17: Learning and Memory

true or false: LTP will still develop at a lower frequency, as long as you get a high number of action potentials

false. you need a very strong, high frequency stimulation to achieve LTP.

in a conditioning experiment, will reward or fear conditioning override the other?

fear conditioning will overrride the good

conditioned reinforcement

first, set up pavlovian condition where a CS light presents with a light. after learning occurs, levers are inserted into the chamber - one lever gives the CS light, the other gives nothing. note that the lever is never associated with reward, just light. rats will press the level just for the CS, even though the lever never gave the reward --> the light becomes reinforcing and animals will work for it. sort of like money in humans lesions to the amygdala: no preference for lever that produced the CS

explain the spatial radial maze task and what area of the brain is important for success with this task

food in the end of each of the 8 arms in the maze. the rat just has to learn which arms to not go back to (where it has already been). the hippocampus is important for this task and lesions to this area will leave the rat unable to perform this task.

what were we able to learn from patient H.M?

his poor performance on long-term memory tasks but not on short term memory tasks supports the two stage model for memory formation his inability to consolidate new memories from short term to long term suggests that memories are stored elsewhere in the brain but the hippocampus is important for converting memories into long term storage because his semantic and procedural memory was relatively in tact, not all types of learning and memory are mediated by the hippocampus.

how is the PFC involved in behavioural flexibility?

(see wisonsin card sorting task) - plus maze, rats must learn a response rule: always turn left, while a visual vue is implanted that they must ignore - next, rats must switch strategy to the visual cue and ignore the old strategy. - *inactivate PFC during initial learning*: no effect - *inactivate PFC during the shift*: major impairment - the PFC is selectively involved in switching strategies, not learning ones.

what are the key components of memory?

*Encoding*: getting sensory info into your brain by translating it into a neural code the brain can understand. just like typing on a keyboard, keystrokes are converted into electrical signals the computer can understand *Storing*: retaining information over time *Retrieval*: the active processes of locating and using stored information

give some examples of tests that H.M struggled with. why was he unsuccessful with these tasks?

*digit span + 1 test*: present 5 digits, have subject repeat back. keep adding digits to remember until the subject makes errors. most people can do 15, H.M could only to up to 8. *matching to sample*: board of 9 different image tiles turned over. the subject presses the sample pad to turn it over, then, it flips back over and the other 8 panels turn face up, subject has to pick the panel that matched the sample. H.M could perform this task with delay up to 40 seconds as long as he was allowed to use repitition to remember - if he was distracted he showed impairment. on nonverbal version of the task he was impaired at intervals greater than 5 seconds because he cannot easily use repitition to remember. these tasks indicated his short term memory was in tact, but his ability to form long term memories was damaged.

summarize the different brain regions involved in memory and what type of memory they encode.

*hippocampus*: declarative memory (humans) spatial/relational memory (rats) *striatum* (basal ganglia, caudate nucleus): procedural memory/skill/habit learning (humans), instrumental conditioning (rats) *amygdala*: pavlovian conditioning for appetitve or aversive events (humans and rats) multiple brain regions can interact to regulate a particular type of memory, however some can work independently, referred to as a *dissociation* of memory systems

the prefrontal cortex is further broken down into two regions. what are they and what are their functions?

*medial and orbital (orbitofrontal):* emotion regulation *dorsolateral*: (in humans and primates) working memory, flexibility and planning

give some examples of memory tests that H.M performed successfully on. why was he successful with these tasks?

*mirror drawing task*: subject has to redraw an object from reflection in the mirror (without being able to see their hand) *rotary pursuit task*: subjects have to keep pen on target thats on a rotating disk on both of these tasks, H.M was tested for several days, each day he couldn't remember having done the task previously, but his performance improved indicating he could learn skills (procedural memory) he could also gradually learn new facts (semantic memory) but not recall learning them

what part(s) of the brain are involved in contextual fear conditioning? support your answer with an animal study.

