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Memory: Key Terms • Explicit memories formed before are left

Memory: Active system that stores, organizes, alters, intact.

and recovers (retrieves) information • The probable cause is damage to
Encoding: Converting information into a useable form hippocampus.
Storage: Holding this information in memory Retrograde amnesia:
Retrieval: Taking memories out of storage • The disruption of memory for the past,
Stages of Memory: Sensory, Short-Term, Long-Term especially episodic memory.
Sensory Memory: Storing an exact copy of • After brain trauma or surgery, there often is
incoming information for less than a second retrograde amnesia for events occurring just
 Icon: A fleeting mental image or visual before.
Representation Infantile/child amnesia:
 Echo: After a sound is heard, a brief • The inability as adults to remember events
continuation of the sound in the that occurred in our lives before about 3 years
auditory system of age.
Short-Term Memory (STM): second stage of memory; • This is possibly due to the fact that the
stores small amounts of information briefly; very hippocampus is not fully developed
sensitive to interruption or interference
 Phonetically: Storing information by sound; how Positional Effects on Memory
most things are stored in STM  Serial Position effect: It is hardest to recall items
 Memory Span: STM is limited to holding seven in the middle of a list
(plus or minus two) information bits at once  Primacy effect: It is easier to remember items
 Chunk: Meaningful units of information in first in a list than items in the middle, because
memory first items are studied the most
Storing Info in STM  Recency effect: It is easier to remember items
 Recoding- Reorganizing or modifying last in a list than items in the middle, because
information in STM the last items were last studied
 Maintenance Rehearsal- Repeating
information silently to prolong its presence in STM Encoding Information into Memory
 Elaborative Rehearsal - Links new Types of Processing
information with existing memories  Automatic processing - Memory processing that
and knowledge in LTM occurs subconsciously and does not require
 Good way to transfer STM attention. How many of you can sing the theme
information into LTM song for Sesame Street? How many learned it
Long-Term Memory (LTM) - - Storing information on purpose?
relatively permanently  Effortful processing - Memory processing that
- Stored on basis of meaning and occurs consciously and requires attention. How
Importance many of you can name all of the divisions of the
Types of Long-Term Memory nervous system? How many learned it on
 Explicit / Declarative Memory - Factual purpose?
knowledge & personal experiences Levels-of-Processing Theory
• Semantic Memory: Impersonal facts and - A theory of information processing in memory that
everyday knowledge assumes that semantic processing leads to better long-
• Episodic Memory: Personal experiences term memory
linked with specific times and places • Physical memory processing: Encoding the word
Implicit / Procedural Memory – Skills, Long- “birthday” by the way it is spelt, b i r t h d a y
term memories of conditioned responses and • Acoustic memory processing: Encoding the word
learned skills, e.g., driving “birthday” by the way it sounds, birth-dayyyyy
• Semantic memory processing: Encoding the word
Loss of Memory / Amnesia “birthday” by its meaning, “a day of joy and celebration
Anterograde amnesia: commemorating the anniversary of one’s birth.”
• The inability to form new explicit long-term Leads to the best recall
memories for events following brain trauma or
Mood and Memory: How are They Linked? information from the senses after a stimulus (e.g. an
Encoding specificity principle: The principle that the image, a sound, a flavour etc) is gone.
environmental cues present at the time information is
encoded into long-term memory serve as the best Memory Techniques How can we improve our
retrieval cues for the information. retention?
State-dependent memory: Long-term memory retrieval Mnemonics - Mnemonics are memory tricks, or
is best when a person’s physiological state at the time techniques which are used to help us remember
of encoding and retrieval is the same. something. You may need to memorize a list of
Mood-dependent memory: Long-term memory retrieval objects, a string of numbers or a sequence of
is best when a person’s mood state at the time of information.
encoding and retrieval is the same. Memory “tricks”, systems, or aids using mental
Pictures, making things meaningful, Making
Measuring Retrieval information familiar, Forming bizarre, unusual
Recall: A measure of long-term memory retrieval that or exaggerated mental associations
requires the reproduction of the information Acronyms - take the first letter of a group of words, to
with essentially no retrieval cues. form a new word
Recognition: A measure of long-term memory retrieval – this is especially useful for remembering words in a
that only requires the identification of the particular order.
information in the presence of retrieval cues. ASAP (As Soon As Possible) or DIY (Do It Yourself) are
Relearning: The savings method, Measures the amount examples of acronyms that might be familiar to you.
