Physiology of Behavior

Learning & Memory

Nathaniel W. Nelson, Ph.D., LP, ABPP University of St. Thomas, GSPP

Overview of Learning and Memory

• Learning − Acquire new information − Our experiences change our nervous system and behavior

• Memory − Long-term changes in the nervous system following learning

Types of Memory

• Sensory Memory

• Short-term (Working) Memory

• Long-term Memory − Non declarative Memory (implicit) − Declarative Memory (explicit)

Types of Memory

Copyright © Allyn & Bacon 2007

Simple model of the learning process.

The Steps of Learning and Memory

The Nature of Learning At least 4 types of learning:

• (1) Sensory/Perceptual • Recognition of a particular stimulus (i.e., that have been perceived

previously); modality nonspecific; thought to be associated with changes in sensory association cortices

• (2) Stimulus-response • Ability to learn to perform a particular behavior in presence of particular

stimulus; includes: • classical conditioning

• Pairing of an unconditioned stimulus (e.g., puff of air) with a conditioned stimulus (e.g., tone), with the result that the usual and unconditioned response (e.g., blinking) is effectively elicited by the CS alone, resulting in a conditioned response (e.g., blinking)

• instrumental (operant) conditioning • When effects of a particular behavior in a particular situation increase

(via reinforcing stimulus) or decrease (via punishing stimulus) the probability of the behavior

The Nature of Learning

• (3) Motor • Differs from (1) and (2) in the degree to which new forms of behavior are learned;

the more novel the behavior, the more the neural circuits in the motor systems of the brain must be modified

• (4) Relational • Complex learning that entails relationships among individual stimuli. Can involve

integration of various sensory modalities, or relationships of stimuli within one modality (e.g., spatial learning). Also includes:

• Episodic learning • Remembering sequences of events (episodes) that requires tracking not only

of individual stimuli but the chronology of presentation

Learning to Recognize Stimuli

− Ventral Stream  WHAT Pathway

− Dorsal Stream  WHERE Pathway

Role of the Extrastriate Cortex in Perceptual Learning

Activation of neural circuits in the sensory association cortex constitutes the “readout” of perceptual memory. Seeing a specific visual stimulus results in a unique pattern of neural activity in the extrastriate cortex. The same visual stimulus, if seen again later, will stimulate the same neural activity in the extrastriate cortex.

Perceptual Learning

• Retaining perceptual information in short-term memory

− Role of extrastriate cortex  Fusiform face area and parahippocampal place area

− Role of prefrontal cortex  “Manipulate and organize to-be-remembered

information, devise strategies for retrieval, and also monitor the outcome” (Miyashita, 2004)

Copyright © Allyn & Bacon 2007

fMRI activation caused by retrieval of auditory (red/orange) and visual (green/blue) memories. Subjects read words that had previously been accompanied with sounds or pictures.

Words paired with pictures primarily activated visual association cortex; words paired with sounds primarily activated auditory association cortex.

A Simple Neural Model of Classical Conditioning

When the 1,000-Hz tone is presented just before the puff of air to the eye, synapse T is strengthened.

Hebb ruleHebb rule – The hypothesis proposed by Donald Hebb that the cellular basis of learning involves The hypothesis proposed by Donald Hebb that the cellular basis of learning involves

strengthening of a synapse that is repeatedly active when the postsynaptic neuron strengthening of a synapse that is repeatedly active when the postsynaptic neuron fires.fires.

Conditioned Emotional Responses

The figure shows the probable location of the changes in synaptic strength produced by the classically conditioned emotional response that results from pairing a tone with a foot shock.

A Simple Neural Model of Operant Conditioning

Stimulus-Response Learning: Operant Conditioning

• Role of Basal ganglia:

– Circuits begin in sensory association cortex (perception) – End in motor association cortex (movements) – Two pathways

▪ Direct transcortical connections ▪ Connections via basal ganglia and thalamus

Operant Conditioning: Pathways

• Transcortical Pathways – Acquisition of declarative, episodic memories

(with hippocampus)

• Basal Ganglia Pathways – As learned behaviors become automatic, they

are “transferred” to basal ganglia – Caudate nucleus and putamen

Stimulus and Response Pathways

• (1) Information from transcortical (1) Information from transcortical pathways to basal ganglia (as behavior pathways to basal ganglia (as behavior becomes automatic). The caudate and becomes automatic). The caudate and putamen receive information from the putamen receive information from the frontal lobes about movements. frontal lobes about movements.

• (2) Information goes to globus pallidus(2) Information goes to globus pallidus

• (3) Information then goes to (3) Information then goes to premotor/supplementary motorpremotor/supplementary motor

• (4) Finally, information goes to the (4) Finally, information goes to the primary motor cortex where the primary motor cortex where the response behavior is initiated.response behavior is initiated.

