Memory: Key Terms
Memory: Active system that stores, organizes, alters,
and recovers (retrieves) information
Encoding: Converting information into a useable form
Storage: Holding this information in memory
Retrieval: Taking memories out of storage
Stages of Memory: Sensory, Short-Term, Long-Term
Sensory Memory: Storing an exact copy of
incoming information for less than a second
 Icon: A fleeting mental image or visual
Representation
 Echo: After a sound is heard, a brief
continuation of the sound in the
auditory system
Short-Term Memory (STM): second stage of memory;
stores small amounts of information briefly; very
sensitive to interruption or interference
 Phonetically: Storing information by sound; how
most things are stored in STM
 Memory Span: STM is limited to holding seven
(plus or minus two) information bits at once
 Chunk: Meaningful units of information in
memory
Storing Info in STM
 Recoding- Reorganizing or modifying
information in STM
 Maintenance Rehearsal- Repeating
information silently to prolong its presence in STM
 Elaborative Rehearsal - Links new
information with existing memories
and knowledge in LTM
 Good way to transfer STM
information into LTM
Long-Term Memory (LTM) - - Storing information
relatively permanently
- Stored on basis of meaning and
Importance
Types of Long-Term Memory
 Explicit / Declarative Memory - Factual
knowledge & personal experiences
• Semantic Memory: Impersonal facts and
everyday knowledge
• Episodic Memory: Personal experiences
linked with specific times and places
Implicit / Procedural Memory – Skills, Long-
term memories of conditioned responses and
learned skills, e.g., driving
Loss of Memory / Amnesia
Anterograde amnesia:
• The inability to form new explicit long-term
memories for events following brain trauma or
surgery.
• Explicit memories formed before are left
intact.
• The probable cause is damage to
hippocampus.
Retrograde amnesia:
• The disruption of memory for the past,
especially episodic memory.
• After brain trauma or surgery, there often is
retrograde amnesia for events occurring just
before.
Infantile/child amnesia:
• The inability as adults to remember events
that occurred in our lives before about 3 years
of age.
• This is possibly due to the fact that the
hippocampus is not fully developed
Positional Effects on Memory
 Serial Position effect: It is hardest to recall items
in the middle of a list
 Primacy effect: It is easier to remember items
first in a list than items in the middle, because
first items are studied the most
 Recency effect: It is easier to remember items
last in a list than items in the middle, because
the last items were last studied
Encoding Information into Memory
Types of Processing
 Automatic processing - Memory processing that
occurs subconsciously and does not require
attention. How many of you can sing the theme
song for Sesame Street? How many learned it
on purpose?
 Effortful processing - Memory processing that
occurs consciously and requires attention. How
many of you can name all of the divisions of the
nervous system? How many learned it on
purpose?
Levels-of-Processing Theory
- A theory of information processing in memory that
assumes that semantic processing leads to better long-
term memory
• Physical memory processing: Encoding the word
“birthday” by the way it is spelt, b i r t h d a y
• Acoustic memory processing: Encoding the word
“birthday” by the way it sounds, birth-dayyyyy
• Semantic memory processing: Encoding the word
“birthday” by its meaning, “a day of joy and celebration
commemorating the anniversary of one’s birth.”
Leads to the best recall
Mood and Memory: How are They Linked?
Encoding specificity principle: The principle that the
environmental cues present at the time information is
encoded into long-term memory serve as the best
retrieval cues for the information.
State-dependent memory: Long-term memory retrieval
is best when a person’s physiological state at the time
of encoding and retrieval is the same.
Mood-dependent memory: Long-term memory retrieval
is best when a person’s mood state at the time of
encoding and retrieval is the same.
Measuring Retrieval
Recall: A measure of long-term memory retrieval that
requires the reproduction of the information
with essentially no retrieval cues.
Recognition: A measure of long-term memory retrieval
that only requires the identification of the
information in the presence of retrieval cues.
Relearning: The savings method, Measures the amount
of time saved when learning information for the second
time.
WHY do we forget??? WHY?????
Encoding Failure Theory - Forgetting is due to the failure
to encode the information into long-term memory
Storage Decay Theory - Forgetting is due to the decay of
physical traces of the information in the brain;
periodically using the information helps to maintain it in
the brain, “Use it or lose it” theory!