- create a CS tone-shock pairing in one distinct context A. - give the CS tone in a seperate context (B). - normal rats, as well as hippocampal lesioned rats, will display fear freezing. - put the rats back in context A without CS tone, normal rats will show fear freezing, hippocampal lesioned rats will *not* show fear freezing. - the hippocampus communicates with the amygdala --> if the amygdala is lesioned and the hippocampus is in tact, there is still no ability to learn fear conditioning.

how is the PFC involved in extinction learning?

- create tone/shock freezing association - keep giving tones, but with no shock - rat has to learn new info that it is not scary, and supress the old fear memory response - rats with PFC damage can learn both associations, however they take *much longer to extinguish the fear response* - PFC is connected with the amygdala, and PFC inputs can inhibit neural activity in the amygdala

explain normal synaptic transmission in a glutamatergic synapse that has the potential for LTP. (to help in understanding of LTP mechanism)

- in the hippocampus, synapses in area CA1 have *NMDA and AMPA receptors* in their postsynaptic membrane. both of these receptors have the potential to respond to glutamate, AMPA admits Na+, while NMDA (when not blocked by MG++) admits Ca++ - under *normal frequency, only AMPA is activated by glutamate, because the NMDA receptor is blocked by MG++*. - in response to glutamate, AMPA receptors open up to allow Na+ inside the cell, depolarizing it

why are abnormal or salient memories easier to remember than everyday events?

- the hippocampus encodes episodic memories - cortical areas feed input from different stimuli (where you are, what you see, what you eat, hear etc.) to the hippocampus, making certain groups of neurons fire in a particular pattern. - the hippocampus keeps record of the bits of info and their relation to each other - everyday episodes will code similarily, whereas something different will code different and therefore stand out - being easier to remember. - remembering an episode will cause the hippocampus to activate the particular regions of the cortex triggering recall. over time (2-3 years) a retrieval cue may be able to activate the cortex for retrieval of the memory without the hippocampus = why the hippocampus isn't involved in long term memory

explain the conditioned place preference task and what area of the brain is important for success with this task

8 arms in the maze, rat receives food in one arm and nothing in the others. the rat will learn to spend more time in the arm where it received food. the amygdala is important, and lesions to this area will leave the rat unable to perform this task.

describe the cellular mechanisms behind induction of LTP

- when *larger quantities of glutamate* are released from the presynaptic membrane, AMPA receptors are stimulated more stongly thus admitting more Na+, and causing the *postsynaptic cell to reach threshold*. - this *drives Mg++ outside of the NMDA receptor, freeing it up to be activated by glutamate which allows Ca++ to now enter the cell.* - the large *influx of Ca++ activates protein kinases* inside the cell such as *calcium-calmodulin* (CaMKII/*CaM kinase*), which *activates latent AMPA receptors* to be *inserted in the membrane* - *CREB* is *activated* by *protein kinase C* and *Tyrosine Kinase*, which has short term and long term effects: - short term: *formation of retrograde messenger like NO* (goes from postsynaptic neuron to presynaptic terminal to promote more glutamate release) - long term: *activation of protein synthesis* that can change dendrite shape/size/number/produce more ion channels

is LTP a mechanism of memory formation? explain with evidence

1. *correlational observations*: the time course of LTP bears strong similarity to the time course of memory formation. 2. *somatic intervention experiments*: pharmacological treatments that interfere with any of the physiological processes that contribute to LTP tend to impair learning. - blocking NMDA receptors during learning in the hippocampus disrupts spatial learning, in the amygdala it disrupts fear conditioning, and in the striatum it disrupts instrumental learning. overexpressing NMDA also has been shown to enhance memory formation. - blocking NMDA after training does not disrupt memory formation (because it's past phase 1); blocking protein synthesis after training does disrupt memory formation (because it is second phase) 3. *behavioural intervention experiments*: fear conditioning produces clear LTP specifically in fear circuits in the amygdala

how can memory be defined by the type of info stored?

