Learning and Memory
Damage to the temporal
lobes can leave a person with some impairment of past memories but particularly incapable of forming new memories, without
any impairment of intelligence.
Learning as the Storage
of Memories
Amnesia: The Failure of Storage or Retrieval
Anterograde amnesia is an inability to form new memories
Retrograde amnesia refers to an inability to recall memories from before the damage. The degree of amnesia
is related to how much damage was done and what structures were damaged
The hippocampus, a structure
within the temporal lobe, is linked to memory
Mechanisms of Consolidation and
Retrieval
Consolidation
is the process that produces a permanent representation of memory. This process continues for some time after learning
Retrieval is the process of accessing stored memories
Where Memories Are Stored
The hippocampus is not the permanent storage place for memories, but instead directs activities (e.g., associating
stimuli with one another, or with responses; storing and retrieving memories)
Memories are stored in different cortical areas, depending upon where the information was processed
Two Kinds of Learning
Declarative memory is memory of facts
Non-declarative
memory involves several kinds of learning not associated with factual material
Working
Memory provides a temporary place for information while it i being used. It is necessary for several activities we perform
every day
Much of the cortex participates in working memory, but the prefrontal area plays a primary role
The prefrontal area may serve as a central executive, directing the neural traffic of working memory
Brain Changes in Learning
Long-Term Potentiation (LTP)
LTP is an increase in synaptic strength following repeated stimulation
The effect can occur in several regions of the brain and last from a few minutes up to a few months
Associative long-term potentiation (ALTP) occurs when weak synaptic connections are potentiated because they are on the same postsynaptic neuron as a strong connection
Long-term Depression occurs when a presynaptic neuron is not firing while the postsynaptic neuron is being fired by other neurons.This weakens the synapse; it can block long-term potentiation
that has already occurred
Associative Long-Term Depression is the weakening of a synapse that occurs when two presynaptic neurons fire at
different times
Theta rhythm in the hippocampus appears to be necessary for some kinds of memory formation. It can facilitate LTP
or block LTP that
occurred earlier. This indicates a primary role for the hippocampus in
managing LTP
Synaptic Changes in LTP
The presynaptic neuron increases its neurotransmitter output
as a result of feedback from the postsynaptic neuron
Activation of AMPA glutamate receptors unblocks NMDA glutamate receptors, allowing the neuron to fire.
As a result of calcium influx and alteration of gene activity:
The number of and sensitivity of AMPA receptors is increased
The role of LTP in Learning
Manipulating LTP increases or decreases learning, so LTP may be fundamental to learning
However, in many cases experimentally induced LTP does not last as long as some memories
Consolidation
Apparently the hippocampus is involved in short-term memory, while the cortex is required for long-term storage
Long-term memories are subject to reconstruction, particularly at the time of retrieval. They must
be reconsolidated after each time they are retrieved, making them vulnerable
Disorders
of Learning
Aging is associated with memory loss, though it is not inevitable
The hippocampus loses synapses
and NMDA receptors
LTP is impaired
Metabolism decreases in the
entorhinal cortex
Neurons lose myelin
The basal forebrain area loses neurons
Alzheimer’s Disease is the most common cause of dementia in elderly individuals
The Diseased Brain: Plaques
and Tangles
Plaques are clumps of amyloid, a type of protein that interferes with neural transmission
Neurofibrillary tangles are webs of neurofilanients that develop inside neurons and are involved with killing
brain cells
Alzheimer’s and Heredity: Four genes have been found that influence the development of Alzheimer’s
disease, and it is suspected there are more
Treatment of Alzheimer’s
Disease has focused on restoring the neurotransmitter acetylcholine
Nicotine supplements also have produced improvements in Alzheimer’ s patients
Anticholesterol drugs
have been helpful
Estrogen supplements
following menopause have helped women
Instead of manipulating
the genes responsible for Alzheimer’s, some doctors implant genes for nerve growth factor. This has restored acetylcholine
levels
Korsakoff’s Syndrome is a form of dementia that is almost always caused by alcohol abuse
The cause of the disease is
an inadequate diet
Alcoholics commonly substitute the calories from alcohol for food
Thiamine diet can relieve some of the
symptoms, but cannot reverse brain
damage