Relational Learning • anterograde amnesia

• Amnesia for events that occur after some disturbance to the brain, such as head injury or certain degenerative brain diseases.

• retrograde amnesia • Amnesia for events that preceded some disturbance to the brain, such as a

head injury or electroconvulsive shock.

• Korsakoff’s syndrome • Permanent anterograde amnesia caused by brain damage resulting from

chronic alcoholism or malnutrition.

• confabulation • The reporting of memories of events that did not take place without the

intention to deceive; seen in people with Korsakoff’s syndrome. Prefrontal cortex (particularly medial and orbital prefrontal) plays role in evaluation of accuracy of memories.

Copyright © Allyn & Bacon 2007

Schematic definition of retrograde amnesia and anterograde amnesia.

Retrograde Amnesia in Patients with Hippocampal Damage

Hippocampal damage appears to disrupt the gradual storage of long-term memories. Memories older than approximately 15 years are relatively intact even in people with retrograde amnesia, which suggest that the storage process requires between 10 and 15 years to be completed. (Data from Bayley et al., 2006.)

Relational Learning and the Case of H.M.

From: https://www.nytimes.com/2008/12/05/us/05hm.html

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

Relational Learning • The case of H.M.

• Age 9, involved in head injury that is thought to have been the cause of what will become an intractable epilepsy (i.e., high-dose anti-convulsants unable to manage seizures through adulthood)

• Undergoes bilateral mesial temporal resection (including hippocampus), which effectively managed epilepsy, but resulted in profound anterograde amnesia.

• Many studies have since been conducted on H.M. given the relatively pure nature of his amnesia. Initial researchers concluded that the hippocampus:

• (1) is not the location of long-term memories or their retrieval • H.M. is able to recall events from remote history, can talk, can dress self, etc.

• (2) is not the location of immediate (‘short-term’) memories • H.M. is able to converse and hold information long enough to do so effectively

• (3) is involved in converting immediate (‘short-term’) into long-term memories • H.M., when presented with new information, seems to understand it and remember it as long as he

thinks about it, even if the information is not permanently encoded • Carlson (2007) provides evidence that these 3 conclusions are too simplistic • Still, early research supports the notion that hippocampus is involved in consolidation

of information: conversion of short-term to long-term memory

Bilateral Amygdala Damage in Patient H. M. (a)

Note the lesions in H. M.’s temporal lobe and hippocampus that differ from a typical brain.

Figure 13.24 Bilateral Amygdala Damage in Patient H. M.(b)

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Relational Learning

• Spared learning abilities • H.M. and others with anterograde amnesia retain:

• Perceptual learning • Broken drawing recognition

• H.M. showed improved performances at 1-hour and 4 months • Recognition of faces and melodies

• Stimulus-response learning • Classical and Instrumental conditioning

• Motor learning • Asterisk sequence task

Examples of Broken Drawings

(Reprinted with permission of author and publisher from Gollin, E. S., Developmental studies of visual recognition of incomplete objects, Perceptual and Motor Skills, 1960, 11, 289–298.)

A broken drawings task. An example of a spatial learning task on which anterograde amnesics are able to demonstrate improved performances after delay periods.

Relational Learning

• Although anterograde amnesics are capable of showing at least some degree of spatial, stimulus-response, and motor learning, they do not recall having learned the tasks previously.

• declarative memory (explicit) • Memory that can be verbally expressed, such as memory in a person’s life.

• nondeclarative memory (non-explicit) • Memory whose formation does not depend on the hippocampal formation; c

collective term for perceptual, stimulus-response, and motor memory.

Relational Learning • episodic memory

• Declarative memory of a collection of perceptions of events organized in time and identified be a particular context.

• semantic memory • Declarative memory of facts and general information.

• semantic dementia • Loss of semantic memories caused by progressive degeneration of the

neocortex of the lateral temporal lobes. Episodic memory may be spared.

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Section through a normal hippocampus.

Section through hippocampus of patient Section through hippocampus of patient with CA1 damage as a result of anoxia. with CA1 damage as a result of anoxia. CA1 is especially rich in NMDA receptors. CA1 is especially rich in NMDA receptors. Various metabolic disturbances (e.g., Various metabolic disturbances (e.g., seizures, anoxia, hypoglycemia) cause seizures, anoxia, hypoglycemia) cause abnormally high release of glutamate, with abnormally high release of glutamate, with excessive NMDA activation, excessive excessive NMDA activation, excessive intracellular Ca, and related neuronal intracellular Ca, and related neuronal destruction.destruction.

Copyright © Allyn & Bacon 2007

Relative durations of retrograde amnesia after damage to CA1, entire hippocampal formation, or hippocampal formation and medial temporal cortex.