusvolume ___ with epilepsy duration on the side of:

A

DECREASES with epilepsy duration but ONLY ON THE SIDE OF THE SEIZURE. Shrinkage does not occur on the contralateral side.

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11
Q

There was severe anterograde amnesia experienced by HM, however, what kind of learning was spared?

A

procedural learning. HM could learn new motor skills (ex/ mirror tracing task- he improved over the course of several days, even though he had no memory of having done the task before).

He also could learn new cognitive skills. ex/ he got betetr with practice at recognizing objects from incomplete, fragmented drawings.

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12
Q

How did researchers study HM’s amnesia (anterograde amnesia) in non humans? Outline the process

A

using the delayed non-matched to sample task.

1) sample phase. monkeys (no HC, inferior temporal cortices (entorhinal or perirhinal cortex), or amygdala) are shown a single object
2) delay.
3) monkeys (no HC, inferior temporal cortices (entorhinal or perirhinal cortex), or amygdala)) are shown the same object again, as well as a novel object.
4) over the course of many trials, the monkeys are trained to always lift up the novel object, the one that does nto match the sample, in order to retrive food hidden underneath

because the trials involve different objects, the monkeys can solve the task only if they remember on each trial which object they saw during the corresponding sample phase. they must recognize which of the two objects seen in the test phase is old and which is new.

5) monkeys with large bilateral lesions in the medial temporal lobe are SEVERELY IMPAIRED in the DNMTS task because this involves OBJECT RECOGNITION MEMORY, and is not a procedural task.

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13
Q

3 regions of the medial temporal lobe that were adjcent to the hippocampus whose direct lesioning most likely memory impairment. proof?

A

1) enterorhianl cortex
2) perirhinal cortex
3) parahippocampal cortex.

When these areas were removed, monkeys demosntrates amnesia compared to that of HM. If you lesioned these areas but kept the amygdala and hippocampsu, monkeys performed the DNMTS task at a SEVERELY IMPAIRED LEVEL.

monkeys with large bilateral lesions of the amygdala dn hippocampus, including the dentate gyrus, the CA fields and the subiculum, but had INTACT entorhinal and perirhinal cortices performed JUSTA S WELL ON DNMTS TASKS, indicating that these cortices play a salient tole in memory and learning.

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14
Q

spontaneous novel recognition tasks in rats have shown that rats still exhibit a reliable preference for novel rather than familiar object. HOwever, whhen the ___ and ___ cortex was removed but NOT the hippocampus, nocel stimulus recognition was not demonstrated.

A

when the perirhinal and post rhinal cortex was lesioned, novel stimulus preference was not demonstrated. This indicates that the peri and post rhinal cortices, but NOT THE HIPPOCAMPUS, are needed for OBJECT RECOGNITION.

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15
Q

explain the double dissociation phenomenon in memory

A

hippocampal lesions affect spatial and temporal relationships (ex/ memory needed to navigate around a city, time patterns) but not object recognition memory, and perirhinal lesions affect object recognition but NOT spatial memory.

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16
Q

relational memory hypothesis

A

the proposal that the perirhinal and postrhinal cortices may be sufficient for forming memories of individual objects, but the hippocampus is needed to CONNECT those objects to one another, through space and across time.

aka the HC is involved in learning about SPATIAL, TEMPORAL OR LOGICAL relationships.

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17
Q

long term potentiaion

A

persistent growth or strengthening of synapses that were active just before or during post synaptic depolarization.

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18
Q

4 components of the hippocampus

A

1) dentate gyrus
2) CA1
3) CA3
4) subiculum.

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19
Q

information generalyl flows from the higher order neocortical areas, through the ___ and ___ cortices into the hippocampus and back out

A

through the perirhinal and entorhinal corticices into the hippocampus and back out.

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20
Q

neurons in the enothinal cortex project into the hippocampus’s ____ ___, whose output cells project to the ___ fields of the cornu ammonis, which projects to the ___ field. Where does this field project into?

A

neurons in the enothinal cortex project into the hippocampus’s DENTATE GYRUS, whose output cells project to the CA3 fields of the cornu ammonis, which projects to the CA1 field. THE CA1 field then projects into the SUBICULUM.

