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Ch 12, 13, 14
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Unconditioned stimulus
naturally occurring stimulus that triggers a response automatically
EX: meat powder
Unconditioned response
natural reaction to UCS
EX: salivation
Neutral stimulus
stimulus that initially produces no response
EX: Bell
Conditioned stimulus
once-neutral stimulus that now triggers a learned response
EX: bell
Conditioned response
a learned reaction to a conditioned stimulus
EX: salivation
Acquisition
process of learning the association between NS and UCS
Extinction
when the CS is presented repeated without UCS and the CR fades
Spontaneous recovery
the reappearance of a learned response after extinction
Generalization
responding to similar stimuli
Discrimination
learning to respond only to a specific stimulus
Operant conditioning
learning through consequences of voluntary behavior
Positive Reinforcement
adding something pleasant to increase behavior
EX: vending machine giving a snack when you insert money
Negative Reinforcement
removing something unpleasant to increase behavior
EX: fastening seatbelt to stop beeping
Positive punishment
adding something unpleasant to decrease behavior
EX: scolding a child for drawing on walls
Negative Punishment
removing something pleasant to decrease behavior
EX: no dessert after being rude
Engram
physical representation of learning
neural trace of memory
Equipotentiality
all cortical areas can take over for damaged areas
Mass action
the brain works as a whole for complex learning
Lashley
experimented with rats running mazes after removing different parts of their cortex to see where memory was stored
Lateral Interpositus Nucleus (LIP)
part of cerebellum crucial for learning conditioned responses
without this activity, no new learning occurs
Red Nucleus
midbrain structure controlling performance (movement)
needed to PERFORM response (not LEARN it)
Short-term memory
temporary holding system, requires rehearsal
EX: remembering a phone number briefly
Working memory
active version of STM for processing info, prefrontal cortex
EX: doing mental math
Delayed response task
test for working memory
EX: monkey waits before responding
Long-term memory
durable storage system, stimulated with cues/hints
EX: remembering bday from years ago
Consolidation
process of storing STM into LTM
Flashbulb memory
highly vivid memory of an emotion event
Rehearsal
repetition to maintain STM
Korsakoff’s Syndrome
Cause: Thiamine (B1) deficiency —> can’t metabolize glucose
Brain damage: mammillary bodies, hippocampus
Symptoms: apathy, confusion, amnesia, confabulation
Mechanism: loss of neurons in memory circuits
Common in: malnutrition & alcoholism
LANDS & LATE
Limbic-predominant Amnesic Neurodegenerative Syndrome
Limbic-predominant Age-related TDP-43 Encephalopathy
TDP-43
protein; if build-up = cause LATE
Alzheimer’s Disease
progressive and irreversible brain disorder that causes memory loss, cognitive decline, and behavioral changes
50% of ppl over 85 have this
Stages of Alzheimer’s
Normal outward behavior: no noticeable symptoms
Very mild changes: occasional forgetfulness
Mild decline: difficulty remembering recent events
Moderate decline: trouble with complex tasks (managing money, travel, etc)
Moderately severe decline: needs help with daily activities
Sever decline: major personality and memory changes and confusion
Very sever decline: loss of ability to communicate, move, or recognize loved ones
Alzheimer’s symptoms
memory loss
difficulty communicating or finding words
confusion about time and place
misplacing belonging
mood swings, poor judgement
social withdrawal
changes in vision or spatial awareness
Genetic components of Alzheimer’s
Down Syndrome: gene for amyloid precursor protein —> increased risk
Early onset (before 65) have mutated APP and PSEN1/2 genes
Environmental factors of Alzheimer’s
50% of late onset have no known relative w disease
Risk factors of Alzheimer’s
physical inactivity
smoking and alcohol abuse
air pollution exposure
head injuries
social isolation
low education levels (less cognitive reserve)
obesity, HTN, diabetes
depression
hearing impairment
high cholesterol after age 40
untreated vision loss
Biological mechanisms of Alzheimer’s
Amyloid-beta proteins clump between neurons, forming plaques (these block neural communication and trigger inflammation in brain)
Tau protein become twisted and form tangles (this disrupts transportation within neuron —> producing MEG3 —> causes cell-death via necrosis)
Alzheimer’s treatment
Increase acetylcholine levels
Curcumin (from turmeric) help reduce amyloid buildup
Infant amnesia
inability of adults to recall memories from before age 3 or 4
Why?
