Chapter 12 - Learning and
Memory
2 TYPES OF LEARNING
Associative learning, occurs when an organism forms a
connection between two features of its environment. Classical conditioning, which
allows organisms to learn about signals that predict important events, falls into this
category.
Non-associative learning, including the processes of habituation and sensitization,
involves changes in the magnitude of responses to stimuli rather than the formation
of connections between specific elements or events.
Habituation, occurs when an organism reduces its response to unchanging,
harmless stimuli, such as the sound of an air conditioner or furnace that becomes
background noise.
Sensitization involves, an increased response to other environmental stimuli due to
repeated exposure to a strong stimulus, seen in exaggerated responses to
movement, light, and noise following major disasters like earthquakes.
In Classical conditioning, organisms learn that stimuli act as signals predicting the
occurrence of important events, with conditioned stimuli (CS) gaining significance
through learning, and conditioned responses (CR) being behaviors learned in
response to stimuli that reliably predict future events.
USING INVERTEBRATES TO STUDY LEARNING
Invertebrates, with their large-celled and simple nervous systems, serve as ideal
subjects for learning research.
“Research on invertebrate learning includes bizarre demonstrations like G. A.
Horridge's (1962) experiment showing that headless cockroaches can learn
classically conditioned responses."
"The sea slug Aplysia californica is commonly used in invertebrate learning
research due to its easily observable nervous system."
"The gill-withdrawal reflex in Aplysia habituates over time when the siphon is
repeatedly touched, resulting in a gradual diminishment of the reflex."
"Eric Kandel and colleagues traced the neural pathways responsible for habituation
in Aplysia, revealing the role of synapses between sensory neurons and motor
neurons."
"Kandel demonstrated that repeated touching of the siphon in Aplysia led to
reduced neurotransmitter release, depleting available neurotransmitter and
producing short-term habituation."
CLASSICAL CONDITIONING OF FEAR
Many emotional responses, such as exam jitters or a child's fear of dogs, are
learned through classical conditioning, with the amygdala playing a crucial role in
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emotional response conditioning (Wilensky et al., 2006).
In classical fear conditioning studies with rats, a stimulus like a tone (CS) paired
with an electrical shock (UCS) results in a conditioned fear response (CR) leading
to a reduction in behaviors incompatible with fear, such as
feeding.
Information about the CS and UCS converges in the amygdala, where a high influx
of calcium triggers events, similar to Aplysia, resulting in protein synthesis and
increased sensitivity to subsequent CS input, making the newly conditioned circuits
respond more strongly to the CS alone (Wilensky et al., 2006)
CLASSICAL CONDITIONING OF THE EYEBLINK
Investigations into conditioned eyeblinks in rabbits by Richard Thompson and
colleagues involve pairing a tone (CS) with a puff of air directed at the rabbit's eye
(UCS), resulting in the movement of the nictitating membrane, an inner eyelid found
in some animals (Christian & Thompson, 2003; Lee & Thompson, 2006; Thompson,
Thompson, Kim, Krupa, & Shinkman, 1998).
The cerebellum, particularly the interpositus nucleus, plays a crucial role in classical
conditioning of eyeblinks, with recordings showing an increase in the interpositus
nucleus's response as learning proceeds (Woodruff-Pak & Disterhoft, 2008;
Thompson, 1986).
Reversible lesion experiments, particularly inactivating the interpositus nucleus by
cooling, effectively prevent classical conditioning, indicating the primary
responsibility of the interpositus nucleus in forming the classically conditioned
response of the nictitating membrane in rabbits (Robleto & Thompson, 2008; Krupa,
Thompson, & Thompson, 1993).
CEREBELLAR CIRCUITS AND CLASSICAL CONDITIONING
The cerebellum, with its unique anatomy, is well-suited for classical conditioning,
particularly in its cortex where Purkinje cells receive climbing fibers from the inferior
olive and parallel fibers from granule cells, forming inhibitory synapses on the
cerebellum's output cells in the deep nuclei.
According to James Albus (1971), learning occurs when climbing-fiber and parallelfiber synapses onto a Purkinje cell are activated simultaneously, a proposition
supported by Masao Ito's (1984) recordings showing a reduction in Purkinje cell
EPSPs lasting up to one hour through long-term depression (LTD).