1. *declerative/explicit memory*: things you know that you can tell others - breaks down into: *episodic*: remembering your first day of school; and *semantic*: knowing the capital of france 2. *procedural/implicit memory*: things you know that you can show by doing - breaks down into: *skill/instrumental learning*: knowing how to ride a bicycle; and *conditioning*: salivating when you see a favorite food

summarize the steps in order that are necessary to induce LTP

1. high frequency stimulation and release of glutamate into the synaptic terminal, which binds to AMPA 2. influx of Na++ that causes enough depolarization to remove Mg++ from NMDA 3. influx of Ca++ through NMDA channel 4. activation of protein kinases that send retrograde messengers, activate latent AMPA receptors, and activate protein synthesis all that help to strengthen the synapse

what are the requirements for LTP?

1. simulataneous activity in pre and postsynaptic neuron. for example, if you depolarize the postsynaptic neuron but not the presynaptic, you won't develop LTP - additionally if you activate the presynaptic neuron but block postsynaptic firing you won't develop LTP. 2. very strong (high frequency) stimulation. for example if you stimulated the neuron to get the same number of action potentials but at a lower frequency, you would't get LTP.

what are the 5 important points of Pavlovian conditioning

1. the CS must reliably predict the US 2. delivery of CS and US are uncontrollable to the organism 3. the CR is also uncontrollable (typically an autonomic response like heart rate, but can also be motor - like moving towards stimuli: called *pavlovian approach*) 4. in humans, the CR typically occurs in the absense of conscious knowledge 5. very long lasting: can be extinguished but reinstated very quickly with another CS-US pairing (never truly forget because you never know when youre going to need that info again)

what are the three main points about the neural basis of memory?

1. there are multiple forms of memory 2. different types of memory are regulated by distinct brain regions 3. one type of memory is regulated by interactions between multiple brain regions

describe the 2 phases of LTP

1st phase: increase in receptors/glutamate release, occurs quickly (<1hr) - more AMPA receptors, retrograde messengers 2nd phase: CREB activates protein synthesis that causes longer lasting changes (>3hrs) - change in dendrite shape and size, more ion channels, more dnendrites

what is the role of AMPA in induction of LTP?

AMPA receptors respond to glutamate to induction of Na+ that allows the postsynaptic cell to depolarize. when enough NA+ has entered the cell, it causes the Mg++ block to be removed from NMDA, so it is open to be activated by glutamate. latent AMPA receptors are also involved in the 1st phase of LTP as CaM kinase activates and inserts them into the membrane to allow more Na+ admittance.

describe the 2nd/late phase of LTP

CREB activates protein synthesis that causes longer lasting changes (>3hrs) - change in dendrite shape and size, more ion channels, more dendrites

what is the role of CREB in induction of LTP?

CREB is activated by protein kinase C and tyrosine kinase. it has both short term and long term effects: short term: formation of retrograde messenger like NO (goes from postsynaptic neuron to presynaptic terminal to promote more glutamate release) long term: activates protein synthesis, that can cause changes in dendrite size/shape, more ion channels, more dendrites etc.

what is the role of Ca++ in induction of LTP?

Ca++ can enter the postsynaptic cell through NMDA receptors, once the cell has depolarized enough to remove Mg++ from NMDA. Ca++ inside the cell activase protein kinases such as CaM kinase, protein kinase C, and tyrosine kinase

what is the role of CaM kinase in induction of LTP?

CaM kinase is activated when NMDA receptors have allowed enough Ca++ into the cell. it activates latent AMPA receptors and brings them to the cell membrane to further increase the strength of the synapse.

short term memory

a form of memory where information is held for short periods while physiological changes needed for long-term memory are being made - limited capacity (7 +/-2 items) - susceptible to distraction, requires acive rehearsal to maintain: last about 30 seconds without rehearsal (although there is a lack of consensus on how long it lasts, seconds to hours) - information lost through displacement (new info pishes it out) or decay - either gets discarded or moves into long term memory

