Learning and Memory

learning

• acquiring new information

• changes in our nervous system and behaviors through experiences

consolidation

• encoding short-term, newly learned info into a longer-term form

memory

• long-term changes in the nervous system following learning

stimulus-respondent learning

• performing some behavior when a stimulus is presented

• classical and operant conditioning

• ex. pack up and leave for this class on MWF at 12:10

motor learning

• changing one’s motor responses to a stimulus

• think riding a bike

• similar to S-R learning, has more to do w/ motor functions

perceptual learning

• learning to recognize stimuli that have been presented. before

• how we recognize things

• identifying and categorizing objects and situations

• ex: identify pencil even though not all pencils look the same

relational learning

• learning relationships among individual stimuli

• includes things like spatial learning (where things are location-wise)

sensory memory

• less than 1 second

• very short period of time where initial sensory info is perceived

• fractions of seconds

working memory

• temporary memory used to manipulate information for tasks

• phone numbers, passwords, etc

• if info isn’t need anymore → discarded

short-term memory (STM)

• memory only held for a few seconds and only a few items at a time

• seconds to minutes

• can be extended through rehearsal

long-term memory (LTM)

• memory after consolidation, lasts a long time

• declarative memory → episodic and semantic

• nondeclarative

declarative memory

• facts, events, needs conscious recall

  • episodic → context specific

  • semantic → not context specific

nondeclarative memory

• automatic, behaviors, doesn’t need conscious recall

learning process steps

encoding → consolidation → storage → retrieval

encoding

first encounter with information

consolidation

moving the short-term info to longer-term form

storage

storing the memory to a more permanent location

retrieval

recalling information to use

reconsolidation

when memories are reactivated, they become fragile and changeable again until re-stored

• fear conditioning rat example → lose fear memory if given anisomycin right after something they were fearfully conditioned by happened

hippocampus

• important for long-term, declarative memories

• non-declarative memories rely more on cortex and basal ganglia

• where consolidation of memories happens

• permanent storage is again in the cortex

patient HM

• had hippocampus removed

• was able to retain procedural memories but suffered anterograde amnesia

classical conditioning

• pairing a conditioned stimulus with an unconditioned stimulus

• amygdala important for [this] involving emotional stimulus (fear conditioning)

  • information about the CS and US converge in the lateral nucleus

  • this pairing is strengthened after repeat trials

operant conditioning

• pairing a voluntary response with some outcome

• transcortical path → initial acquisition of declarative, episodic memories; initial acquisition of more complex behaviors

• basal ganglia path → when learned behaviors become more automatic, they move to the basal ganglia

• basal ganglia gets info about stimuli present as we make responses

• over time, basal ganglia learns what to do, freeing the transcortical pathway

Hebb rule

• if a synapse is repeatedly active when the postsynaptic neuron fires → the synaptic connection strengthens

• huge reason why we can learn/remember things

habituation

decrease in response strength after repeated stimulation

sensitization

increase in response strength after repeated stimulation

aplysia

• sea slug that has been used for classical conditioning

• touching the siphon of the slug stimulates a gill withdrawl reflex

• this reflex would habituate after repeated trials, until a tail shock was added

  • once the tail shock was paired with siphon stimulation, reflex sensitized

reinforcement

• dopaminergic neurons play a large role here

• ventral tegmental area (VTA) holds lots of dopamine neurons

  • this projects to areas like the amygdala, hippocampus, and nucleus accumbens (NAC)

• activity of these neurons is important for RFT

• responses are heavier for unexpected RFT

  • based on Reward Prediction Error (RPE): the difference between an expected and actual reward

Premack principle

• given two responses of different likelihoods (H, L) performing the higher probability one after the lower will reinforce the lower

  • L → H = L RFT

  • ex. asking child to eat veggies before dessert → reinforce veggie eating

• reverse direction (H → L) doesn’t reinforce L

• uses extrinsic motivation to achieve a desired behavior

extinction

• unlearning a conditioned response → still considered a form of learning

• repeated CS w/o US does not equal CR

• it takes about 3x as long to unlearn a CR

ventral medial prefrontal cortex (vmPFC)

• inhibits conditioned responses during EXT

• inputs to the [this] tell us what is happening in the environment

• has top-down control over the amygdala → can essentially override it

  • can also modulate expressions of fear

• outputs affect our responses behaviorally and physiologically

  • this includes emotional responses organized by the amygdala

• needed for recall of EXT memories

  • if damaged → EXT memories may come back

spontaneous recovery

• increase in responding after a period of EXT

renewal

• recovery of CR when context features present during EXT are changed

  • EXT in context A doesn’t translate to context B

  • suggests that EXT is context dependent

reinstatement

• recovery when exposed to US or reinforcer

• ex. over nicotine, but then see friend smoking → back to nicotine bc of exposure

resurgence

• reappearance of R caused by extinction of some other behavior

• EXT of A (nicotine addiction) → EXT of B (working on OCD) → resurgence of A (nicotine)

long-term potentiation (LTP)

• causes the neuron to be more readily excitable to a particular stimulus

  • makes it easy to recognize patterns in what you see

• occurs when presynaptic neuron releases NTs to a postsynaptic neuron that is already depolarized

  • called pre-to-post pairing

• primarily studied in hippocampus

early-phase LTP

• changes in the synaptic strength involving NMDA and AMPA receptors

  • particularly AMPA recycling

late-phase LTP

• involves protein synthesis and more permanent changes to the synapse

NMDA receptors

• drive LTP

• Ca++ enters through these, causing cascades that let LTP work

• activated by glutamate and glycine

• can only work if the membrane depolarized (Mg++ blocks the main pore!)

• two ways to depol

  • back-propagating action potentials

  • AMPA receptor activation

back-propagating action potentials

• when an action potential happens, some of the positivity that spreads down the neuron can go backwards

• this isn’t a new action potential, but rather some additional positivity

• by going backwards, BAPs can get into the dendritic spines where NMDA receptors live

• this depolarization can help to remove Mg++ block in NMDA receptors

AMPA receptors

• responsible for early-phase LTP changes

• AMPA receptors are excitatory so they allow action potentials to begin in the postsynaptic neuron

• play a huge role in removing Mg++ block in NMDA receptors

• after repeated activation of the synapse → AMPA receptors can be recycled into the dendritic spine membrane

• adding more receptors allows the synapse to depolarize more quickly

  • more receptors = more excitability

silent synapses

• some synapses in your brain don’t activate because they lack AMPA receptors (these would be synapses that aren’t used)

• it’s a lot harder for NMDA receptors to boot out the MG++ block w/o AMPA

• AMPA recycling can turn them on

spines

• LTP can change size and shape of dendritic spines

  • remember that certain spines make it easier to send APs

• there can also be the creation of new spines

  • this would be a postsynaptic change

protein synthesis

• used in late-phase LTP

• protein PKM-zeta can auto-transcribe itself when Ca++ enzymes turned on

• PKM-zeta activates NSF which helps move AMPA receptors to the dendritic spine membrane (LTP!)

• can suppress Pin1 to keep continuous transcription going (long-lasting LTP)