Chapter 12: Learning & Memory Flashcards

Non-Associative Learning - Habituation - Sensitization Associative Learning - Classical Conditioning Memory Systems Amnesia Encoding, Consolidation, and Retrieval

1
Q

What is Learning?

A

Relatively long-lasting change in an organism’s behavior (or thought) as a result of experience.

Learning is a relatively permanent change in behavior that marks an increase in knowledge, skills, or understanding.

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2
Q

Learning is Distinct from Reflexes or Instincts

A

Reflex: Involuntary response to stimuli.

Instinct: Automatic complex behavior (such as, Mating or parenting behavior).

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3
Q

Types of Learning

A

Non-associative learning involves change in the magnitude of response to environmental events
–Habituation
–Sensitization

Associative learning involves a connection between two elements or events
–Classical conditioning
–Instrumental conditioning

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4
Q

Habituation

A

Decrease in strength or occurrence of behavior after repeated exposure to stimulus

Purpose:
Allows organism to focus on learning new or important information

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5
Q

Orienting Response

A

Innate reaction to novel stimuli.
Purpose:
Allows organism to focus on learning new or important information

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6
Q

Sensitization

A

Experience of one (startling) stimulus heightens responding to subsequent stimuli.

Purpose:
Allows organism to focus on potentially dangerous stimuli

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7
Q

Learning with Aplysia

A

Invertebrate learning offers a simpler system in which to isolate neurobiological correlates of learning.

Aplysia:

  • Simple nervous system (~20,000 neurons)
  • Neuronal development hard-wired
  • Identifiable individual neurons
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8
Q

Aplysia

A

Aplysia is a genus of medium-sized to extremely large sea slugs, specifically sea hares, which are one clade of large sea slugs, marine gastropod mollusks. The general description of sea hares can be found in the article on the superfamily Aplysioidea.

The gill-withdrawal reflex occurs when touching the siphon produces a retraction of the gill.

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9
Q

Habituation in Aplysia

A

Less glutamate released onto motor neuron.

  1. Repeated stimuli to siphon.
  2. Sensory neuron releases less neurotransmitter.
  3. Motor neuron releases less neurotransmitter.
  4. Gill shows weak withdrawal.
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10
Q

Sensitization in Aplysia

A

Shocking the head or tail results in an enhanced gill-withdrawal reflex following siphon touch.

Serotonin (interneuron) release promotes enhanced glutamate (sensory neuron) release.

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11
Q

Sensitization in Aplysia:

The Process

A

Serotonin (interneuron) release promotes enhanced glutamate (sensory neuron) release.

  1. Shocking the tail is followed by a stimulus to the siphon.
  2. Sensory neuron in tail releases neurotransmitter.
  3. Facilitating interneurons release serotonin, which causes the siphon sensory neuron to release increased amounts of neurotransmitter.
  4. Motor neuron releases increased amounts of neurotransmitter.
  5. Gill shows stronger-than-normal withdrawal.
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12
Q

Long-term Changes in Habituation and Sensitization

A

Control Aplysia have ~1300 axon terminals on sensory neurons.
Aplysia experiencing sensitization have ~2800 terminals.
Aplysia experiencing habituation have ~800 terminals.

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13
Q

Pavlov

A

Identified and developed an empirical approach for studying classical conditioning.

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14
Q

unconditioned stimulus (US)

A

a biologically relevant stimulus (like food)

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15
Q

unconditioned response (UR)

A

an unlearned reaction to the US (like salivation)

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16
Q

conditioned stimulus

A

an initially neutral stimulus that acquires the ability to signal important biological events (like a bell).

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17
Q

conditioned response

A

a learned reaction to the CS (like salivation)

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18
Q

Classical Eyeblink Conditioning

A

Best understood form of classical conditioning—behavior and neural substrates.

US: Airpuff
UR: Eyeblink to airpuff
CS: Tone
CR: Eyeblink to tone

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19
Q

Eyeblink Conditioning Neural Circuit

A

???