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21
Q

after receiving input from the CA1 field, the subiculum projects out of the hippocampus to the ___ ___, and to several subcortical targets, including:

A

projects to the entorhinal cortex and to several subcortical targets, including the amygdala and hypothalamus

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22
Q

what is the perforant path of the hippocampus? What is the mossy fiber pathway? How does the CA3 project to CA1?

A

the projection from the entorhinal cortex to neurons in the dentate gyrus and CA3

The mossy fiber pathway connects the dentate gyrus to CA3.

the neurons of CA3 project to CA1 AND TO OTHER CA3 NEURONS via recurrent collaterals.

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23
Q

what’re the three major input pathways that hippocampal CA3 neurons receive?

A

1) from entorhinal cortex
2) from the dentate gyrus
3) from other CA3 neurons.

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24
Q
A
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25
Q

T/F mossy fiber connecions between CA3 and dentate gyrus is seen to undergo LTP

A

false. in this connection system, the boost in synaptic strength is not dependent on post synaptic depolarization and therefore not LTP

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26
Q

Which connections of the hippocampus exhibit LTP (following hebbs rule)

A

LTP is observed at synapses connecting CA3 to CA1, as well as the synapses that connect CA3 neurons TOGETHER. synpases onto CA3 neurons can be strengthened by applying a strong, high-frequency stimulus (a long tetanic stimulus) to the axons of other CA3 neurons.

this hebbian plasticity might be a reason that allows certain neurons to be capable of storing info about their own patterns of activity.

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27
Q

the CA3 neurons in the hippocampus exhibit Hebbian plasticity and become more strongly connected to one anotehr. Eventually, all the activated CA3 neurons becoem capable of activating each other. These interconnected neurons form a ___ ___

A

CELL ASSEMBLY.

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28
Q

each cell assembly of CA3 neurons is a potential ____, a memory trace.

A

ENGRAM

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29
Q

in the CA3, what happens when only a subset of the neurons in a fully fromed cell assembly are activated by some external input? What’s this process known as?

A

as a result of prior LTP, the activated CA3 neurons have become strongly connected to the other neurons in the same assembly. through these previously strngthened connections, neural activity spreads from the initial subset of active neurons to the entire assembly, even to the neurons in the assembly that weren’t first excited by the initial external stimulus. this is known as PATTERN COMPLETION. See the “cued recall” diagram

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30
Q

how is LTP involved in learning and rememboring TEMPORAL SEQUENCES

A

the key notion here is that LTP preferentially stengthens not only synapses that were active simiultaneously, but also synapses that were active a few milliseconds earlier.

this temporal asymmetry in LTP (spike timing dependent plasticity) makes sequence learning possicle. Ex/ if neuron A is consistenyl active 10 ms before neuron B fires and AP, then the synapse from A to B will be strengthened, whereas the synapse from B to A will remaine weak. Afterwards, activation of A can trigger a spike in B, but B activation cannot trigger a spike in A.

Therefore, this 2 neuron network has stored info about the TEMPROAL SEQUENCE of the original firing pattern.

autoassociative networks with spike timing-dependent LTP are capable of storing sequences.

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31
Q

why is cell assembly segregation so important?

A

each cell assembly represents different experiences, and must remain segegated from one another. Although individual neurons may participate in multiple cell assemblies, the overlap between different assemblies must be MINIMAL or else we would not be able to separate memories.

to counteract this problem, we ensure that even similar experiences activate different sets of CA3 neurons from the outset during the intiial encoding of the memory

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32
Q

what hippocampal structures are involved in the process of pattern separation to prevent the overlapping of cell assemblies and thus memories? Evidence?

A

dentate gyrus. it receives projections from the neocortex in a pretty random manner with NONOVERLAPPING neurons. Nonoverlapping sets of neurons in the dendate gyrus fire, and these distinct sets of dentate neurons influence the CA# neurons in such a way that they too respond with very different patterns of activity to similar patterns of neocortical input.

the dentate gyrus is helping to “pull apart” the cell assemblies in CA3.

there is evidence for this because by blocking NMDA receptors in dentate gyrus of rats prevents them from discriminating between two slightly different environments.

