Psychobiology: Learning & Memory, WEEK 2 Flashcards

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1
Q

Timescales of memory + how we study it

A
  • Memories exist across different timescales
  • studied using Pavlovian fear conditioning as it can be learnt in one trial > researcher knows exactly when shock is delivered thus learnt + test when it is later expressed.
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2
Q

Stages of visual memory

A
  • Iconic/Immediate memory > lasts for less than 1 seconds + shown using Sperling array (show letters + numbers for a second or less + recall)
  • Visual short-term memory > eg spot the difference > don’t directly compare images but look at one image + take in the information and hold it while looking at the other > would not remember these details the next day (decays)
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3
Q

Pavlovian fear conditioning

A
  • Key method used to understand timescale of mem from a biological view,
  • Fear conditioning = rat is put in a conditioning chamber where stimuli (eg sound) is heard, followed by electric shock from floor of the cage. > rat learns + predicts the shock when they next hear the stimuli
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4
Q

Theory of memory consolidation

A
  • Distinguishes between short-term + long-term memory (STM + LTM)
  • After acquiring info, a process allows the memory to stay in the STM, another process allows the memory to stay in LTM or transfer info from LTM to STM.
  • Memory consolidation is the process of moving info into the STM + LTM (aka cellular consolidation)
  • Once you learn, STM can be expressed but decays quickly, after the info has to transfer into the LTM but it takes time
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5
Q

Biological mechanisms of memory consolidation

A
  • Primary mechanism of memory consolidation = protein synthesis. > production of new proteins enables cells to carry out functions (in neurons + brain)
  • Proteins synthesise by transcription of DNA into mRNA > translate this into amino acid chains > plays into memory + can impair this process using toxin produced bacteria like anisomycin
  • Anisomycin blocks synthesis of ALL proteins > eg: if anisomycin is released into amygdala, STM wont be impacted but the LTM will.
  • Another mechanism is NMDA receptors
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6
Q

Mechanisms of memory consolidation + protein ARC.

A
  • Only certain proteins are important for Pavlovian fear conditioning. > one is ARC (activity-related cytoskeletal associated protein)
  • Can look at protein expression using antibodies made for it specifically (binds only to ARC)
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7
Q

Ploski et Al, 2008: ARC

A
  • uses antibodies which bind to ARC using learning periods of stimulus followed by footshock.
  • Found in rat brain after learning that, in the paired condition where rats learn and associate footshock to stimuli, there was more ARC in the amygdala compared to the condition where there was no learning. > ARC is associated with learning.
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8
Q

Anti-sense technology

Ploski et Al, 2008

A
  • Can block translation of certain mRNA > Ploski used anti sense to block translation of mRNA (arc)
  • Ploski then looked at ability of rats to express the memory in STM (1 hour after learning) > no effect on STM
  • Ploski et Al then looked at expression of memory a day later, assessing LTM, and anti-sense inhibition of arc reduced memory
  • LTM was impaired but STM was not > arc is relevant to memory consolidation
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9
Q

NMDA receptors as a mechanism of memory consolidation

A
  • Memory consolidation links to surface of neurons too.
  • Studies show impairing action of NMDA receptors using receptor antagonists = impairment of STM + LTM
  • NMDA receptors are important for acquisition of info > because memory isnt acquired by NMDA receptors, the STM cannot initiate its mechanisms nor can LTM.
  • NMDA receptors + arc protein are linked in a complex process.
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10
Q

Why are mechanisms of memory consolidation important?

A
  • Epilepsy is associated w/ memory deficit > BDNF expression in people w/ epilepsy impairs the consolidation process > if we can repair BDNF, memory consolidation can be repaired.
  • Lubin (2015) uses Met supplementation to try boost BDNF expression > Parrish + Lubin (2015) found memory improved substantially with Met during fear conditioning > can lead to intervention for humans.
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11
Q

Synaptic plasticity

Donald Hebb, 1949

A
  • The idea that strength of a synapse is subject to alteration > a synapse could be made to be stronger which increases likeliness of a memory being consolidated
  • A synapse could be made weaker too which decreases likeliness.
  • This depends on firing potential + the stimulation it receives. (excitatory will increase strength/inhibitory reduces)
  • Different forms of synaptic plasticity can co-exist in the same area (e.g: cerebellum)
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12
Q

Synaptic transmission

A
  • The process by which information transfers from the pre-synaptic neuron to the post-synaptic neuron past the synaptic cleft > enables processing in the brain for memory + other functions
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13
Q

What is long-term potentiation (LTP)

Tim Bliss & Terje Lømo (1973)

A
  • Long lasting increase in synaptic strength
  • Form of synaptic plasticity where connection between synapses improve with increasing stimulation > if a synapse experiences LTP, it is more likely for info to pass through + be conserved.
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14
Q

Research on LTP

Tim Bliss & Terje Lømo (1973)

A
  • LTP is studied using extracted brain slices of an animal which exposes neurons which can be manipulated + record activity.
  • Bliss + Lømo studied rabbit hippocampus where they stimulated inputs + recorded activity from hippocampal neurons
  • Learning period induced by high frequency stimulation which led to an increase in synaptic strength.
  • Without learning stimulation, synaptic strength stays uniform throughout.
  • Bliss + Lømo record 24 out of 35 pathways tested showed LTP hours after testing > supports hyp
  • Shows introduction + retention of memory however as it was found in an extracted brain, this can’t be behaviourally linked
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15
Q

Associative + non-associative LTP

A
  • Non-associative LTP is where there is an intense stimulation of an input (LTP) which results in a greater response
  • Associative LTP is necessary to suggest LTP is relevant to consolidation in Pavlovian fear conditioning.
  • Associative LTP does exist so if there are two neurons and only one experiences high stimulation while the other gets normal stimulation, both inputs will still be strengthened after LTP which increases degree of output
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16
Q

LTP evaluation

Does LTP underlie memory consolidation?

A
  • Pavlovian fear conditioning is reliant on amygdala, not the hippocampus where synaptic plasticity is >suggests LTP cant underlie fear conditioning (but some say LTP can be induced in the amygdala)
  • Mem consolidation needs protein synthesis, if LTP underlies mem consolidation, LTP needs to synthesise
  • Evidence shows LTP needs NMDA receptors as when they are antagonised, it blocks early + late LTP (similarly to how it blocks STM + LTM) > underlies conditioning
  • Some evidence suggests LTP does work in a intact brain + amygdala in fear conditioning
  • ARC should be important for LTP if it underlies memory consolidation. Ploski et Al found LTP stimulation in amygdala = increased expression of ARC
  • If we know what neurons need to be wired together to make a memory, we can artificially make a memory of an event which hasn’t happened (eg: induce fear in a rat w/o ever presenting the stimuli to them) > Johansen et Al mimicked this with optogenetics + found mice never had the shock but the brain acted like it did
17
Q

Long-term depression (LTD)

A
  • Long lasting decrease in synaptic strength
  • when low frequency stimulation leads to a decreased response to test stimulation (doesn’t mean LTD = forgetting)
  • LTD is mainly linked to the cerebellum (links to motor learning) > this type of learning relies on LTD more
  • LTP + LTD could both be in the cerebellum which could increase strength despite LTD presence
  • LTD at the right point in a synapse can increase the output strength dependant on whether the potential fired is inhibitory or excitatory (eg: inhibitory LTD can increase strength)