LTD involves a decrease in the number of available glutamate receptors in the
Purkinje cell membrane, essential for learning the eyeblink conditioned response
(CR) in the inferior olive-climbing fiber system.
TRACE CONDITIONING AND EXTINCTION
Classical conditioning can be categorized into delay conditioning, where the CS and
UCS overlap without a stimulus-free interval, and trace conditioning, which involves
a stimulus-free interval between the CS and UCS, requiring the participation of
forebrain areas.
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Research with mutant mice and human patients with cerebellar lesions revealed
that abnormal cerebellums interfered with delay conditioning but not trace
conditioning, indicating different learning processes for these two types.
Trace conditioning, involving forebrain structures like the sensory cortex,
hippocampus, and prefrontal cortex, requires conscious, declarative processes,
making it a valuable model for studying declarative memories across species.
MEMORY
Types of memory
In the Atkinson-Shiffrin model, information initially enters sensory memory, which
can hold a large amount of data briefly.
Selected data moves to short-term memory, with a limited capacity of about five to
nine items, often leading to loss of previous information. Short-term memory is
temporary and involves temporary storage areas managed by a "central executive"
process.
The final destination is long-term memory, which has few limitations on capacity or
duration. Long-term memories include semantic, episodic, and procedural
memories, with semantic and episodic memories grouped as declarative memories,
recalled consciously, while procedural memories are recalled unconsciously.
The model distinguishes explicit and implicit memories, illustrated in cases of
anterograde amnesia where patients can form implicit memories despite a lack of
explicit recall.
The search for the engram, the physical representation of memory in the brain,
remains a focus in psychology.
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BRAIN MECHANISMS IN MEMORY
The search for the engram, the physical representation of memory in the brain,
involved early efforts by psychologists like Karl Lashley and neurosurgeon Wilder
Penfield. Lashley conducted experiments on rats, concluding that all parts of the
cortex contribute equally to learning and memory, a concept known as
equipotentiality.
However, this idea is now considered a mistake, as more recent data suggest
uneven participation of different cortex areas in memory.
Wilder Penfield, through cortical mapping of patients undergoing seizure disorder
surgery, found experiential responses linked to temporal lobe stimulation, focusing
interest on the temporal lobe's role in long-term memory.
Other researchers using single-cell recordings provided evidence for specific,
localized memory storage, with neurons showing relationships to particular types of
information, challenging Lashley's equipotentiality concept.
THE TEMPORAL LOBE AND MEMORY
The temporal lobe's role in memory was explored through studies on patients with
anterograde amnesia, such as the well-known case of patient H. M. H. M., who
underwent extensive surgery, including removal of parts of the temporal lobe,
demonstrated a profound inability to transfer new information from short-term longterm memory while retaining procedural memory.
This case supports the distinction between explicit and implicit memories, as well as
the Atkinson-Shiffrin model's stage approach to memory. While H. M.'s damage
impacted explicit memories, it did not affect implicit memories or stored long-term
memories, suggesting that the hippocampus may not be the storage location for the
engram.
Further studies on monkeys with medial temporal lobe lesions, including the
amygdala, hippocampus, and surrounding areas, showed impaired performance on
a delayed nonmatching to sample task, emphasizing the role of these structures in
the formation of long-term memories.
LONG-TERM POTENTIATION (LTP)
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Long-Term Potentiation (LTP), explored since the 1970s, involves neural
mechanisms in the hippocampus crucial for learning and memory. The
hippocampus, consisting of Ammon's horn and the dentate gyrus, plays a
central role. Input from the cortex enters through the parahippocampal and rhinal
cortices, reaching the hippocampus.
LTP, demonstrated through rapid electrical shocks, enhances synapses’ efficiency,
lasting a long time, and requiring only seconds of input. LTP aligns with Donald
Hebb's cellular learning model, involving associativity and cooperativity.
NMDA glutamate receptors facilitate these processes. While initially observed in the
hippocampus, LTP has been identified throughout the central nervous system,
emphasizing its significance in understanding memory formation.
LTP AND SPATIAL MEMORY
Studies on spatial memory, examining an organism's ability to map locations,
provide additional evidence linking Long-Term Potentiation (LTP) to memory.
Researchers, like O'Keefe and Dostrovsky, demonstrated that mice use distinct
hippocampal activation patterns to represent spatial locations, forming stable maps
within minutes of entering a new environment.