Interference Theory - Forgetting is due to other
information in memory interfering, Can be proactive or
retroactive
Some Ways to Improve Memory
Recitation -Summarizing aloud while you are Recitation
learning
Rehearsal - Reviewing information mentally (silently)
Selection - Selecting most important Selection concepts
to memorize
More Ways to Improve Memory
Organization: Outlining items into chunks; a
type of reordering
Overlearning: Studying is continued beyond bare
mastery
Spaced Practice: Alternating study sessions with
brief rest periods
How to Help Your Memory
We have 5 main senses: Vision Audition Gustation
Olfaction Tactile/Somatosenses
Our sensory memory allows us to retain impressions of
information from the senses after a stimulus (e.g. an
image, a sound, a flavour etc) is gone.
Memory Techniques How can we improve our
retention?
Mnemonics - Mnemonics are memory tricks, or
techniques which are used to help us remember
something. You may need to memorize a list of
objects, a string of numbers or a sequence of
information.
Memory “tricks”, systems, or aids using mental
Pictures, making things meaningful, Making
information familiar, Forming bizarre, unusual
or exaggerated mental associations
Acronyms - take the first letter of a group of words, to
form a new word
– this is especially useful for remembering words in a
particular order.
ASAP (As Soon As Possible) or DIY (Do It Yourself) are
examples of acronyms that might be familiar to you.
Acronyms are even more useful if they also spell out a
word e.g. the health campaign for helping someone
suffering from a stroke, uses the
acronym FAST, which stands for:FaceArmSpeechTime to
call
Sentence Acrostics -Acrostics are similar to acronyms,
taking the first letter of each word you wish to
remember. But rather than creating a word, that letter
is used to create a new word, which forms part of a
sentence. e.g. If you wanted to remember a list of
neurotransmitters:
Dopamine, Glutamate, Oxytocin, Acetylcholine,
Norepinephrine, Serotonin.
You might remember it as: Don’t Go Out At Night, Silly.
The Story Method -In order to remember a list of words
or objects, you could try a storytelling approach. Using
your imagination, picture the words or objects you want
to remember by placing them in your story.
Alzheimer’s Disease- First described by Alois
Alzheimer in 1906, Begins with mild memory
problems and ends with personality changes,
disorientation, and agitation
Alzheimer’s Disease- This is caused by irreversible
deterioration of brain tissue, Characterized by beta-
amyloid plaques outside neurons and neurofibrillary tau
tangles inside the neurons, which cause neuronal death
• These are generally present in the hippocampus, the
area responsible for memory
• Neurotransmitters involved: less acetylcholine and
more glutamate, Time to death: 12 years
Brain Areas Affected by Plaques and Tangles
Hippocampus, Frontal, temporal, and parietal lobes
Enlargement of ventricles, Cerebellum, spinal cord,
motor/sensory areas
Etiology
• A heritability estimate of 79 percent is reported.
• Late-onset cases of AD have apolipoprotein E4 alleles
in chromosome 19.
• This is related to glucose metabolism and the
formation of plaques.
• One E4 allele increases risk to 30 percent.
• Two E4 allelles increase risk to >90 percent.
Environmental Factors
• Account for 21 percent of the development of AD
• Strong cognitive ability offers some protection from
Alzheimer’s.
• In a retrospective study of nuns, low linguistic ability
was found in 90 percent of those who developed AD.
• Frequent cognitive activity is related to a 46 percent
decrease in risk, despite plaques and tangles in the
brain.
What are Neurotransmitters?
▪ Recall that at the level of the synapse, chemicals are
released between neurons.
▪ These chemicals are generally known as
neurotransmitters; they light up the brain with life.
Criteria
1. The molecule is synthesized in the neuron.
2. The molecule is present in the presynaptic neuron
and released on depolarization in significant amounts.
3. When administered exogenously as a drug, the
exogenous molecule mimics the effects of the
endogenous neurotransmitter.
4. A mechanism in the neurons or synaptic cleft acts to
remove or deactivate the neurotransmitter.
Neurotransmitters vs. Neuromodulators
▪ Neuromodulators serve to alter the effects of
neurotransmitters.
– They can prolong or limit the release of, or the effect
of a neurotransmitter.
– They are able to do this by diffusing to their target
neurons of the region.
– However, their effects are limited only to a small area
within the neuron which releases them.
Classification
▪ Neurotransmitters are classified according to their
structure.
▪ Currently, there are three major types of
neurotransmitters. Biogenic amines, Amino acids,
Peptides
Biogenic amines- Best known and most understood,
Present in the least number of neurons, Form a large
part of psychopharmacology
Amino acids- Present in 70 percent of neurons
Peptides- Intermediate in terms of percentage of
neurons that contain them. Outnumber the other two
categories in terms of number of types (200-300)
Biogenic Amines
▪ Synthesized in distinct groups of neurons in the brain
and exert their influence throughout tracts.
▪ Of central importance to the pharmacological therapy
of thought, mood, and anxiety disorders.