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20
Q

Think Long-term Depression (LTD)

A

Purkinje cell, conditioned response.

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21
Q

Think Long-term Potentiation (LTP)

A

Interpositus, conditioned response.

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22
Q

Long-term Potentiation / Depression

A

NMDA receptor activation leads to changes in synaptic efficacy—i.e., AMPA receptors (which gate sodium) are inserted (LTP) or removed (LTD) from the terminal

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23
Q

Interpositus cell activity

A

LTP-dependent increase in neuronal firing across trials.

NMDA receptor activation leads to changes in synaptic efficacy—i.e., AMPA receptors (which gate sodium) are inserted (LTP) or removed (LTD) from the terminal

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24
Q

AMPA receptors gate

A

sodium

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25
Q

Interpositus (IP) cell activity… cont.

A

LTP-dependent increase in neuronal firing across trials.

Neuronal activity in IP corresponds to generation of eyeblink CR, suggesting IP neurons “drive” the behavioral response.

26
Q

Purkinje cell activity

A

Sole output from cerebellar cortex.
Inhibitory: releases GABA onto IP neurons.
Decrease in firing rate due to LTD.

27
Q

Extinction of eyeblink CR

A

Presentation of CS in absence of US.

  • Not simply unlearning
  • New, opposing response acquired
  • Learned response is unexpressed
  • Spontaneous Recovery: CR recovers with passage of time
  • Renewal: CR is context-specific
  • Reinstatement: US reminder reinstates CR

Behavior and neural circuit is conserved across most mammalian species.

28
Q

Eyeblink Conditioning in Humans

A
Lateral interpositus nucleus
Ventral Striatum
Corpus Collasum
Inferior Thalamus
Red Nucleus
Anterior Cerebellar Vermis
29
Q

Atkinson-Shiffrin Model of Memory

A

Sensory Input&raquo_space; Sensory Memory&raquo_space; Short-Term Memory&raquo_space; Long-Term Memory

30
Q

Sensory Memory

A
  • Large Capacity
  • Lasts up to 1-2 seconds

Sensory input is either discarded from the sensory memory (forgotten) or sent to Short-term memory via attention

31
Q

Short-term or Working Memory

A
  • Small Capacity (5-9 items)
  • Lasts up to 15-18 seconds.
  • Active and temporary representation of information that is maintained for short periods of time
  • Different systems maintain phonological and spatial-visual information
  • Central Executive: Monitors and manipulates WM information
32
Q

Long-term Memory

A
  • Unlimited Capacity

- Lasts indefinitely

33
Q

PFC as the Central Executive

A
  • WM
  • Attention
  • Cognitive flexibility
34
Q

Long-term Memory

A

Declarative or Explicit Memory: memories for facts or events

Non-Declarative or Implicit Memory: memories for skills, habits, and emotions

35
Q

Declarative Memory:

A

Explicit.

Memories for facts or events

36
Q

Implicit Memory

A

Non-Declarative.

Memories for skills, habits, and emotions

37
Q

Long-term Memory

A

Declarative or Explicit Memory: memories for facts (semantic) or events (episodic)

Non-Declarative or Implicit Memory: memories for skills (procedural), habits (nonassociation), and emotions

38
Q

Declarative Memory:

A

Explicit.
Memories for facts or events.

Semantic Memory:
“What is a…?”

Episodic Memory:
“What happened…?”

39
Q

Implicit Memory

A

Non-Declarative.
Memories for skills, habits, and emotions.

Procedural Memory: “How to…?”
Associative Learning: Classical & Operant Conditioning
Non-Associative Learning: Habituation & Sensitization

40
Q

Factual vs. ____

Semantic vs. ____

Knowing vs. ____

A

Factual vs. Autobiographical Memory

Semantic vs. Episodic Memory

Knowing vs. Remembering

41
Q

Episodic Memory

A

Repeated exposure can weaken Episodic Memory.