This rapid formation and stability align with features of both long-term memories and
LTP. Investigations using genetic mutations disrupting LTP-related pathways, such
as NMDA receptor components, show a negative impact on spatial memory. While
animals with impaired LTP can still form spatial maps, these maps lack stability.
The impairment leads to the formation of new maps instead of reactivating previous
ones, resembling the behavior of patients with memory deficits. Applying NMDA
receptor antagonists also impairs spatial learning in rodents and prevents the
development of LTP in the hippocampus.
THE DIENCEPHALON AND MEMORY
The hippocampus and the temporal lobe are closely linked to the thalamus, and
disruptions to these structures or their connections can lead to amnesia.
Case studies, such as that of patient N. A., who suffered a thalamic lesion from a
fencing foil accident, show similarities to the memory loss experienced by H. M. N.
A. exhibited anterograde amnesia, preserving intelligence and short-term memory
but struggling with forming new explicit memories. Chronic alcoholics with
Korsakoff's syndrome, often resulting from thiamine deficiency, display similar
anterograde amnesia symptoms.
Thiamine deficiency damages the dorsomedial thalamus and mammillary bodies in
the diencephalon. Patients with Korsakoff's syndrome also suffer severe retrograde
amnesia, possibly due to lesions in various brain areas, including the cerebellum,
brainstem, cortex, and diencephalon. Animal studies support these findings,
showing that monkeys with thalamic and mammillary body lesions struggle with
memory tasks.
SEMANTIC MEMORY AND THE CEREBRAL CORTEX
Semantic knowledge, encompassing basic facts and language, is widely distributed
in the cortex. Different areas of the association cortex activate during semantic
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memory tasks based on specific concept characteristics.
PET scans by Alex Martin and colleagues revealed that when naming animals,
participants activated the left medial occipital lobes associated with visual
processing, while naming tools activated the left premotor area and the left middle
temporal gyrus associated with tool-use concepts.
Case studies of patients with association cortex damage, like the one by McCarthy
and Warrington, further support the distributed nature of semantic knowledge.
Retrieving these memories involves coordinated efforts, and Antonio Damasio
suggests the existence of a
"convergence zone" responsible for assembling various aspects of a memory into a
cohesive whole.
Likely candidates for this convergence zone in semantic memories include areas
along the left lateral inferior frontal gyrus. These areas become more active when
language rules or world knowledge are violated compared to correct language
usage or factual information.
EPISODIC MEMORY AND THE CEREBRAL CORTEX
Episodic memory, involving personal experiences, is distinct from semantic memory.
Patients with cortical damage, particularly in the prefrontal areas, may experience
source amnesia, retaining semantic knowledge but forgetting how and when they
learned specific information.
For instance, Patient K. C. retained general semantic knowledge but couldn't
remember details about learning to play chess after sustaining damage to specific
cortical areas. Episodic memories contribute to our sense of self, and brain imaging
studies suggest the involvement of the anterior prefrontal cortex and posterior
cingulate cortex in retrieving personal episodic memories.
The distinction between fantasy and reality relies on episodic memory, as evidenced
by brain activity patterns when participants were asked about the possibility of
conversing with real or fantasy figures. Brain areas associated with episodic
memory were active when considering reality, while areas linked to semantic
processing were more active when contemplating fantasy. Disturbances in this
distinction may underlie delusions in some psychological disorders.
SHORT-TERM MEMORY AND THE BRAIN
The Atkinson-Shiffrin model suggests that short-term memory (working memory)
involves the central executive, the phonological loop, the visuo-spatial sketchpad,
and an episodic buffer. In terms of brain localization, the dorsolateral prefrontal
cortex (DLPFC) and the anterior cingulate cortex (ACC) are believed to underlie the
central executive.
These areas contribute to attentional aspects of short-term memory. Patients with
prefrontal cortex lesions struggle with tasks like the Wisconsin card-sorting test,
indicating difficulties in shifting attention and adjusting to new rules. Research on
memory development, such as the object permanence test, suggests that a mature
prefrontal cortex is necessary for short-term memory.
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The ACC also plays an executive role in short-term memory, as evidenced by
studies comparing people with large or small short-term memory capacities. People
with larger capacities show more ACC activation and use different memory
strategies, supporting the ACC's involvement in processing verbal information in
short-term memory.