Pavlovian (classical) conditioning

a fundamental and highly adaptable form of learning for virtually all animals; helps organism prepare for biologically significant events in response to cues that predict those events. includes 4 key elements: *unconditioned stimulus (US)*: the biologically significant event *unconditioned response (UR)*: normal response to significant event *conditioned stimulus (CS)*: previously neutral cue that reliably predicts significant event *conditioned response (CR)*: the body's response to the CS alone.

cell assembly

a large group of cells that tend to be active at the same time because they have been activated simultaneously or in close sucession in the past

what is meant by an increase in synaptic strength? what causes this?

a long term change in a synapse where the presynaptic neuron will induce more depolarization in the postsynaptic cell. it is caused by reverbatory circuits --> cells that wire together fire together causes: 1. the presynaptic neuron increases amount of NT it releases 2. the postsynaptic neuron increases the number of receptors it has 3. both 4. other types of physical changes (change in shape, number of dendrites, etc)

hippocampal "place cells"

a neuron within the hippocampus that selectively fires when the animal is in a particular location

what is Long Term Potentiaion (LTP)?

a stable and enduring increase in the effectiveness of synapses following repeated strong stimulation

iconic memory

a very brief type of memory that stores the sensory impression of a scene; a sensory buffer

animals or humans with lesions to what area of the brain would display the inability to develop new fears?

amygdala

animals or humans with lesions to what area of the brain would display "fearless" like behaviours? e.g: with a lesion to this area, primates who are innately scared of snakes will not be afraid

amygdala

perseveration

an error made in wisconsin card sorting task by individuals with PFC damage where they are able to learn the first task, but not able to learn the new task.

what might be an underlying cause of PTSD?

an exaggerated type of memory modulation caused by noradrenaline during highly emotional events. a potential preventative treatment for PTSD is administering beta blockers at traumatic events

tower of london task

assesses planning of movement sequences "move the balls from the start position to the final position in as few moves as possible" - PFC damage patients need many more moves to reach the goal position, often don't reach it

instrumental conditioning

association with a particular action/motor response and its consequences (i.e: reinforcement) here the organism can control what happens. reinforcer: something that increases or decreases likelihood of response occuring again this body action = this response happens (learning how to ride a bike)

how can memory systems be dissociated?

by how long it lasts: *(iconic), short term, (intermediate), and long term* or by the *type* of information being stored: 1. *declerative memory*: things you know that you can tell others - breaks down into: *episodic*: remembering your first day of school; and *semantic*: knowing the capital of france 2. *procedural memory*: things you know that you can show by doing - breaks down into: *skill/instrumental learning*: knowing how to ride a bicycle; and *conditioning*: salivating when you see a favorite food

how do we measure changes in synaptic strength?

changes in EPSPs (excitatory post synaptic potential) evoked by an input from a presynaptic neuron. an increase in EPSP = increase in synaptic strength

retrograde amnesia

difficulty retrieving memories formed before the onset of amnesia

what would neural activity of PFC neurons look like during the delay period of a delayed response task?

during the delay period there is increase activation in the PFC. the less activity during delay = the more likely animal is to make an error

experiment: plus shaped aparatus (use N/S/E/W for direction) in "T" configuration where the north arm is blocked off and the rat begins in the south arm. during the training period food is always in the east arm of the T, and there are spatial cues around the apparatus. during the probe period, the rat begins instead from the north arm of the plus. (the food is still in the east arm and the spatial cues remain in the same places) explain the results you expect to see if you do the probe trial: early on in training later in training with a lesion to the hippocampus with a lesion to the dorsal striatum what does this experiment tell us about different memory systems?