42
Q

Semantic Memory

A

Repeated exposure can strengthen Semantic Memory.

43
Q

Animal Model of Amnesia

A

Monkeys with medial temporal lobe damage do poorly on delay non-match to sample (DNMS) task

44
Q

Henry Gustav Molaison (H.M.): 1926-2008

A

Two-thirds of medial temporal lobes removed in 1953, including hippocampus, amygdala, and surrounding cortex.

  • Profound anterograde amnesia—able to retain information for only short periods of time.
  • Personality unchanged; IQ increased.
  • Memory highly dependent on attention.
45
Q

Stages of Memory

A

Encoding, Storage/Consolidation

Retrieval

46
Q

Systems of Memory

A

Sensory
Short-term
Long-term

47
Q

Consolidation

A

Process of forming a physical representation of a memory (storing).
- Neural trace formed via synaptic plasticity across many neurons and brain regions.

48
Q

Retrieval

A

Process of accessing stored memories (remembering)

49
Q

Hippocampal Consolidation

A

Memory assessed in control and hippocampal-lesioned rats 1 or 28 days following training.

Necessity of hippocampus diminishes across time.

Memory is consolidated in extra-hippocampal substrate.

50
Q

Standard Consolidation Theory

A

Hippocampus binds many components (sight, sound, etc) of memory together.

As consolidation occurs, memory becomes hippocampal-independent.

As consolidation occurs, memory looses specificity or detail.

51
Q

Memory Consolidation

A
  • Similar context more fear-evoking than distinct context.

- Freezing to generalized context increases with time.

52
Q

Habituation

A

Think less gltuamate

53
Q

Sensitization

A

Think more Serotonin&raquo_space;> more glutamate

54
Q

Prefrontal Cortex plays key role in WM

A
  • Maintains info in WEM

- Places long-term memories into WM

55
Q

How is LTP linked to memory

A

Long-term potentiation (LTP) is a long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously. It is one of several phenomena underlying synaptic plasticity, the ability of chemical synapses to change their strength. As memories are thought to be encoded by modification of synaptic strength, LTP is widely considered one of the major cellular mechanisms that underlies learning and memory.

56
Q

What is the role of the NMDA receptors in LTP

A

NMDA receptors, as part of a large multi-protein complex, in facilitating long-term potentiation (LTP).

57
Q

Do the Purkinje cells excite or inhibit the IP?

A

Purkinje cells (Fig. 1), which strongly inhibit their target neurons in the interpositus nucleus.

58
Q

How does excitatory activity in the IP interact with inhibitory activity from Purkinje cells to produce eyeblink CR?

A

??

59
Q

What behavioral procedures indicate extinction is new learning, not forgetting?

A

In each of them, the extinguished response returns to performance. All of them therefore indicate that extinction is not the same as unlearning, and because all of them can be seen as context effects, they also support the idea that performance after extinction is context-dependent. Extinction involves new learning, and it therefore leaves the CS with two available “meanings” or associations with the US. As is true for an ambiguous word, the context is crucial in selecting between them.
Perhaps the most fundamental of these effects is the renewal effect. In this phenomenon, a change of context after extinction can cause a robust return of conditioned responding. Several versions of the renewal effect have been studied. In the most common one, “ABA renewal,” conditioning is conducted in one context (context A) and extinction is then conducted in a second one (context B). (The contexts are typically separate and counterbalanced apparatuses housed in different rooms of the laboratory that differ in their tactile, olfactory, and visual respects.) When the CS is returned to the original conditioning context (context A), responding to the CS returns. In a second version, “ABC renewal,” conditioning is conducted in context A, extinction is conducted in context B, and then testing is conducted in a third, “neutral” context—context C. Here again, a renewal of responding is observed. In a final version, conditioning and extinction are both conducted in the same context (context A) and then the CS is tested in a second context (context B). Here again, conditioned responding returns, although there is currently less evidence of this “AAB renewal” effect in operant conditioning than in Pavlovian conditioning.

