exam 3 - learning and memory

patient EP

• virus destroyed part of hippocampus and brain tissue around it

  • able to copy complex drawings; able to repeat short list of words; able to recall past job relating to electronics; recalled childhood house

• researchers repeatedly revisited EP to ask him questions; he had no memory of the researchers’ names; no awareness of repeating stories about being in electronics; not able to recall things that happened fifteen minutes ago

• shows the importance of hippocampus to shorter”er” term/newer memory, consolidating memory into long-term; impairments to hippocampus affect declarative (episodic, semantic) memory; but hippocampus can’t be the permanent storage site for long-term memory

engram

the neural representation of memories

Karl Lashley’s experiments for brain mechanisms of learning and memory

• examined learning in rats following leasions and transactions of different cortical regions

• assumed cortex was critical to memory & focused there

• cortical transactions → failed to block learning

• cortical lesions → impaired learning, but size determined impairment rather than a specific location of lesions

• conclusion: cortex is not likely to affect memory and learning very significantly

equipotentiality

all areas of cortex are equally involved in memory

mass action

ability to form memories depends only on the mass (amount) of brain in the cortex

patient HM (Henry Molaison)

• suffered from epilepsy as a child; had strong attacks, affected daily life

• epileptic center in the hippocampus (strong, overactive firing of neurons in brain area + affects neighboring areas)

• 1953 - doctors removed hippocampus and adjacent structures: allowed relief for epilepsy but HM lost ability to form new memories

  • relation btwn hippocampus and ability to form new memories

anterograde amnesia

unable to form new declarative memories going forward in time; past memories are retained

retrograde amnesia

impairs memories before the event; new memories can still be formed

did patient HM suffer mainly from anterograde or retrograde amnesia?

anterograde amnesia

• only mainly affected his episodic and semantic memory

• retained memories from childhood

• still able to learn skilled movements and form procedural memories such as tracing a star only viewing through a mirror

Clive Wearing

• extrememly short-term memory - less than thirty seconds (a sentence or two)

• only remembered his wife

• lesioned hippocampus and adjacent structures in the temporal lobe

Morris water maze

• tests memory in rodents

• rats placed in pool of water and non-transparent liquid; must look for hidden platform suspended in the water; rats will stand on platform and stop swimming; rats have motivation to remember location of the platform for next trial

• quantifying memory: how quickly the rat reaches the platform, how long the rat travels

lesions to hippocampus in rats in the Morris water maze

• no hippocampus and hippocampal lesions: no improvement or learning in time taken to get to platform

• no memory formed of where the platform was & unable to use it for next trials

synaptic plastitcity hypothesis

experience can leave a memory trace by causing long-lasting changes in synaptic connections

what does it mean for a synapse to have strengthened?

• increased amount of neurotransmitter released from neuron A to B

• before: action potential causes neuron A releases x amount of neurotransmitter and elicits an EPSP in B

• strengthened: same action potential causes neuron A releases 2x amount of neurotransmitter and elicits a higher EPSP in B

• bigger EPSP in B makes B more likely to fire its own action potential

Hebbian plasticity/learning

if cell A continuously and repeatedly excits cell B, the efficacy of the synapse between them will increase; “fire together, wire together”

trisynaptic circuit

info about experiences travels through three stations:

1. entorhinal cortex → dentate gyrus in the hippocampus

2. dentate gyrus → CA3 region

3. CA3 region → CA1 region (output station)

long-term potentiation (LTP)

• a potential mechanism for experience-dependent synaptic plasticity

• repetitive, high-frequency, intense stimulation of a presynaptic neuron induces a long-term increase of the synapse with the postsynaptic neuron

• leads to a stronger EPSP from a similar stimulation

strong input from the cortex may drive LTP in the _ and includes info about

hippocampus; aspects of experience - odors, sounds, senses

LTP works because of two types of postsynaptic receptors:

• AMPA receptor

• NMDA receptor

• both bind to glutamate

AMPA and NMDA receptors interact when/because

strong and persistent depolarization through Na+ glutamate channel AMPA repels the Mg2+ the blocks calcium flow through the NMDA receptor

what happens after NMDA receptors are open (Mg removed)?

entry of calcium → second messengers and cascade → modify the cell

• AMPA receptors free-floating inside the cell are transported and anchored onto membranes

• gene expression changes → production of more AMPA receptors

increased number of AMPA receptors will lead to higher reception of glutamate & higher amounts of depolarization

LTP is particularly prevalent in the hippocampus because

it is more plastic and modifiable than other areas (“quick learner”)

pattern completion

reinstatement of a memory from a partial cue

network of neurons → LTP more prone to give rise to a pattern associated with a past experience → memory

mice and baited arm experiment

hippocampus has time-limited role in memory too; memory representation moves elsewhere over time

• mice trained to locate position of baited arm (one chamber with food among many other empty chambers)

• one group: next day → hippocampus inactivated; other group: after 30 days of training → hippocampus inactivated

• mice in next-day group were not really able to find the chamber; mice in the 30-day group were very successful

true/false: the hippocampus is connected bidirectionally to the cortex, allowing memory to propagate out

true

memory encoding (during experience, online)

info is temporarily stored in hippocampus via LTP or something similar

memory consolidation (after experience, offline)

info in hippocampus is gradually transferred from the hippocampus to cortex; occurs at times with no experiences, like sleep

two-stage model

• stage 1: sensory experience → sensory processing in cortex → hippocampus: synaptic plasticity/LTP, temporary storage of experience

• stage 2: during sleep, etc info moves from hippocampus to cortex → repeated transfer of same info →long-term memory (memory remains in cortex)

spatial coding in rodents is possible in the hippocampus because of

“place cells” - neurons fire at particular locations/place fields, which varies by neuron

• as a rodent travels, neurons fire sequentially along a path; from a sequence, you can decode the path taken

• suggests that place and trajectories in space are mainly what rodent hippocampi are interested in

hippocampal replay

reactivation of temporal sequence of neural activity during sleep (out of experience)

• very short time scale

• reflects recent experience (ex. rodent’s path from left to right replays)

• coordinated with cortical regions (info is sent to cortex during rehearsal)