33
Q

it is seen that each individual CA3 cell assumbly represents one memory. is activation of CA3 sufficient to generate a full blown memory experience?

A

actually no. there is neocortical involvement. it was found that recalling images activates a subset of neocortical areas that were involved in the INITIAL PERCEPTION (ex/ asking to recall a sound a dog makes activates the auditory cortices).

thus, memory recall appears to reinstate at least part of the neocortical activity pattern that existed when the memory was formed.

NOTABLE< it was found that the entorhinal cortex responds selectively when the clips of movies are initially displayed, and then JUST BEFORE the clips are remembered. Activation of entorhinal cortex prior to recall impries that memory recall involves at least some neocortical neurons.

In diagram:

One entorhinal neuron (A) increased its firing rate whenever the patient was watching brief (5-sec) clips of a Simpson’s episode.

The graphs in (B) show the same neuron’s activity when the patient was later asked to recall which clips he viewed.

Remarkably, the neuron increased its firing rate just before the patient reported remembering “the Simpsons.”

Similar recall-related activity has also been recorded in the hippocampus.

34
Q

what is reinstatement hypothesis

A

memory recall appears to reinstate at least part of the neocortical activity pattern that existed when the memory was formed.

35
Q

how is the entorhinal and neocortex activated in response to memory recall?

A

reactivation of the neocortex is facilited by the hippocampus.

pathways from the neocortex into hippocampus are paralleled by pathways going in the opoiste direction, from hippocampus to entorhinal cortex, perirhinal cortex, and ultimately, a variety of other cortical areas.

thus we can think of info flowing from the neocortex to the HC during memory encoding, and in the opposite direction during subsequent memory recall.

36
Q

what is retrograde amnesia

A

the inability to remember events that had formed prior to an event (surgery or something)

37
Q

T/F: lesioning of temporal medial lobe causes retrograde amnesia

A

false. lesioning the HC actually didn’t cause people like HM to lose old childhood memories. they did cause LIMITED retrograe amnesia, but in monkeys, the amnesia does not last very long.

38
Q

why is it that the HC damage interferes with mostly recent memories and not old memories?

A

it is hypothesized that memories are initiailly stored in the hippocampus but then someow transfered to the neocortex.

The HC-driven reinstatement of neocortical activity will, if it occurs repeatedly cause the formation of neocortical cell assemblies, which can then be reactivated even without a functioning hippocampus. hippocampus “teaches” the neocortex, and then the HC is no longer required to reinstate the neocortical activity patterens that existed when the memory was formed.

39
Q

memory and systems consolidation

A

memory consolidation: the gradual strengthening of memories

systems consolidation: the idea that memory consolidation involves the relocation of memories to the neocortex.

ie/ neocortex activation (perception) causes memory formation by forming cell assemblies in HC (Ca3). Reinstatement/lots of recal from HC then causes neocortical neurons to strengthen, leading to the formation of a neocortical cell assembly that can be activated without involving the HC.

40
Q
A
41
Q

proof of systems consolidation

A

neuronal activity in the HC is LOWER during a memory test at 25 days after training, rather than at 5 days after training. Conversely, activity levels in several neocrotical areas are significantly HIGHER during recall at 25 days than at 5 days after training.

42
Q

neocortical ___ ___ ___ is required for memories lasting longer than a day or two in mice, indiciating the necessity of systems consolidation

A

neocortical LONG TERM POTENTIATION

43
Q

T/F: neocortical cell assembblies form more slwly than hippocampal cell assemblies

A

true

44
Q

the ___ serves as an initial, temporary store of rapidly acquired info. Some of this info is hten transmitted to the ___, where it is gradually integrated with info that was learned ____. What the neocortex stores tends to be less ___ and better ___ with previously acquired info.

A

the HC serves as an initial, temporary store of rapidly acquired info. Some of this info is hten transmitted to the NEOCORTEX, where it is gradually integrated with info that was learned EARILIER. What the neocortex stores tends to be less DETAILED and better INTEGRATED with previously acquired info.

45
Q

when is the hippocampus teaching the neocortex?