▪ Examples include dopamine, serotonin,
norepinephrine, histamine, and acetylcholine.
Dopamine
▪ Synthesis: – Transformed by tyrosine
hydroxylase from 3,4- dihydroxyphenylalanine (L-DOPA)
– Cell groups in the midbrain's substantia nigrae and
ventral tegmental areas (VTA).
▪ Important Tracts:
– Nigrostriatal
– Mesolimbic-mesocortical
– TuberoinfundibularThe Effects of Dopamine
▪ Nigrostriatal Tract
– Control of movement by its actions on the basal
ganglia
– Too little dopamine results in Parkinson’s disease or
symptoms similar to it
The Effects of Dopamine
▪ Mesolimbic / Mesocortical – Heighten the awareness
of pleasure, increases motivation and activity
– Too much dopamine results in psychotic symptoms
(hallucinations and delusions)
– This dopamine pathway has been consistently linked
to pleasure and reward!The Effects of Dopamine
▪ Tuberoinfundibular– Regulates the menstrual cycle
and lactation
– Too little dopamine results in galactorrhea,
amenorrhea, or gynecomastia
Examples of Abnormal Dopamine Levels
High in Dopamine - Psychosis, mania, and substance
abuse (cocaine, amphetamines)
Low in Dopamine - Parkinson’s disease and treatment
with antipsychotics
Dopamine and Antipsychotics
▪ Abnormally increased levels of dopamine in the
mesolimbicand mesocortical areas cause psychotic
symptoms of disorders like schizophrenia.
▪ Antipsychotics are medications which have been
formulated to block postsynaptic dopamine receptors,
hence preventing the dopamine from reaching target
receptors.
– These work by directly blocking D2 receptors in all
dopamine pathways
– Examples include haloperidol and chlorpromazine.
– Side effects include Parkinson-like symptoms and
gynecomastia.
Termination of Action
▪ Reuptake by the presynapticdopamine transporter
▪ Metabolized by two enzymes:
– Monoamine oxidase
– Catechol-O-methyltransferase
Serotonin
▪ In the brain, the raphe nuclei are the principal source
of serotonin release.
▪ However, most serotonin in the human body is found
in the gastrointestinal tract, where it is used to regulate
intestinal movements.
▪ Made from the amino acid tryptophan, which we
ingest in our diet.
– Tryptophan is generally found in protein-rich
foods such as legumes, meat, and dairy.
– Another important source of tryptophan is
chocolate
The Tracts of Serotonin
▪ Subcortical nuclei including the centrally located
thalami; the surrounding corpus striata including the
nucleus accumbens; the hypothalamus, hippocampus,
and amygdala,
▪ Cingulate cortex, including the cingulum, a tract of
association fibers connecting the corpus callosum with
the hippocampus,
▪ Neocortex
The Effects of Serotonin
▪ A well-regulated level of serotonin produces feelings
of satisfaction, contentment, sleepiness, and a general
sense of well-being.
▪ Abnormally high serotonin levels result in agitation,
vomiting, somnolence, sexual dysfunction, diarrhea,
and headache.
▪ Abnormally low serotonin levels result in depression,
irritability, hunger, and anxiety.
Examples of Abnormal Serotonin Levels
High - Mania, LSD,Ecstasy (MDMA)
Low - Depression Anxiety
Termination of Action:
Application to Antidepressants
▪ Reuptake by the serotonin transporter
Selective serotonin reuptake inhibitors (SSRIs)
prevent reuptake of serotonin by the
presynaptic neuron after firing
Leaves more serotonin in the synapse
Examples: Fluoxetine (Prozac) and Sertraline
(Zoloft)
▪ Metabolized by monoamine oxidase
Monoamine oxidase inhibitors (MAOIs) keep
MAO from deactivating serotonin, hence
increasing levels
Example: Tranylcypromine (Parnate)
Norepinephrine
▪ Synthesis:
– The locus ceruleus, “blue spot”, which is also located
within the pons of the brain stem
– Synthesized from dopamine through dopamine-B-
hydroxylase
▪ Pathways:
– Cerebral cortex
– Limbic system
– Thalamus
– Hypothalamus
Norepinephrine’s Role in Our Lives
▪ Norepinephrine mediates arousal in two ways:
– It relays messages in the sympathetic nervous
system, as part of the autonomic nervous system's
fight-or-flight response.
– It prepares the brain to encounter and
respond to stimuli from the environment, thereby
facilitating vigilance.
▪ With respect to mood disorders, norepinephrine
works in tandem with serotonin.
▪ Norepinephrine is also the precursor of epinephrine,
which drives the fight-or-flight response.