early in training: most rats will use the "hippocampal" strategy, and turn right using spatial cues to find the east arm late in training: most rats will use the "striatal" strategy and automatically turn left to find food, even though turning left is a new (west) spatial location with a lesion to the hippocampus: even if early in training, most rats will switch to the striatal strategy with a lesion to the striatum: even if late in training, most rats will switch back to the hippocampal strategy tells us: 1. different memory systems can learn independently and in parallel to each other 2. suppression of one system allows behaviours driven by another to emerge 3. different systems learn at different rates (hippocampal = rapid, striatal = gradual)

describe one of the first studies to support the idea of LTP

experimenters planted electrodes in the glutamatergic neurons of the rat hippocampus so that the presynaptic terminal could be stimulated and the electrical response in the postsynaptic terminal could be recorded. when they stimulated the presynaptic terminal with a low activation they saw stable, predictable response in the postsynaptic neuron they next applied *tetanus* to the presynaptic neuron creating high frequency of APs when they stimulated again at the baseline frequncy, the same frequency caused larger EPSP's, indicating the synapse had become stronger/more efficient

true or false: LTP provides a basis for short term memory

false. LTP provides a basis for long term memory

true or false: LTP has only been observed in vivo (living), awake animals

false. it has been observed in vivo, in vitro, anesthetized or awake animals

true or false: LTP has only been demonstrated in the hippocampus

false. it was originally observed in the hippocampus, but it has been seen in all glutamate synapses, such as those in the cortex, amygdala, striatum, and cerebellum.

if you define by how long it lasts, what are the different types of memory?

iconic: very brief, stores the memory impression of a scene short term: information is held for short period while physiological changes needed for long term memory are being made long term: can last lifetime of organism, is relatively stable.

what is the key difference between pavlovian and instrumental conditioning?

in instrumental conditioning the sobject has control of the situation, in pavlovian it does not

anterograde amnesia

inability to form new memories beginning with the onset of amnesia

describe the 1st/early phase of LTP

increase in receptors/glutamate release, occurs quickly (<1hr) - more AMPA receptors, retrograde messengers

what is a *reverberatory circuit* and what does it have to do with synaptic plasticity?

it provides a basis for short term memory: a cell assembly that continues to respond after the original stimulus that excited it has ceased. if the activity in the circuit is strong enough/lasts long enough/salient enough long term alterations can occur making the memory more permanent

what is the role of the amygdala in fear conditioning? describe what happens with lesions to the amygdala

lesions to the amygdala abolish auditory fear conditioning in rodents (freeze in response to a CS tone from a US shock) lesions both prior to conditioning and after conditioning disrupt the CR = *amygdala necessary for learning and retrieval of the fear response* - note similar results in humans with amygdala damage: disrupted fear conditioning shown via HR and BP auditory info and pain info converge in lateral amygdala, fire together (wire together) to produce the response without the pain; increase activation in amygdala to CS after conditioning

the dorsolateral PFC is to primates is as the ________ is to rats

medial prefrontal cortex

long term memory

memory that cn last days, weeks or years, lifetime - very large capactiy (potentially unlimited) - can be active or passive - information can be forgotten or recalled inaccurately

intermediate term memory

memory that lasts longer than short term but not as long as long term memory. for example remembering todays weather forecast but not that of a few days ago. used by some but not all researchers.

who is patient H.M?

patient with severe epilepsy that has seizures originating bilaterally in medial temporal lobes --> had them surgically removed, included most of the hippocampus, amygdala, and adjacent temporal cortex. relief from seizures but presented with severe anterograde amnesia - couldn't form new memories (also mild retrograde amnesia ~3 years prior to surgery) normal short term memory, but couldn't transfer info into long term memory.

pavlovian approach

pavlovian conditioning can elicit the organism to approach a "place" or behaviour that becomes attractive based on reward.

the amygdala

plays an essential role in both innate fears and in learning and preparing to be afraid of potentially harmful things

what is the function of the PFC

plays major roles in: *working memory* (see delay response task) and *behavioural flexibility* (wisconsin card sorting and the plus maze) *extinction learning* (takes longer to extinguish a fear conditioned response) *planning* (see tower of london and dinner party problem)

Conditioned Stimulus (CS)

previously neutral cue that reliably predicts significant event ex: the bell (that signifies the arrival of meet powder or the tuft of air blown into rabbits eye)

which regions of the brain are involved in procedural (implicit) memory?