language skills aren’t fully developed yet
hippocampal growth and brain aren’t matured yet
infants lack a stable sense of self
H.M. (Henry Molaison)
Suffered from severe epilepsy so he surgically removed hippocampi which stopped his seizures but his memory decreased
Effects of HM on diff types of memories
Anterograde amnesia (couldn’t form new long-term memories)
Retrograde amnesia (lost some memories from just before surgery)
Working memory (remained the same)
Episodic memory (severely impaired)
Implicit & Procedural memory (intact)
Explicit memory (impaired)
Hippocampal functions
supports declarative memories (memory for facts)
damage leads to amnesia or memory loss
constantly communicates with cerebral cortex to consolidate memories
produces “sharp-wave ripples” strengthen and store episodic memories very well
spatial memory (helps us remember and navigate spaces)
Sharp-wave ripples
brief bursts of synchronized neural activity between hippocampus and cerebral cortex
Hippocampal spatial memory cells
Place cells
activated when animal is in a specific location and it receives input from entorhinal cortex (which has grid cells that form a coordinate system for space)
Time Cells
activates at specific moments during a task/experience
Striatum (basal ganglia)
supports procedural and habit learning (especially probabilistic learning, which is the brain learning patterns based on reward and feedback)
Amygdala
involved in emotional memory, especially fear learning and conditioning
Parietal lobe
helps w/ “piecing info together” integrating sensory details into coherent memories and concepts
Temporal lobe
support sematic memory (facts)
Aplysia
marine invertebrate (sea slug) used in neuroscience
very few neurons
touch results in the withdrawal response
Withdrawal reflex
when you touch an aplysia, it’ll withdraw its gills
can be modified by experience (habituation & sensitization)
Habituation
decrease in response to a repeated, harmless stimulus
Sensitization
increase in response following a strong or harmful stimulus
Long-term Potentiation (LTP)
long-lasting increase in synaptic strength following rapid, repeated stimulation of a synapse
postsynaptic neuron becomes more reactive
Properties of LTP
Specificity: only the synapse that receives stimulation is strengthened
Cooperativity: several weak inputs can combine to produce LTP
Associativity: pairing weak input with strong one strengthens both
Long-term Depression (LTD)
long-term weakening of synaptic strength, occurs when synapses are rarely active while surrounding neurons are active
Biochemical mechanisms of LTP
LTP depends on neurotransmitter glutamate, which binds to two receptors:
AMPA: opens Na+ channels —> depolarizes the cell
NMDA: normally blocked by Mg2+ but when dendrite is depolarized, glutamate can bind
How LTP happens
Glutamate binds to AMPA: Na+ enters and depolarizes dendrite
NMDA channel opens: Mg2+ block removed —> Ca2+ enters postsynaptic cell
Ca2+ triggers enzymes (like CaMKII) —> activated CREB (a gene-regulating protein)
These changes causes the neuron to make more AMPA and NMDA receptors, make new dendritic branches/synapses, and strengthen existing connections
BDNF (brain-derived neurotrophic factor) further enhances these effects, promoting neuron growth and survival
Retrograde transmitter (NO) acts as a positive feedback neurotransmitter
LTP & Behavior
Abnormal NMDA receptor —> poor learning
More NMDA receptors —> improved learning
No AMPA receptors —> no LTP or memory
Drugs that block LTP —> blocks learning
Drugs that enhances LTP —> improves learning
Left Hemisphere
Interpreter, specialized for language, scientific facts, right hand
Right hemisphere
specialization in music awareness, artistic ability, 3D spatial reasoning, imagination/creativity, emotional tone of language, & left hand
Contra-lateral connections
left hemisphere controls right hand and visual field while right hemisphere controls left hand and visual field
Lateralization
each hemisphere does some tasks more efficiently, even though they cooperate
Commissures
axon pathways that connect the left an right hemispheres (allow sensory, motor, emotional, and memory information to be shared)
Corpus callosum
commissure
primary information highway between hemispheres
enables coordinating movement