– Epinephrine is released into the bloodstream
when dangerous circumstances occur, in an emergency
requiring immediate action, and in stressful situations
or environments.
Examples of Abnormal Norepinephrine Levels….
High – Mania Anxiety & Social Phobia Tremors
Low – Depression
Termination of Action
▪ Reuptake by the presynaptic transporter
– Serotonin-norepinephrine reuptake inhibitors
are anti-anxiety and antidepressant medications. These
work by blocking the reuptake pathway for serotonin
and norepinephrine, causing increased levels in the
synaptic cleft.
– Example: desvenlafaxine (Pristiq)
▪ Metabolized by two enzymes:
– Monoamine oxidase
– Catechol-O-methyltransferase
▪ Autoreceptor regulation
– A special kind of antidepressant called mirtazapine
(Remeron) prevents the autoreceptors from diminishing
the amount of norepinephrine released from the
presynaptic terminal.
Acetylcholine
▪ Synthesized at the nucleus basalis of Meynert from
acetyl CoA and choline.
▪ Termination through enzymatic degradation
(acetylcholinesterase) and reuptake and recycling of
Choline
Tracts and Functions of Acetylcholine
▪ In the central nervous system, it is involved in
wakefulness, attentiveness, anger, aggression,
sexuality, thirst, and memory.
– It increases responsiveness to peripheral
stimuli.
▪ Importantly, acetylcholine mediates the functions of
the parasympathetic system.
– Acetylcholine serves to slow down the
heart rate, increase stomach peristalsis, and constrict
the pupils.
– It also serves to activate skeletal muscle.
Acetylcholine: Clinical Applications
▪ Nicotine serves to increase levels of dopamine and
acetylcholine, increasing concentration and memory.
▪ Depletion of acetylcholine in the central nervous
system causes memory problems and Alzheimer’s
disease.
– Acetylcholinesterase inhibitors are used to
slow down Alzheimer’s disease. They inhibit the enzyme
which breaks down acetylcholine. Examples: donepezil,
rivastigmine
Peptide Neurotransmitters
▪ A peptide is a short protein consisting of less than 100
amino acids.
▪ Peptide neurotransmitters are made in the neuronal
cell body and stored in the vesicles of the presynaptic
axon terminal.
▪ Peptide neurotransmitters include opioids,
corticotropinreleasing factor, and substance
P.Endogenous Opioids
▪ Endogenous opioids have remarkable analgesic and
psychological effects.
– Their effects are similar to the drug morphine,
which is extracted from the poppy.
▪ Opioids act on three major receptors: mu,
kappa, and delta.
– Their interactions with these receptors are
involved in the regulation of stress, pain, and
mood.
▪ Opioid-containing neurons have been found in the
hypothalamus, diencephalon, pons, hippocampus, and
midbrain, with their axons projecting widely.
Amino Acid Neurotransmitters
▪ Amino acids are the building blocks of proteins.
▪ The two major amino acid neurotransmitters are
glutamate and GABA (gamma-aminobutyric acid).
Glutamate: Excitatory
GABA: Inhibitory
Glutamate
▪ Glutamate is synthesized from glucose and glutamine
in presynaptic neuron terminals and stored in synaptic
vesicles.
– Glutamate release is also stimulated by the
nicotine in cigarette smoke.
▪ It is the primary neurotransmitter in the cerebellum,
striatum, cortex, and thalamus.
▪ Its action is terminated through reuptake into the
presynapticneuron or adjacent glia.
Glutamate: Abnormal Levels and Clinical Applications
Excitotoxicity: Prolonged stimulation leads to
destruction of neuronal integrity, seen also in
Alzheimer’s disease. Glutamate receptor blockers serve
to slow down the progress of Alzheimer’s.
Psychosis: Reduction in glutamate receptor activity is
thought to cause symptoms of psychosis. This has
also been shown in PCP use.
GABA
▪ This neurotransmitter is found almost exclusively in
the brain and is synthesized from glutamate.
– Its highest concentrations are in the midbrain.
▪ As an inhibitor, it can suppress seizure activity,
anxiety, and mania, while causing drowsiness.
– Drugs that simulate GABA activity include
anticonvulsant, barbiturates and
benzodiazepines such as diazepam (Valium).
GABA, ANXIETY, AND BENZODIAZEPINES
▪ Historically, barbiturates were first used for the
treatment of anxiety.
▪ However, due to the increased risks for lethal side
effects, the preferred medication class in modern times
is the benzodiazepine.
▪ Benzodiazepines have demonstrated benefit in almost
all of the anxiety disorders.
– However, they are best combined with
psychotherapy due to their potential for addiction and
production of severe withdrawal symptoms.