Several facts about the renewal effect are worth noting. First, it has been observed in virtually every conditioning preparation in which it has been investigated. Second, it can occur after very extensive extinction training. In fear conditioning (conditioned suppression) in rats, Bouton and Swartzentruber (1989) observed it when 84 extinction trials followed eight conditioning trials. Other evidence suggests that it can occur after as many as 160 extinction trials, although a recent report suggests that it might not survive an especially “massive” extinction treatment (800 extinction trials after eight conditioning trials. Third, the role of the context is different from the one anticipated by standard models of classical conditioning. Those models accept the view that the context is merely another CS that is presented in compound with the target CS during reinforcement or nonreinforcement. It therefore enters into simple excitatory or inhibitory associations with the US. In the ABA renewal effect (for example), context A might acquire excitatory associations with the US, and context B might acquire inhibitory associations. Either kind of association would summate with the CS to produce the renewal effect (inhibition in B would reduce responding to the CS, whereas excitation in A would enhance it). However, a number of experiments have shown that the renewal effect can occur in the absence of demonstrable excitation in context A or inhibition in context B. These findings, coupled with others showing that strong excitation in a context does not influence performance to a CS unless the CS is under the influence of extinction, suggest that direct associations in a context are neither necessary nor sufficient for a context to influence responding to a CS. The implication is that the contexts modulate or “set the occasion” for the current CS-US or CS-no US association. Put another way, they activate or retrieve the current relation of CS with the US.

A further important characteristic of the renewal effect is that it implies that extinction learning is more context-specific than is original conditioning. Notice that this must be true if one observes ABC and AAB renewal; in either case, conditioning transfers better to the final test context than extinction. But our experiments on renewal have often involved comparisons of groups that received extinction training in the context in which conditioning had occurred or in a discriminably different context. Strikingly, there was no measurable effect of switching the context after conditioning on responding to the CS. In contrast, extinction itself was relatively context-specific, as the renewal effect itself suggests. Recent research suggests that both conditioning and extinction become somewhat context-specific after extinction has occurred. But there is little question that extinction is still more context-dependent than is the original conditioning. We have therefore emphasized the fact that extinction learning is especially context-dependent.

A final fact about the renewal effect is that it appears to be supported by many kinds of contexts. For example, when fear extinction was conducted in the interoceptive context provided by benzodiazepine tranquilizers chlordiazepoxide and diazepam, renewed fear was observed when the rat was tested in the original nondrug state had reported compatible evidence with alcohol, and we have recently collected similar observations with the benzodiazepine midazolam. State-dependent learning or retention can be conceptualized as the drug playing the role of context.

Spontaneous Recovery
The passage of time might also bring about changes in internal and external stimulation that provide a gradually-changing context. Pavlov (1927) first observed another well-known extinction effect. In spontaneous recovery, if time is allowed to pass following extinction, the extinguished response can recover. There are several available explanations of spontaneous recovery, and it seems likely to be multiply determined. However, we have argued that just as extinction is relatively specific to its physical context, so it may be specific to its “temporal context.” Spontaneous recovery can be seen as the renewal effect that occurs when the CS is tested outside its temporal context. Both are due to a failure to retrieve memories of extinction outside the extinction context. Consistent with this perspective, a cue that is presented intermittently during the extinction session can attenuate either spontaneous recovery or renewal if it is presented just before the final test. The parallel results suggest that the two effects might be controlled by a common mechanism: a failure to retrieve a memory of extinction outside the extinction context. Interestingly, changing the physical context and temporal context together can have a bigger effect than changing either context alone, as if their combination creates an even larger context change.