A

The hippocampus can teach the neocortex every time you recall a memory by reinstating a neocortical activity pattern.

repeated reactivation of hippocampal memory traces leads to the creation of neocortical cell assemblies that can be activated without the hippocampus

46
Q

How does unconcious replay of memories work?

A

hippocampal cell assemblies can reinstate neocortical activity patterns not only during ordinary memory recall, when we are awake, but also when we are asleep.

In rats, after learning a placement activity, the hippocampal place cells frequentyl fired in the same stereotyped sequence that they had followed when the rat had run along the track while the rat slept, more often than chance.

47
Q

how does attention enhance the memory encoding? What is the underlying neural mechanism?

A

attention enhances the neural signals carrying the attended info. it makes the attended stimulit 1) easier to detect and identify, and 2) increases the liklihood it would be remembered long term.

mechanism: the stronger a sensory input pattern, the more likely it is to cause the formation of robust hippocampal cell assemblies. strong hippocampal cell assemblies in turn are likely to drive neocrotical neurons strongly enough to form assemblies of their own.

48
Q

how does behavioral arousal heighten sensory encoding?

A

behavioral arousal involves the activation of locus coeruleus, which then boosts any sensory signals that are being processed at the time while suppressing background activity. therefore, behvarioal arousal boosts memories for whatever happens during the period of arousal.

49
Q

Behavioral arousal activates the ___ ____ of the ____ , as well as the locus coeruleus, which then enhances memories while they are formed, while they are consolidated, or both.

A

Behavioral arousal activates the basolateral complex of the amygdala, which then enhances memories while they are formed, while they are consolidated, or both.

rats and humans who have taken emphetamines or epinephrine remember better than control rats what happened shortly before the injections. This points to how important behavioral arousal is for memory consolidation and retention.

50
Q

what is post training memory enhancement?

A

when behavioral arousal enhances memories for things that happened earlier, shortly before the arousal got underway.

51
Q

why is post training memory enhancement beneficial?

A

its normall beneficial because the better an organism can remember what led up to a negagtive emotional experience, the better it can avoid similar experiences in the future.

52
Q

genetic basis of posttraumatic stress disorder

A

the lifetime probability of developing PTSD is influenced by a single nucleotide substitution in the gene for catecholomethyltransferase; an enzyme involved in the ianctivation of catecholamines.

survivors of genocides who are HOMOZYGOUS for this mutation were found to have an increased likelihood of developing ptsd, even if their trauma exposure was relatively low.

this is important, especially because NE has been implicated in arousal-based memory enhancement.

53
Q

treatment of PTSD

A

1) exposure therapy
2) D-cycloserine enhancement, an NMDA agonist that enhances EXTINCTION LEARNING (gradual decrease in response to a conditioned stimulus that occurs when the stimulus is presented without reinforcement.)
3) SSRIS

54
Q

the neural mechanisms underlying arousal-driven, post training memory enhancement have been studied extensively. a key player is the ___ ___ ___, whose neurons increase their firing rates after behaviorally arousing events, regardless if they are negative or positive.

A

the neural mechanisms underlying arousal-driven, post training memory enhancement have been studied extensively. a key player is the BASOLATERAL AMYGALA COMPLEX, whose neurons increase their firing rates after behaviorally arousing events, regardless if they are negative or positive.

55
Q

how is the basolateral amygdala complex arousal response initiated?

A

driven by noradrenergic inputs from the LOCUS COERULEUS because NE levels in the basolateral amygdala correlate with arousal.

56
Q

proof that the basolateral amygdala complex is involved in arousal driven post training memory enhancement and memory consolidation.

A

post training infusions of beta blockers interfered with memory consolidation in rats and resulted in rats exploring objects they were already exposed to. injection of NE boost memory, and the rats “remembered “ the objects and didn’t explore them as much.

the basolateral amygdala is involved in CONSOLIDATION and not necessarily recall or perception because these drugs were administered post exposure and a long time before the test. therefore, the manipulations can be interpreted as affecting memory consolidation rather than other aspects of memory

57
Q

_____ activation of the basolateral amygdala complex is necessary and sufficient for post training memory enhancement

A

NORADRENERGIC.