Anterior commissure
smaller than corpus callosum
connects anterior parts of hemisphere
involved in pain sensation, emotion, and some aspects of olfaction
Hippocampal commissure
connects right and left hippocampi
important for memory formation and spatial navigation
Corpus callosum
main information highway between hemispheres
responsible for communication between sides of body
Visual Connections to Hemispheres
what is visible at any moment
both eyes can see both visual fields
right visual field goes to left half of both retinas (which goes to left hemisphere) vice versa
Auditory Connections to Hemispheres
each ear receives sound waves from just one side of head but sends information to both sides of brain
Absence of Corpus Callosum
prevents exchange of information between hemisphere
it’s cut as treatment for sever epilepsy —> split brain behavior
Plenum Temporale
section of temporal cortex that is plays a role in auditory and language processing
Language
system of communication involving spoken, written, or gestured symbols arranged according to a grammar
must have symbols that carry meaning
must be independent of situation it’s being used
must have possibility to produce new symbols/signals to represent ideas
Phonological loop
a working memory system used for speech sounds
language evolution
language likely evolved after mouth/hand gestures
Evidence against the idea that language is a result of intelligence
undamaged brains can still have impaired language
impaired intelligence can still have normal language (EX: williams syndrome)
Language acquisition device (LAD)
by Noam Chomsky
children learn language naturally and quickly, without formal teaching
they learn more than what they are explicitly taught (poverty of stimulus argument)
suggests humans are biologically prepared for language
FoxP2 gene
FoxP2 gene
gene associated with speech and language development (located on chromosome 7) which is involved in motor control of speech organs (jaw & throat)
Critical periods for language learning
there’s a sensitive developmental window during childhood where the brain is especially ready to learn language.
Language production
ability to produce spoken language (speaking)
brain area: broca’s area
Language comprehension
ability to understand language (hearing)
brain area: wernicke’s area
aphasia
sever language impairment caused by brain damage, usually to left hemisphere
Non-fluent aphasia
person knows what they want to say but struggles to form words
Fluent aphasia
speech is fluent and smooth, but does not make sense
Dyslexia
learning disorder that involves a significant impairment in reading ability
more common in boys and English-language readers
more symmetrical cerebral cortex
cause: sound processing impairment, and attention differences
Dysphonic dyslexia
trouble sounding out words
Dyseidetic dyslexia
trouble recognizing whole words by sight
Mind-brain relationship
how the mind and brain relate to each other
is the mind the same as the brain, or something separate?
Dualism
the mind and body (brain) are separate things
Rene Descartes
Monism
only one kind of substance exists
Materialism: all is physical
mentalism: only the mind exists
identity: mind and brain are the same things, but with different names
Masking
visual technique used to study which stimuli enter consciousness
awareness depends not just on sensory input, but on continued synchronized brain activation (coordinated, widespread neural firing)
Binocular rivalry
when each eye is shown a different image, you don’t see a blend, instead your conscious awareness switches back and forth between the two images
Threshold Phenomenon
There’s a minimum level of neural activation required for a stimulus to become conscious
Phi Phenomenon
visual illusion where static images shown rapidly in sequence appear to move
Attention
concentration of mental activity
associated with increased neural activity
required for highest perceptual accuracy
Inattentional blindness
when people fail to perceive an obvious stimulus because attention is focus elsewhere
Agonist
Mimics or increases effects of a neurotransmitter
Antagonist
Blocks or takes away from effects of the neurotransmitter
Affinity
ability to bind a receptor
Efficacy
how well the drug activates the receptor