THE STRIATUM AND PROCEDURAL MEMORY
The striatum, encompassing the basal ganglia and nucleus accumbens, plays a
crucial role in procedural memory formation. Involved in motor system functions,
these structures are particularly associated with learning and remembering motor
patterns. The nucleus accumbens contributes emotional and reward-related aspects
to procedural memory. During trial-and-error learning, the striatum encourages
exploration and participates in the evaluation of changes leading to greater
accuracy and reward. Studies with rats in a maze task revealed that the striatum's
neuronal activity is involved in both exploration and exploitation phases of learning.
In a specific study with rats learning maze tasks, it was observed that the striatum’s
role is more pronounced in procedural than declarative memories. Rats with lesions
in structures associated with the hippocampus struggled with declarative memory
tasks, where explicit episodic memories are crucial, but performed normally in
procedural memory tasks. On the other hand, rats with lesions in the basal ganglia
had difficulty with procedural tasks but showed little impairment in declarative tasks.
This provides evidence for the distinct involvement of the striatum in procedural
memory formation.
SHORT-TERM SENSITIZATION PROCESS
Single session produces behavior changes lasting minutes. [repetition]
Serotonin activates adenylyl cyclase, converting ATP to cAMP.
cAMP activates protein kinase A (PKA).
PKA effects include prolonged action potential, increased vesicle movement, and
opening of more Ca2+ channels, enhancing glutamate release. [retrieval]
LONG-TERM SENSITIZATION PROCESS
Repeated and spaced-out sensitization trials result in behavioral changes lasting
weeks.
cAMP-PKA-MAPK-CREB pathway activated.
PKA, recurrently activated, triggers MAP kinase.
PKA and MAP kinase transported to neural cell body, activating CREB-1 and
inhibiting CREB-2.
CREB-1 and MAP kinase block inhibitory actions of CREB-2, allowing gene
transcription.
Two genes expressed: one for ubiquitin carboxyterminal hydrolase (maintaining
PKA activity) and another for C/EBP (stimulating new synaptic terminal growth).
Biochemical and structural changes account for long-term presynaptic changes.
THE EFFECTS OF STRESS ON MEMORY
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Yerkes-Dodson Law and Stress Effects on Memory
Stress effects on memory depend on task complexity.
Simple tasks show linear improvement with increasing stress.
Complex tasks show improvement up to a point, then decline with stronger
stress.
Timing and Stress-Related Memory Formation
Stress initially enhances memory formation.
This enhancement is followed by a refractory period impairing memory
formation.
This refractory period may protect important memories from interference.
Hippocampus and Amygdala Interaction
Stress impacts hippocampus and amygdala independently.
Case study: Emotional component processed by the amygdala, but
hippocampus unable to encode declarative details.
Prefrontal Cortex and Stress
Stress affects prefrontal cortex functions (coping, decision making, planning,
multitasking).
Inverted U-shaped relationship with dopamine and norepinephrine release.
Implications and Potential Interventions
Understanding these processes may help prevent and treat traumatic and false
memories.
Glucocorticoids released during stress (e.g., cortisol) correlated with more false
memories.
Propranolol, blocking glucocorticoid effects, might prevent traumatic memories.
Manipulation of enzymes in animals shows progress in "erasing" long-term
memories, offering potential PTSD treatment approaches.
AGING AND MEMORY
Age-Related Changes in Learning and Memory
Eyeblink conditioning is more difficult and takes longer in older participants.
Most cognitive abilities in healthy older adults remain stable.
Brain modifications may compensate for age-related declines in function.
Brain Activity and Aging
Decreased blood flow observed in brain regions essential for memory and
cognition.
Areas of increased activation suggest brain reorganization to maintain
stable cognitive performance despite age-related deficits.
Comparisons in Memory Encoding
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Young and older adults show no differences in hippocampal activation
during successful
encoding of face-name pairs.
Young participants exhibit reduced activation in parietal lobe and posterior
cingulate cortex
during successful encoding.
High-performing older participants show similar areas of deactivation, while
lower-performing
ones may be in early dementia stages.
Alzheimer's Disease and Memory Encoding
Participants at risk for Alzheimer's or with mild cognitive impairment
demonstrate increased
hippocampal activity during encoding.
Increased activity may represent the brain's compensatory effort.
Eventually, compensation fails as dementia progresses, leading to reduced
hippocampal activity
below healthy older controls.
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