Rapid Reacquisition
A third effect further indicates that conditioning is not destroyed in extinction. In rapid reacquisition, when new CS-US pairings are introduced after extinction, the reacquisition of responding can be more rapid than is acquisition with a novel CS, indicating that the original learning has been “saved” through extinction. Unfortunately, the early literature on rapid reacquisition was often difficult to interpret because many early designs were not equipped to rule out less interesting explanations. To add to the complexity, studies of fear conditioning and flavor aversion learning, have shown that reacquisition can be slower than acquisition with a new CS. (It is more rapid than initial acquisition with a CS that has received the same number of nonreinforced trials without conditioning.) In fear conditioning, slow reacquisition requires extensive extinction training; more limited extinction training yields reacquisition that is neither fast nor slow (Bouton 1986). At least part of the reason these preparations support slow reacquisition is that both typically involve very few initial conditioning trials. In contrast, procedures in which rapid reacquisition has been shown (rabbit nictitating membrane response (NMR) conditioning and rat appetitive conditioning) have usually involved a relatively large number of initial conditioning trials. Consistent with a role for number of trials, Ricker and Bouton (1996) demonstrated that slow reacquisition occurred in an appetitive conditioning preparation when the procedure used the number of conditioning and extinction trials that had been used in previous fear conditioning experiments. In rabbit NMR and heart rate conditioning, extensive extinction training has abolished rapid reacquisition, although slow reacquisition has yet to be observed.

Ricker and Bouton (1996) suggested that rapid reacquisition may partly be an ABA renewal effect that occurs when the animal has learned that previous USs or conditioning trials are part of the original “context” of conditioning. That is, the animal might learn that recent CS-US pairings are part of the context of conditioning, whereas recent CS-only presentations are part of the context of extinction. When CS-US pairings are resumed after extinction, they would thus return the animal to the original conditioning context. The hypothesis is compatible with Capaldi’s (1967, 1994) sequential analysis of extinction, which has made excellent use of the idea that responding on a particular trial is determined by how the animal has learned to respond in the presence of similar memories of previous trials (see below). Presumably, conditioning preparations that use a relatively large number of conditioning trials allow ample opportunity for the animal to learn that previous reinforced trials are part of the context of conditioning. Ricker and Bouton (1996) also reported evidence that high responding during the reacquisition phase was more likely after a reinforced than a nonreinforced trial, which presumably signaled conditioning and extinction, respectively.

In more recent experiments, Bouton et al. (2004) reasoned that if rapid reacquisition is caused by recent reinforced trials generating ABA renewal, then an extinction procedure that includes occasional reinforced trials among many nonreinforced trials should slow down rapid reacquisition by making recent reinforced trials part of the context of both conditioning and extinction. Consistent with this hypothesis, a very sparse partial reinforcement procedure in extinction slowed reacquisition in a final phase compared with a group that had received simple extinction. Such a result is consistent with the idea that rapid reacquisition is at least partly an ABA renewal effect. Because the partial reinforcement treatment involved many more CS-US pairings than did simple extinction, it is difficult to reconcile with the view that rapid reacquisition is a simple function of the strength of an association that remains after extinction.

Reinstatement
A fourth context-dependent extinction phenomenon is reinstatement. In this effect, the extinguished response returns after extinction if the animal is merely reexposed to the US alone. If testing of the CS is contemporaneous with US delivery, then the USs may cause a return of responding because they were encoded as part of the conditioning context. On the other hand, in many studies of reinstatement, testing is conducted at an interval of at least 24 h after US re-exposure; here one still observes reinstatement compared with controls that were not re-exposed to the US. In this case, evidence strongly suggests that the effect is due to conditioning of the context. When the US is presented after extinction, the organism associates it with the context; this contextual conditioning then creates reinstatement. For example, if the reinstating USs are presented in an irrelevant context, there is no reinstatement when the CS is tested again. Independent measures of contextual conditioning also correlate with the strength of reinstatement. And if the animal receives extensive extinction exposure to the context after the reinstatement shocks are presented, reinstatement is not observed. These results indicate that mere re-exposure to the US is not sufficient to generate reinstatement. It is necessary to test the CS in the context in which the US has been re-exposed.

