Chapter Introduction

CHAPTER 14

How Do We Learn
and Remember?

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CLINICAL FOCUS 14-1 REMEDIATING DYSLEXIA

14-1 CONNECTING LEARNING AND MEMORY

STUDYING LEARNING AND MEMORY IN THE LABORATORY

EXPERIMENT 14-1 QUESTION: DOES AN ANIMAL LEARN THE ASSOCIATION BETWEEN EMOTIONAL EXPERIENCE AND ENVIRONMENTAL STIMULI?

TWO CATEGORIES OF MEMORY

WHAT MAKES EXPLICIT AND IMPLICIT MEMORY DIFFERENT?

WHAT IS SPECIAL ABOUT PERSONAL MEMORIES?

14-2 DISSOCIATING MEMORY CIRCUITS

DISCONNECTING EXPLICIT MEMORY

DISCONNECTING IMPLICIT MEMORY

CLINICAL FOCUS 14-2 PATIENT BOSWELL’S AMNESIA

14-3 NEURAL SYSTEMS UNDERLYING EXPLICIT AND IMPLICIT MEMORIES

NEURAL CIRCUIT FOR EXPLICIT MEMORIES

CLINICAL FOCUS 14-3 ALZHEIMER DISEASE

CLINICAL FOCUS 14-4 KORSAKOFF SYNDROME

CONSOLIDATION OF EXPLICIT MEMORIES

NEURAL CIRCUIT FOR IMPLICIT MEMORIES

NEURAL CIRCUIT FOR EMOTIONAL MEMORIES

14-4 STRUCTURAL BASIS OF BRAIN PLASTICITY

LONG-TERM POTENTIATION

MEASURING SYNAPTIC CHANGE

ENRICHED EXPERIENCE AND PLASTICITY

SENSORY OR MOTOR TRAINING AND PLASTICITY

EXPERIMENT 14-2 QUESTION: DOES THE LEARNING OF A FINE MOTOR SKILL ALTER THE CORTICAL MOTOR MAP?

RESEARCH FOCUS 14-5 MOVEMENT, LEARNING, AND NEUROPLASTICITY

EXPERIENCE-DEPENDENT CHANGE IN THE HUMAN BRAIN

EPIGENETICS OF MEMORY

PLASTICITY, HORMONES, TROPHIC FACTORS, AND DRUGS

EXPERIMENT 14-3 QUESTION: WHAT EFFECT DO REPEATED DOSES OF AMPHETAMINE, A PSYCHOMOTOR STIMULANT, HAVE ON NEURONS?

SOME GUIDING PRINCIPLES OF BRAIN PLASTICITY

14-5 RECOVERY FROM BRAIN INJURY

DONNA’S EXPERIENCE WITH TRAUMATIC BRAIN INJURY

THREE-LEGGED CAT SOLUTION

NEW-CIRCUIT SOLUTION

EXPERIMENT 14-4 QUESTION: DOES NERVE GROWTH FACTOR STIMULATE RECOVERY FROM STROKE, INFLUENCE NEURAL STRUCTURE, OR BOTH?

LOST NEURON REPLACEMENT SOLUTION

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Katherine Streeter

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CLINICAL FOCUS 14-1

Remediating Dyslexia

As children absorb their society’s culture, acquiring language skills seems virtually automatic. Yet some people face lifelong challenges in mastering language-related tasks. Educators classify these difficulties under the umbrella of learning disabilities.

Dyslexia, impairment in learning to read, may be the most common learning disability. Children with dyslexia (from Greek words suggesting bad and reading) have difficulty learning to write as well as to read.

In 1895, James Hinshelwood, an eye surgeon, examined some schoolchildren who were having reading problems, but he could find nothing wrong with their vision. Hinshelwood was the first to suggest that children with reading problems were impaired in brain areas associated with language use. Norman Geshwind and Albert Galaburda (1985) proposed how such impairment might come about.

Struck by the finding that dyslexia is far more common in boys than in girls, they reasoned that hormones influence early brain development. They examined postmortem the brains of a small sample of people who had dyslexia and found abnormal collections of neurons, or warts, in and around the brain’s language areas.

This relation between structural abnormalities in the brain and learning disabilities is further evidence that an intact brain is necessary for healthy human functioning. Geshwind and Galaburda also found abnormalities in the auditory thalamus, suggesting a deficit in auditory processing. More recently, brain imaging has determined that, relative to the brains of healthy participants, activity is reduced in the left temporoparietal cortex of people with dyslexia.

Michael Merzenich and his colleagues designed a remedial treatment program based on the assumption that the fundamental problem in learning disabilities lies in auditory processing, specifically of language sounds (e.g., Temple et al., 2003). Remediation involves learning to make increasingly difficult sound discriminations, for example, discriminating ba and da.

When the sounds are spoken slowly, discriminating between them is easy, but as they grow briefer and occur faster, discrimination becomes more difficult. Previous studies using rats and monkeys showed that discrimination training stimulates neural plasticity in the auditory system, making it capable of discrimination of sounds that previously was not possible.

The representative fMRIs shown here reveal decreased activation in many brain regions in untreated dyslexic children compared with typical children. With training, dyslexic readers can normalize their brain activity and presumably its connectivity.

The extent of increased brain activation in the language-related regions (circled in the images) correlates to the amount of increased brain activation overall. The results suggest that the remedial treatment both improves brain function in regions associated with phonological processing and produces compensatory activation in related brain regions.

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Regions of the frontal and temporoparietal cortex that showed decreased activation in children with untreated dyslexia.
“Neural Deficits in Children with Dyslexia Ameliorated by Behavioral Remediation: Evidence from Functional MRI,” by E. Temple, G. K. Deutsch, R. A. Poldrack, S. L. Miller, P. Tallal, M. M. Merzenich, and J. D. E. Gabrieli, 2003, Proceedings of the National Academy of Sciences (USA) 100, pp. 2860–2865.

Neuroplasticity is the nervous system’s potential for physical or chemical change that enhances adaptability.

The brain is plastic. It changes throughout life, allowing us to modify our behavior, to adapt and learn, and to remember. If we reflect on our own lives, we can easily compile a list of experiences that must change the brain:

Learning is common to all these experiences. Understanding how the brain supports learning is fundamental in neuroscience. At the level of the neuron, synapses change with experience—learning new information, for example. Such changes can take place anywhere in the brain.

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We can investigate neuronal changes that support learning specific types of information by describing changes in cells exposed to specific sensory experiences. Or we can look at the neural changes that mediate brain plasticity—recovery from brain injury, addiction to drugs, or conquering a learning disability. This chapter’s goal is to move beyond the general concept of neuroplasticity toward understanding what stimulates plastic change in the brain. We inspect changes related to environment and experience, learning and memory, electrical stimulation, chemical influences, and brain injury.