58
Q
A
59
Q

the ___ nucleus of the amygdala, which is part of the basolateral complex, facilitates the flor of info from the ___ into the ____. more specifically, it appears that area ___ of the ____ cortex acts as a gate for info flow.

A

the LATERAL nucleus of the amygdala, which is part of the basolateral complex, facilitates the flor of info from the NEOCORTEX into the HIPPOCAMPUS. more specifically, it appears that area 35 of the PERIRHINAL cortex acts as a gate for info flow.

60
Q

POST TRAINING ACTIVATION of the basolateral complex of the amygdala increases hippocampal levels of the ___ protein, which is linked to ___ ___. These findings imply that activity in the BL complex of the amygdala can influence hippocampal activity not only during the learning episode but also afterwards, during the memroy consolidation phase.

A

POST TRAINING ACTIVATION of the basolateral complex of the amygdala increases hippocampal levels of the ARC protein, which is linked to SYNAPTC PLASTICITY. These findings imply that activity in the BL complex of the amygdala can influence hippocampal activity not only during the learning episode but also afterwards, during the memroy consolidation phase.

61
Q

electrical stimuluation of area ___ of the perirhinal area and the ___ ___, but not of either area by itself, allows activity to spread into the ___ ___ an the ___ ___.

A

electrical stimuluation of area 35/36 of the perirhinal area and the LATERAL AMYGDALA , but not of either area by itself, allows activity to spread into the ENTERHINAL CORTEX AND THE DENTATE GYRUS

This demonstrates the the Lateral amygdala stimulation opens the “gate”
for information flowing into the hippocampus

diagram: show that electrical stimulation of area 36 and the lateral amygdala, but not of either area by itself, allows activity to spread into the entorhinal cortex and dentate gyrus.

62
Q

people with a lesioned amygdala but intact hippocampus do not remember ___ ___ images any better than neutral images

A

people with a lesioned amygdala but intact hippocampus do not remember EMOTIONALLY AROUSAL images any better than neutral images.

this finding is consistent with the hypothesis that part of the amygdala modulates memory for arousing experiences in humans.

amygdala activation at the time of memory formation (encoding) correlates positively with memorys trengthw hen subjects are tested severeal weeks later.

63
Q

In auditory fear conditioning, rats learn to ____ in response to a tone previously paired with an aversive stimulus. The underlying neural circuits run through the ____ and ____ nuclei of the amygdala.

A

In auditory fear conditioning, rats learn to FREEZE in response to a tone previously paired with an aversive stimulus. The underlying neural circuits run through the BASOLATERAL and CENTRAL nuclei of the amygdala.

64
Q

a key player is the ___ ___ of the amygdala, which projects to the autonomic control regions involved in the fight or flight response. this structure then projects to the ___ ___, which coordinates the freezing response to auditory fear conditioning.

A

a key player is the CENTRAL NUCLEUS of the amygdala, which projects to the autonomic control regions involved in the fight or flight response. this structure then projects to the PERIAQUEDUCTAL GRAY, which coordinates the freezing response to auditory fear conditioning.

65
Q

what are the the three unconditioned fear pathways that reach the central nuclei of the amygdala. what does this allow for?

A

the central nucleus receives input from the 1) Parabrachial nuclei, the 2) dorsal thalamus, and 3) from the basolateral complex.

the multiplicity of the uconditioned fear pathways make the system fault tolerant.

66
Q

How does inactivation of the maygdala interfere with auditory fear conditioning?

A

In auditory fear conditioning, testing is performed in a novel chamber to control for the possibility that the rat learned to fear the chamber, rather than the tone.

Inactivating the central nucleus of the amygdala with muscimol (a GABA agonist) during training or testing reduces the freezing response (B).

Injecting muscimol into the basolateral complex likewise reduces the freezing response (C).

67
Q

where specifically does auditory info enter the unconditioned fear pathway, and where does the synaptic strengthening take place?

A

single neurons in the lateral nucleus respond to sounds as well as to foot chock, and their auditory responsees are strengthened by training. auditory info converges with pain info in the CENTRAL NUCLEUS of the amygdala and in the dorsal thalamus, both of which exhibit synpatic plasticity. therefore, auditory fear conditioning involves synaptic strengthening in multiple brain aea.