This effect of context conditioning is especially potent with an extinguished CS. For example, Bouton (1984) compared the effects of US exposure in the same or a different context on fear of a partially extinguished CS or another CS that had reached the same low level of fear through simple CS-US pairings (and no extinction). Although contextual conditioning enhanced fear of the extinguished CS, it had no impact on the nonextinguished CS. This result is consistent with the effects of context switches mentioned above: An extinguished CS is especially sensitive to manipulations of the context. One reason is that contextual conditioning may be another feature of the conditioning context; its presence during a test may cause a return of responding after extinction because of another ABA renewal effects.

In summary, a variety of research indicates that responding to an extinguished CS is susceptible to any of a number of recovery effects, suggesting that extinction is not unlearning. Indeed, based on the results of a number of tests that allow a specific comparison of the strength of the CS-US association before and after extinction has suggested that extinction involves no unlearning whatsoever; the original CS-US association seems to survive essentially intact. Extinction must thus depend on other mechanisms. The renewal effect, and the fact that extinction leaves the CS so especially sensitive to manipulations of context, is consistent with the idea that extinction involves new learning that is especially context-dependent. We have therefore suggested that extinction leaves the CS under a contextually modulated form of inhibition: The presence of the extinction context retrieves or sets the occasion for a CS-no US association.

Other Phenomena With Theoretical Links to Extinction

Several behavioral phenomena have been linked theoretically with extinction, and it is worth considering them to see what insights they provide.

60
Q

delay non-match to sample

A

Delayed nonmatch-to-sample

A developmental task that tests for explicit learning and memory is the delayed nonmatch to sample (DNMS) task. The DNMS task requires the subject to compare a presented sample object with a previously presented comparison object and encourages the selection of a novel object with an object’s second presentation. An edible reward is given to the subject to encourage the novel item selection. After learning the rule for avoiding the familiar object in favor of novelty, the delay period between object demonstrations is increased from 10 to 120 seconds and the number of displayed objects requiring recollection increases. The DNMS task is likely both implicit and explicit in nature. Its use of reward conditioning is likely implicit in nature (Squire, 1992). Its use of positive emotional conditioning helps to pair and associate item novelty with reward salience. This shapes the subject’s learning toward identifying novelty as the desired object quality for selection. The DNMS task itself is also likely explicit; it requires the infant or child to recognize an object’s previous exposure, to differentiate its qualities from that of a new object, to hold this information in mind during a delay period, and is characterized by rapid learning in developmentally capable older children and adults.

Surgical removal of either the hippocampal region’s perirhinal cortex or the ventromedial prefrontal cortex (vmPFC) in the nonhuman primate impairs the ability for acquiring the cognitive strategy needed for performing explicit aspects of the DNMS task (Bachevalier, Beauregard, Alvarado, 1999; Bachevalier & Mishkin, 1986; Malkova, Mishkin, & Bachevalier, 1995). This suggests that both brain regions are needed for successful completion of the DNMS task. Human research findings further demonstrate that human amnesics incurring damage limited to the hippocampus proper and damage extending into surrounding structures like the entorhinal cortex (Bayley, Hopkins, & Squire, 2003; Squire & Zola, 1997) are unable to both declare the inherent principle and perform as well as normal comparison controls on the DNMS task (Squire, Zola-Morgan, & Chen, 1988). According to these findings, amnesics also experience significant reductions in accuracy as DNMS task-dependent delays increase beyond 5 seconds.