of time saved when learning information for the second Acronyms are even more useful if they also spell out a
time. word e.g. the health campaign for helping someone
suffering from a stroke, uses the
WHY do we forget??? WHY????? acronym FAST, which stands for:FaceArmSpeechTime to
Encoding Failure Theory - Forgetting is due to the failure call
to encode the information into long-term memory Sentence Acrostics -Acrostics are similar to acronyms,
Storage Decay Theory - Forgetting is due to the decay of taking the first letter of each word you wish to
physical traces of the information in the brain; remember. But rather than creating a word, that letter
periodically using the information helps to maintain it in is used to create a new word, which forms part of a
the brain, “Use it or lose it” theory! sentence. e.g. If you wanted to remember a list of
Interference Theory - Forgetting is due to other neurotransmitters:
information in memory interfering, Can be proactive or Dopamine, Glutamate, Oxytocin, Acetylcholine,
retroactive Norepinephrine, Serotonin.
You might remember it as: Don’t Go Out At Night, Silly.
Some Ways to Improve Memory The Story Method -In order to remember a list of words
Recitation -Summarizing aloud while you are Recitation or objects, you could try a storytelling approach. Using
learning your imagination, picture the words or objects you want
Rehearsal - Reviewing information mentally (silently) to remember by placing them in your story.
Selection - Selecting most important Selection concepts
to memorize Alzheimer’s Disease- First described by Alois
Alzheimer in 1906, Begins with mild memory
More Ways to Improve Memory problems and ends with personality changes,
Organization: Outlining items into chunks; a disorientation, and agitation
type of reordering Alzheimer’s Disease- This is caused by irreversible
Overlearning: Studying is continued beyond bare deterioration of brain tissue, Characterized by beta-
mastery amyloid plaques outside neurons and neurofibrillary tau
Spaced Practice: Alternating study sessions with tangles inside the neurons, which cause neuronal death
brief rest periods • These are generally present in the hippocampus, the
area responsible for memory
How to Help Your Memory • Neurotransmitters involved: less acetylcholine and
We have 5 main senses: Vision Audition Gustation more glutamate, Time to death: 12 years
Olfaction Tactile/Somatosenses
Our sensory memory allows us to retain impressions of Brain Areas Affected by Plaques and Tangles
Hippocampus, Frontal, temporal, and parietal lobes Biogenic amines- Best known and most understood,
Enlargement of ventricles, Cerebellum, spinal cord, Present in the least number of neurons, Form a large
motor/sensory areas part of psychopharmacology
Etiology Amino acids- Present in 70 percent of neurons
• A heritability estimate of 79 percent is reported. Peptides- Intermediate in terms of percentage of
• Late-onset cases of AD have apolipoprotein E4 alleles neurons that contain them. Outnumber the other two
in chromosome 19. categories in terms of number of types (200-300)
• This is related to glucose metabolism and the
formation of plaques. Biogenic Amines
• One E4 allele increases risk to 30 percent. ▪ Synthesized in distinct groups of neurons in the brain
• Two E4 allelles increase risk to >90 percent. and exert their influence throughout tracts.
Environmental Factors ▪ Of central importance to the pharmacological therapy
• Account for 21 percent of the development of AD of thought, mood, and anxiety disorders.
• Strong cognitive ability offers some protection from ▪ Examples include dopamine, serotonin,
Alzheimer’s. norepinephrine, histamine, and acetylcholine.
• In a retrospective study of nuns, low linguistic ability Dopamine
was found in 90 percent of those who developed AD. ▪ Synthesis: – Transformed by tyrosine
• Frequent cognitive activity is related to a 46 percent hydroxylase from 3,4- dihydroxyphenylalanine (L-DOPA)
decrease in risk, despite plaques and tangles in the – Cell groups in the midbrain's substantia nigrae and
brain. ventral tegmental areas (VTA).
