last updated:

APRIL 25, 2021

[Brain Image]    

PSY 340 Brain and Behavior

Class 32 Learning, Memory, and Memory Loss [OUTLINE]


I. Localized Representations in Memory

Karl Lashley's FAILED Search for the Engram

[Lashley's Search for the

In the period from roughly 1920 to 1955, Lashley searched after the "engram"

Cortical Cuts

Tissue Ablation

Lashley's Principles for the Nervous System. Lashley rejected the notion of localized learning.

  • Equipotentiality: All parts of the cortex contribute equally to learning; one part can substitute for another part. 
  • Mass Action: The cortex works as a whole; performance improves when more of the cortex is involved.

We know that Lashley was wrong. Why? He assumed (1) the engram (memory trace) is only in the cortex and (2) all memories are the same physiologically.

Modern Search for the Engram

Conditioning & the Lateral Pontine Nucleus of the Cerebellum

[Lateral Pontine Nucleus]
  • Rabbit eyes will blink (= UR: unconditioned response) if a puff of air hits them (= US: unconditioned stimulus).
  • Richard F. Thompson conditioned rabbits using a tone (= CS: conditioned stimulus) which he paired with the US. Eventually, the rabbits learned to blink (= CR: conditioned response) when they heard the CS alone.
  • Learning the CS:CR connection increased the activity level of the lateral pontine nucleus (LPN; called the lateral interpositus nucleus in the text) of the cerebellum.
1. Suppressing the LPN temporarily prevented rabbits from learning the CS:CR connection

2. Suppressing the red nucleus temporarily prevented the rabbits from responding (the CR), but not the learning itself 
  • Conclusion: Learning seems to have taken place at the Lateral Pontine Nucleus. Further, this and other research points to conditioned learning in the cerebellum

II. Types of Memory

Short- and Long-Term Memory

Donald O. Hebb proposed in the late 1940s a model of memory with two different components:

  • short-term memory (STM; up to 20 seconds)
    • rehearsal 
    • George Miller noted, the storage capacity of STM is limited: 7 +/- 2 chunks of information
  • long-term memory (LTM; 20-60 seconds to a lifetime): anything that happened in the past which you can remember
  • Brain consolidates memories by means of a reverberating circuit within the nervous system; gradually causes some type of permanent change in the chemical or structural make-up of the nervous system.

Changing Views of Consolidation

  • Time for consolidation varies considerably
  • Memories are labile (changeable or vulnerable to alteration). When memories are recalled, they are frequently reconsolidated

Alan Baddeley's "Working Memory" (WM): A Modern Advance

[Baddeley's Working Memory

[Dorsolateral prefrontal cortex]

Testing the "working memory" model uses delayed response tasks = respond to a stimulus that was seen or heard a short time ago with a time delay inserted between the perception and the response.

dorsolateral prefrontal cortex as site for rehearsed memory. The rest of the prefrontal cortex is also involved in WM.

III. Memory Loss (Amnesia)

A. Korsakoff's Syndrome & Other Prefrontal Damage

Wernicke's encephalopathy
• deficiency of thiamine (vitamin B-1).
• 80% of patients surviving Wernicke's encephalopathy develop Korsakoff's Syndrome (KS). 

KS is a chronic brain disorder characterized by severe memory problems: both anterograde and retrograde memory is usually damaged. Patients also show apathy and confusion.

[Mammillary bodies]  [dorsomedial nucleus]

The brain area damaged includes the mammillary bodies (beneath the hypothalamus) and the dorosmedial (or mediodorsal) thalamus (nucleus connected to pre-frontal cortex).

Patients with KS often show

B. Auguste Deter
                - 1st person to be diagnosed with ADAlzheimer's Disease (AD)

Dementia: A broad notion encompassing multiple diseases including AD. Dementia involves

History. First identified in 1906 by Dr. Alois Alzheimer in a 55-year-old patient, Auguste Deter, in Frankfurt, Germany. Autopsy examination of her brain revealed the characteristic presence of amyloid plaques and neurofibrillary tangles of tau (discussed below)

Incidence of AD by ageAD appears in two forms

Prevalence/Incidence of AD

AD is a progressive disorder which initially involves minor forgetfulness. Over the course of about 8 to 10 years following diagnosis, AD patients experience increasing symptoms including severe memory loss, confusion, depression, hallucinations, delusions, restlessness, sleeplessness, and loss of appetite. Eventually, the disease will lead to death.

Genetic Factors

Cellular Pathology

          of AD in the brain
AD brain tissue
  • Amyloid plaques
  • Neurofibrillary tangles (tau protein)

Brain Pathology

[Brain: Normal vs. Alzheimer's