Furthermore neuroimaging findings reference a significant role for the right hippocampus proper during DNMS training’s encoding phase and a trend for familiar-novelty comparisons and item recognition during the retrieval phase. A neuroimaging study by de Zubicaray and colleagues (2001) monitored and tracked brain activity with positron emission tomography (P.E.T.) regional cerebral blood flow (rCBF) during the encoding, retention, and retrieval phases of DNMS training. It found significant lateral-medial activation shifts from more ventrolateral regions of the anterior prefrontal cortex or frontal pole region to the ventromedial prefrontal cortex and a posterior to anterior shift in the dorsolateral prefrontal cortex (dlPFC) from encoding to retention and retention to retrieval phases. Sensory cortical activations also shifted from posterior visual regions in the occipital lobe and lingual gyrus in the encoding phase, to the parietal lobe in the retention phase, and then to both the parietal and occipital lobules in the retrieval phase, suggesting successful engagement of visual areas during DNMS dependent short delays. Activation in the caudate tail during encoding and retention phases was probably associated with its receipt of visuomotor information from the occipital lobe and return relay to this structure (Brown, Desimone, & Mishkin, 1995) to facilitate successful subsequent task-related classification accuracy (Seger & Cincotta, 2005). Transient ventrolateral prefrontal cortical activity during the retention phase likely helped to facilitate increased cognitive demands during periods of increasing long delays (Elliott & Dolan, 1999) to avert tendencies for perseverative interference (Kowalska, Bachevalier, & Mishkin, 1991). Transient activations during the retrieval phase in the perirhinal cortex of the hippocampal region were likely evidence of the developing ability for cue-dependent retrieval that characterizes visual long-term memory recognition and familiarity (Buffalo, Ramus, Squire, & Zola, 2000; Hadfield, Baxter, & Murray, 2003; Holscher, Rolls, & Xiang, 2003; Malkova, Bachevalier, Mishkin, & Saunders, 2001). In total these findings suggest differential task-related activation sites for encoding, retention, and retrieval during DNMS learning. They also reflect that different brain regions are involved in task-related encoding, retention, and retrieval processes. They support that memory is not a single entity and is characterized by many different multiple systems which interact in a structurally time-dependent manner during the DNMS task. The nature “of representation stand(ing) between perception and production” (Meltzoff & Moore, 1997, p. 182) may be the developmental response of multiple memory systems underlying processes and abilities for storage, retention, and retrieval of representational memory and associated task-related behaviors.

The DNMS is developmentally more complex than deferred and elicited imitation tasks. Overman (1990) hypothesized that this “may be primarily due to slow learning of the (object’s) novelty- (external) reward rule and secondarily due to the inability to remember a particular item or rule” (p. 380). Because certain objects inherently possess their own rewarding qualities of color, texture, size, shape, etc. it is likely that a sample object’s intrinsic rewarding quality in the youngest of subject populations may distract and interfere in the establishment of the associational learning required for the novelty-initial presentation reward rule in infants. Infants older than four months can eventually acquire the DNMS strategy, with 4 month olds tolerating up to 10 second delays, 6 month olds tolerating 3 minute delays, and 12-9 month olds tolerating up to 10 minute delays between object demonstrations (Diamond, 1990). According to Overman (1990) and Overman and colleagues (1992) twelve to fifteen month old child can acquire the adult standard of the DNMS and reach performance criterion with up to 478 errors in 69-75 test days depending upon task-related age-dependent modifications (Overman, Bachevalier, Turner, & Peuster, 1992). Eighteen to twenty month olds can learn the DNMS strategy with up to 127 errors in 24-25 days over 10 weeks of testing. Twenty-two and thirty-two month olds can acquire it with up to 40 total errors in 11-14 days over four weeks of testing. The oldest children aged 45-81 months perform at levels similar to adults but with accuracy scores below those of adult. Finally adults can learn the DNMS strategy in two-three days with incurring an average of four errors.

Therefore increasing developmental age is associated with increased accuracy of DNMS performance and task related item complexity paired with increasing ability for managing the duration of delay periods between object presentations. These increasing capabilities are also likely supported by increasing developmental expression of memory systems supporting perception, retention, storage, and retrieval.