68
Q

What is contextual fear conditioning? What two structures does it involve?

A

Contextual fear conditioning involves both the amygdala and the hippocampus

In contextual fear conditioning, a rat is asked whether it remembers the chamber (the context) in which it experienced a footshock (A).the question is not whether the animals learned to fear the tone but whether they leaned to fear the chamber

Inactivating the basolateral amygdala (BLA) complex with muscimol, either during training or during testing, impairs context conditioning, as assessed by the freezing response (B).

The expression of contextual fear is also impaired by hippocampal lesions, as long as the lesions are made within 14 days after training (C) (recall that HC is more involved with memory encoding and is not the true stroage place. if lesioning happens after 14 days, the memory is most likely not in the HC anymore and so lesioning it wouldn’t affect results).

Auditory fear conditioning is not affected by those same lesions.

69
Q
A
70
Q

difference behind the neural circuitry of contextual fear conditioning and auditory fear conditioning

A

they are the same in terms of activating the basolateral amygdala. however, contextual fear conditioning is also impared by hippocampal lesions, which do not affect auditory fear conditioning (as long as the lesions are made beofer 14 days). the overall conclusion is that the neural circuits involved in contextual fear conditioning overlap with those for auditory fear conditioning but include some extra elements, notably the hippocampus.

71
Q

what is inhibitory avoidance training?

A

in this paradigm, animals are taught to FEAR A PLACE, but in contrast to contextual fear conditioning, learned fear is assessed by determining whether the trained animals AVOID THE DANGEROUS PLACE.

researchers measure how long it takes the animal to enter the dark half after being shocked in it.

The longer it takes, the stronger the fear memory.

72
Q
A
73
Q

what’re the temporal changes in neural circuitry seen during inhibitory avoidance training?

A

it is found that:

1) a funcitonal HC and amygdala are required for rats to show inhibitory avoidance on the post training DAY 1
2) entorhinal cortex remaines required for at least 30 DAYS.
3) parietal cortex is needed to express the memory for at least 60 DAYS.

this data is consistent with the standard model of memory consolidation in which theneocortex is needed for long term storage.

this was tested by inhibiting a variety of structures with AMPA glutamate inhibitor CNQX.

74
Q

what is the role of the hippocampus and the basolateral amygdala in the social transmission of food preference?

A

large hippocampal lesions impair social transmission of food preference in rats. rats with damaged HC cannot learn from others which food to eat. the basolateral complex must also ibe intact for rats to learn about a novel food from other rats. HOWEVER, once the preference has been established, the BL amygdala is not requried to exhibit foor preference.

Large hippocampus lesions impair socially transmitted food preference (STFP) when performed 1 day after training but not at 21 days after training (B), as predicted by the standard model of memory consolidation. Inactivating the basolateral amygdala during the sniffing phase, but not during testing, eliminates STFP

this implies that the BL Complex is involved in the INITIAL LEARNING OF SOCIALLY TRANSMITTED FOOD PREFERENCES but that those memories are stored else where.

75
Q
A
76
Q

neurosn in the ___ ___ repond to both saccharin and lithium in conditioned taste aversion tests. how was this tested? what does this indicate?

A

neurosn in the BASOLATERAL AMYGDALA repond to both saccharin and lithium in conditioned taste aversion tests. tested by quantifying arc protein, which is involved in synaptic plasticity. the more arc, the more active those neurons were.

it appears that the association between taste and nausea is formed within the basolateral amygdala

77
Q
A
78
Q

which form of memory does a rat rely on in the cross maze paradigm?

A

it depends on how many days of training the animal had. short amount of time = hippocampal activation and place learning. after a long amount of time = the STRIATUM. Habit has formed, it no longer involves true navigation.

it all depends on how activated the hippocampus is relative to the striatum, and vice versa. Infusing glutamate into the hippocampus after each training trial causes the experimental rats to exhibit place learning on day 16, when normal (saline-infused) rats have switched to being guided by the force of habit (B). In contrast, animals receiving glutamate infusions into the striatum exhibit habit learning already on day 8, when control rats normally exhibit place learning (C).