▪ Important Tracts:
What are Neurotransmitters? – Nigrostriatal
▪ Recall that at the level of the synapse, chemicals are – Mesolimbic-mesocortical
released between neurons. – TuberoinfundibularThe Effects of Dopamine
▪ These chemicals are generally known as ▪ Nigrostriatal Tract
neurotransmitters; they light up the brain with life. – Control of movement by its actions on the basal
Criteria ganglia
1. The molecule is synthesized in the neuron. – Too little dopamine results in Parkinson’s disease or
2. The molecule is present in the presynaptic neuron symptoms similar to it
and released on depolarization in significant amounts. The Effects of Dopamine
3. When administered exogenously as a drug, the ▪ Mesolimbic / Mesocortical – Heighten the awareness
exogenous molecule mimics the effects of the of pleasure, increases motivation and activity
endogenous neurotransmitter. – Too much dopamine results in psychotic symptoms
4. A mechanism in the neurons or synaptic cleft acts to (hallucinations and delusions)
remove or deactivate the neurotransmitter. – This dopamine pathway has been consistently linked
to pleasure and reward!The Effects of Dopamine
Neurotransmitters vs. Neuromodulators ▪ Tuberoinfundibular– Regulates the menstrual cycle
▪ Neuromodulators serve to alter the effects of and lactation
neurotransmitters. – Too little dopamine results in galactorrhea,
– They can prolong or limit the release of, or the effect amenorrhea, or gynecomastia
of a neurotransmitter. Examples of Abnormal Dopamine Levels
– They are able to do this by diffusing to their target High in Dopamine - Psychosis, mania, and substance
neurons of the region. abuse (cocaine, amphetamines)
– However, their effects are limited only to a small area Low in Dopamine - Parkinson’s disease and treatment
within the neuron which releases them. with antipsychotics

▪ Neurotransmitters are classified according to their Dopamine and Antipsychotics
structure. ▪ Abnormally increased levels of dopamine in the
▪ Currently, there are three major types of mesolimbicand mesocortical areas cause psychotic
neurotransmitters. Biogenic amines, Amino acids, symptoms of disorders like schizophrenia.
Peptides ▪ Antipsychotics are medications which have been
formulated to block postsynaptic dopamine receptors,
hence preventing the dopamine from reaching target Leaves more serotonin in the synapse
receptors. Examples: Fluoxetine (Prozac) and Sertraline
– These work by directly blocking D2 receptors in all (Zoloft)
dopamine pathways ▪ Metabolized by monoamine oxidase
– Examples include haloperidol and chlorpromazine. Monoamine oxidase inhibitors (MAOIs) keep
– Side effects include Parkinson-like symptoms and MAO from deactivating serotonin, hence
gynecomastia. increasing levels
Termination of Action Example: Tranylcypromine (Parnate)
▪ Reuptake by the presynapticdopamine transporter
▪ Metabolized by two enzymes: Norepinephrine
– Monoamine oxidase ▪ Synthesis:
– Catechol-O-methyltransferase – The locus ceruleus, “blue spot”, which is also located
within the pons of the brain stem
Serotonin – Synthesized from dopamine through dopamine-B-
▪ In the brain, the raphe nuclei are the principal source hydroxylase
of serotonin release. ▪ Pathways:
▪ However, most serotonin in the human body is found – Cerebral cortex
in the gastrointestinal tract, where it is used to regulate – Limbic system
intestinal movements. – Thalamus
▪ Made from the amino acid tryptophan, which we – Hypothalamus
ingest in our diet.
– Tryptophan is generally found in protein-rich Norepinephrine’s Role in Our Lives
foods such as legumes, meat, and dairy. ▪ Norepinephrine mediates arousal in two ways:
– Another important source of tryptophan is – It relays messages in the sympathetic nervous
chocolate system, as part of the autonomic nervous system's
The Tracts of Serotonin fight-or-flight response.
▪ Subcortical nuclei including the centrally located – It prepares the brain to encounter and
thalami; the surrounding corpus striata including the respond to stimuli from the environment, thereby
nucleus accumbens; the hypothalamus, hippocampus, facilitating vigilance.
and amygdala, ▪ With respect to mood disorders, norepinephrine
▪ Cingulate cortex, including the cingulum, a tract of works in tandem with serotonin.
association fibers connecting the corpus callosum with ▪ Norepinephrine is also the precursor of epinephrine,
the hippocampus, which drives the fight-or-flight response.
▪ Neocortex – Epinephrine is released into the bloodstream
when dangerous circumstances occur, in an emergency
The Effects of Serotonin requiring immediate action, and in stressful situations
▪ A well-regulated level of serotonin produces feelings or environments.
of satisfaction, contentment, sleepiness, and a general Examples of Abnormal Norepinephrine Levels….
sense of well-being. High – Mania Anxiety & Social Phobia Tremors
▪ Abnormally high serotonin levels result in agitation, Low – Depression
vomiting, somnolence, sexual dysfunction, diarrhea,
and headache. Termination of Action
▪ Abnormally low serotonin levels result in depression, ▪ Reuptake by the presynaptic transporter
irritability, hunger, and anxiety. – Serotonin-norepinephrine reuptake inhibitors
Examples of Abnormal Serotonin Levels are anti-anxiety and antidepressant medications. These
High - Mania, LSD,Ecstasy (MDMA) work by blocking the reuptake pathway for serotonin
Low - Depression Anxiety and norepinephrine, causing increased levels in the
Termination of Action: synaptic cleft.
