there was a backlash to Skinner. Psychologists felt that cognitive models were needed for things like language, perception, reasoning.
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Modern summary of Nature vs. Nurture
Nurture (the environment) uses Nature (heritable individual differences in biological mechanisms) to make changes to cells, systems, organisms, and behavior. While knowledge is learned. (Empiricism), the biological mechanisms of learning can be heavily influenced by inherited traits (nativism)
\-In sum Nature and Nurture both contribute to Conditioning and Learning.
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Behavior
Activity that can be observed or measured brains and neurons are not required
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Learning
A relatively permanent change in behavior based on experience
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Other ways to change behavior that are not learning:
\-Fatigue (response fatigue) decrease in behavior due to repeated or excessive use of muscles
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Other ways to change behavior that are not learning:
\-Physical Maturation/growth-change in behavior due to physical capability
ex: tadpole vs. adult frog jumping abilities
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Other ways to change behavior that are not learning:
sensory adaptation -change in function of the sensory apparatus that changes detection of stimuli
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Elicited Behavior
Behavior in response to a stimulus
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Reflex Behavior
\-Simplest form of elicited behavior
\-Stimulus→Response
(response behavior in relatively rare without eliciting stimulus)
Return in behavioral responding after a long time delay between exposures
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Neural Basis of Learning
applies to associative and non-associative
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EEG
Electroencephalography measures neural activity ≠ summed over large areas High temporal resolution , low spatial resolution measurement to limited to cortex activity
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MRI
Magnetic Imaging, View Structure of brain
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DTI
Variation on MRI (Structural) to see connections between brain areas uses the flow of water as a tool to indicate brain structure
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FMRI
Functional MRI, measures changes in blood flow associated with brain acitivity; spatial resolution does depend on magnet strength (TESLA) , typical medical ( research in 3T, although 2IT exists and it gets closer to neuron-level spatia) resolution.
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Microscopy Analysis
post-mortem brain collection, tissue on microscope slides limited to one timepoint over due lifespan (analysis)
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Genetic Manipulations in animals
can control genes over days or lifetimes
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In Vivo Electrophysiology
Record from individual or multiple neurons via probe within brain
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Chronic In Vivo
measuring weed out of Ca^a+
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TMS
Transcranial magnetic stimulation-used to manipulate brain activity
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In Vivo Microscopy
Calcium imaging of individual Neurons
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TDCS
Transcranial direct
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Where is Learning in the brain?
Are we looking for change in a single location or is it distributed?
Single Location: 1 to 1 relationship between learning and Brain
1800s -Francis Gall
Phrenology-Now debunked that experiences changes
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Santaigo Ramon y Cajal
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hypothesized that learning happens at connections between cells.
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1929
Karl Lashley attemepted 1st experiment to identify the location of memory in the Brain \[He found no lesions on the Brain impairing learning→learning is distributed\]
\-His experiment =Training Rats on mazes, then lesioned different parts of neocortex to evaluate effects, no single are imported male memory; he concludes that learning is distributed.
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Donald O. Hebb
(student of Lashley) “ neurons that fire together, wire together” Learning occurs in circuits (cover broad areas, connecting different brain locations, circuits are strengthened or weakened by experience at the contacts between Neurons (synapses)
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What is the magnitude of brain change associated with Learning/ Experience?
\-Two groups of Rats : typal housing & enriched housing
\-Less Anxiety-Like Behavior, 9-10% Larger Brain Mass, Neurons live in Cortex are more elaborate with more branching more synapses\]
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Domarian Children in Orphages
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Severe social/sensory deprivation -atypical social behavior, impairments in cognitive Function, Less Gray Matter ( Seen on MRI) , Less dense white matter (Fibers), Connecting brain areas , seen with DTI, Atypical neural activity with EEG.
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Brain change magnitude
in association with magnitude of experience
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What is learning at the neuronal circuit level?
Synaptic Plasticity (changes at Synapses)
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Bliss & Velmo
1 neuron stimulates and the other Records
\-Neuron in circuit hooked to another Neuron→lFinding How Neurons talk to each pother
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Bliss & Velmo
If Stimulate A has a weak stimulation at first then Record B will have a Weak Response, if it has a strong stimulation it will have a strong response.
\ They learned: after experience in the circuit it learns about input and it is ready for a stronger response next time there is a weak stimulation.= Learning exists and after Long term potentiation
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Long term Potentiation (LTP)
Brief Bursts of Large inputs can increase the strength of future inputs
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Long Term Depression (LTD)
Repeated Exposures to very weak input weakens synapses
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In a neuron…
Vesicle filled with glutamate (neurotransmitter)
Glutamate Receptor (AMPA Receptor)
NMDA Receptor (also glutamate)
MG++ Block ( Magnesium)
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1\.Depolarization
(Na enters) on presynaptic side
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2. Vesicles
move to synaptic membrane and release neurotransmitter
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3. Neurotransmitter
binds to AMPAR on post-synaptic side to convey one signal
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4. If the inhibitory signal is large enough
(lots of NA+ flows in; Large depolarization) then the MG++ leaves the doorway of NMOA r)
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5\.Calcium
Pushes in Through NMDAR
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Calcium starts
making changes to post synaptic
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within 10 minutes
CA++ changes the stabilization of scaffolding on post synaptic side (The inside structure of cells) within 30 minutes -2 hours consolidation =increated insertion of more AMPA R at post synaptic side
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Maintenance
Keeping a larger quantity of AMPA R @ Postsynaptic side
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Drugs to break synaptic plasticity: CNQX
A drug that block (inhibits, antagonists)AMPA R eliminates neural transmission
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\n Drugs to break synaptic plasticity:
APV (APS)
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A DRUG THAT blocks NMDA R Blocks LTP (leaves neural trasnmission intact)