regions such as the striatum (skill/instrumental) and amygdala (conditioning)

would a patient with amnesia resulting from hippocampus damage show impairment in the primacy effect or recency effect?

they would show a reduced primacy effect but retain the recency effect as their STM is still in tact

the striatum

regulates action selection (damage: intention tremor in parkinsons) and instrumental conditioning. receives inputs from the sensory/motor cortex and dopamine system. involved in late learning when responses become more automatic/habitual (there is a transition from early learning where responses are goal directed, then later become more automatic, this is mediated by dorsal striatum) also takes input from the amygdala to influence intrumental action (reaching into the cupboard for a certain food even if you know its not there)

explain how episodic memories become consolidated and no longer require the hippocampus for retrieval

remembering an episode will cause the *hippocampus* to activate the particular regions of the cortex triggering recall. over time (2-3 years) a retrieval cue may be able to activate the cortex for retrieval of the memory without the hippocampus, indicating the memory has reached 'long term memory' status. note: the hippocampus is responsible for remembering the association of all the stimuli together, the memories may be held elsewhere (this is why H.M can still remember)

how does emotion influence memory? provide examples to support your answer

strong emotional states enhance memory consolidation, likely mediated in part by noradrenaline and the amygdala. 1. 2 groups of subjects shown the same set of pictures, one group told emotionally charged stories to associate with images, the other told emotionally neutral stories. the group told the emotional stories remembered the images better than the neutral group. when given noradrenaline beta-receptor antagonist (block adrenaline) the group told the emotionally charged story had recall similar to the neutral group, despite reporting an emotional response to the stories. 2. stimulating the amygdala post 1 day of training = improved memory consolidation tested on day 2

what evidence do we have for hippocampal involvement in spatial memory of humans?

studies using virtual 3D environments: - humans with hippocampal damage are impaired when navigating through space and remembering routes - imaging studies in healthy individuals show increased activity in hippocampus when people learning routes in virtual environment taxi drivers how increased hippocampal activation when recalling taxi routes - recall of landmarks that drivers did not know/remember = no hippocampal activion

dinner party problem

subjects are given a real world planning task: - 6 errands to run, get answers to 4 questions, do not enter shops unnecessarily and finish as quickly as possible - PFC damage patients are very ineficcient, broke rules

describe an experiment of appetitive conditioning using humans

task: find a red ball and you get a food reward and a pleseant tone. find the black ball, you get a buzzer and no reward. the background behind each ball is different preference test: subjects shown the different patterns, the ones that were behind the red ball were prefered when controls asked why do you prefer this one: they had no conscious association with the pattern and reward and gave answers like "it looks like the sun" or "reminds me of pizza" etc. patients with amygdala lesions showed no preference reward-associated cues can control our behaviour, sometimes without us being aware

delayed response task

tests PFC - animal aquires info, has to hold it over a delay and then use it to guide a response. - trials are given in rapid succession with short inter-trial intervals, on each trial subject needs to distinguish the information to remember on that trial, vs previous ones - during the response phase animal must figure out where food may be based on what it saw humans and primates with *dorsolateral PFC lesions* are impaired even at the shortest delay, suggesting the PFC is responsible for working memory (in rats the medial PFC impairs)

wisconsin card sorting task

tests PFC, behavioural flexibility (ability to change strategies) - subject have to sort cards by one stimulus dimension (ex: number) - then task switches, patient have to ignore old strategy and switch to new one (ex: shape) - patients are not told what to do, they are given feedback like yes that is right or no that is wrong - patients with damage to PFC are able to learn the first discrimination but *not able to switch strategy = perseveration*

how is the PFC involved in planning?

the PFC keeps track of/helps you plan sequences of action (*temporal organization of behaviour*) - PFC damage: can remember particular items, but cannot remember them in order - impaired recall in temporal order of events in memory (did you go to the gym or the store first? remembers both but not what came first) - see tower of london task and dinner party problem

which region(s) of the brain are involved in conditioning (aversive or appetitive) memory?