Application to Antidepressants – Example: desvenlafaxine (Pristiq)
▪ Reuptake by the serotonin transporter ▪ Metabolized by two enzymes:
Selective serotonin reuptake inhibitors (SSRIs) – Monoamine oxidase
prevent reuptake of serotonin by the – Catechol-O-methyltransferase
presynaptic neuron after firing ▪ Autoreceptor regulation
– A special kind of antidepressant called mirtazapine mood.
(Remeron) prevents the autoreceptors from diminishing ▪ Opioid-containing neurons have been found in the
the amount of norepinephrine released from the hypothalamus, diencephalon, pons, hippocampus, and
presynaptic terminal. midbrain, with their axons projecting widely.

Acetylcholine Amino Acid Neurotransmitters

▪ Synthesized at the nucleus basalis of Meynert from ▪ Amino acids are the building blocks of proteins.
acetyl CoA and choline. ▪ The two major amino acid neurotransmitters are
▪ Termination through enzymatic degradation glutamate and GABA (gamma-aminobutyric acid).
(acetylcholinesterase) and reuptake and recycling of Glutamate: Excitatory
Choline GABA: Inhibitory
Tracts and Functions of Acetylcholine ▪ Glutamate is synthesized from glucose and glutamine
▪ In the central nervous system, it is involved in in presynaptic neuron terminals and stored in synaptic
wakefulness, attentiveness, anger, aggression, vesicles.
sexuality, thirst, and memory. – Glutamate release is also stimulated by the
– It increases responsiveness to peripheral nicotine in cigarette smoke.
stimuli. ▪ It is the primary neurotransmitter in the cerebellum,
▪ Importantly, acetylcholine mediates the functions of striatum, cortex, and thalamus.
the parasympathetic system. ▪ Its action is terminated through reuptake into the
– Acetylcholine serves to slow down the presynapticneuron or adjacent glia.
heart rate, increase stomach peristalsis, and constrict Glutamate: Abnormal Levels and Clinical Applications
the pupils. Excitotoxicity: Prolonged stimulation leads to
– It also serves to activate skeletal muscle. destruction of neuronal integrity, seen also in
Alzheimer’s disease. Glutamate receptor blockers serve
Acetylcholine: Clinical Applications to slow down the progress of Alzheimer’s.
▪ Nicotine serves to increase levels of dopamine and Psychosis: Reduction in glutamate receptor activity is
acetylcholine, increasing concentration and memory. thought to cause symptoms of psychosis. This has
▪ Depletion of acetylcholine in the central nervous also been shown in PCP use.
system causes memory problems and Alzheimer’s
disease. GABA
– Acetylcholinesterase inhibitors are used to ▪ This neurotransmitter is found almost exclusively in
slow down Alzheimer’s disease. They inhibit the enzyme the brain and is synthesized from glutamate.
which breaks down acetylcholine. Examples: donepezil, – Its highest concentrations are in the midbrain.
rivastigmine ▪ As an inhibitor, it can suppress seizure activity,
anxiety, and mania, while causing drowsiness.
Peptide Neurotransmitters – Drugs that simulate GABA activity include
▪ A peptide is a short protein consisting of less than 100 anticonvulsant, barbiturates and
amino acids. benzodiazepines such as diazepam (Valium).
▪ Peptide neurotransmitters are made in the neuronal GABA, ANXIETY, AND BENZODIAZEPINES
cell body and stored in the vesicles of the presynaptic ▪ Historically, barbiturates were first used for the
axon terminal. treatment of anxiety.
▪ Peptide neurotransmitters include opioids, ▪ However, due to the increased risks for lethal side
corticotropinreleasing factor, and substance effects, the preferred medication class in modern times
P.Endogenous Opioids is the benzodiazepine.
▪ Endogenous opioids have remarkable analgesic and ▪ Benzodiazepines have demonstrated benefit in almost
psychological effects. all of the anxiety disorders.
– Their effects are similar to the drug morphine, – However, they are best combined with
which is extracted from the poppy. psychotherapy due to their potential for addiction and
▪ Opioids act on three major receptors: mu, production of severe withdrawal symptoms.
kappa, and delta.
– Their interactions with these receptors are
involved in the regulation of stress, pain, and