the amygdala

what is the role of the amygdala in appetitive conditioning?

the amygdala regulates the *conditioned place preference* for a location where the organism experienced a rewarding stimuli the place becomes attractive: pavlovian approach lesions to the lateral amygdala disrupt conditioned place preference for all types of rewards (do not disrupt consumption of reward, only interferes with how the CS linked with the reward affects behaviour)

Unconditioned Stimulus (US)

the biologically significant event ex: meat powder in Pavlov's dogs mouth; tuft of air blown into rabbit's eye; something that can be sensed and will produce an unconditioned response

Conditioned Response (CR)

the body's response to the CS alone. ex: salivating or blinking to the bell

what part of the brain is involved in spatial memory? give examples of animal studies to support your answer

the hippocampus is critical for learning about relationships between different stimuli, including contexts and what events occur in those contexts. in a *radial arm maze*, a rat navigates around the maze to locate food using spatial cues around the room. normal rats remember where they've been and do not re-enter arms, but hippocampal lesions cause rats to make more errors - they keep re-entering arms they've been into in a *morris water maze*, a pool is filled with opaque water and a rat has to find a platform that is just below the surface. normal rats learn to find the platform quickly, but rats with hippocampal lesions never learn to find the platform efficiently.

which region(s) of the brain are involved in declarative memory?

the hippocampus. when lesioned in humans, a deficit is seen in declarative memory and procedural memory is left intact

Unconditioned Response (UR)

the normals response to a significant event ex: salivation (in response to meat powder)

consolidation

the process by which information in short term memory is transferred to long term memory believed to involve physical changes in the way neurons are connected to each other in the brain

which region(s) of the brain are involved in skill (humans) and instrumental (rats) learning?

the striatum (caudate nucleus, basal ganglia)

what part of the brain is is involved in instrumental conditioning?

the striatum (part of a larger subcortical system: the basal ganglia)

primacy effect

the superior performance seen in a memory task for items at the start of a list; usually ttributed to long term memory

recency effect

the superior perfrmance seen in a memory task for items at the end of a list; attributed to short term memory

explain the locally cued-radial arm maze task and what area of the brain is important for success with this task

there are some arms with lights lit and others where they are not. So the rat has to choose a certain type of action (walk down arms with lights, and not down arms with no lights). learning the specific type of action and how they direct their bodies to move towards some arms and not others is an important function of the striatum

true of ralse: in order for LTP to establish, the presynaptic and postsynaptic terminals must be simultaneously activated

true. if you stimulated one but blocked the other, LTP would not develop.

what is the role of NMDA in induction of LTP?

under normal stimulation the NMDA channel is blocked by Mg++, when the cell becomes depolarized enough the Mg++ block is removed, leaving NMDA open to be activated by glutamate. when NMDA is active it allows an influx of Ca++ into the cell, which activates multiple enzyme pathways to increase EPSPs.

describe the three radial arm maze tasks that provided evidence to support a triple dissociation of memory systems

use the same apparatus with 8 arms for each 3 tasks, slightly changed what the animal had to learn *spatial radial maze*: food in each bit of the arms, rat has to learn to not go back to where it's already been. rats with *hippocampal lesions show impairment* whereas lesions to the amygdala or the dorsal striatum show no impairment. *conditioned place preference*: give food in one arm, in another arm it gets nothing. on test day the animal goes to spend time in the arm where it received food. rats with *lesions to the amygdala show impairment* whereas lesions to the hippocampus and dorsal striatum show no impairment. *locally cued-radial arm maze*: put curtains around the maze so the animal can't use spatial cues to see which is different. at the end of each arm there was a light and food, light turns off when the food has been eaten. rat has to learn: go to arms with lights. rats with *lesions to the dorsal striatum showed impairment* whereas lesions to the hippocampus and amygdala performed fine.

what is meant by the "dissociation" of memory systems?

when we observe that 2 or more brain regions are independently involved in separate forms of learning (i.e: lesions to one area impair on one task but not others)