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PSY1202 Introduction to biological psychology > Learning, memory and plasticity > Flashcards

Learning, memory and plasticity Flashcards

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1
Q

neural plasticity

A
  • Changes that are caused by previous experience can be observed at the level of
  • Behaviour (actions, emotions, knowledge)
  • Neurons (neural network activity)
  • Synapses (interactions between individual neurons)
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2
Q

what is learning?

A

the process of acquiring new information

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3
Q

what is memory?

A

the ability to store and retrieve information

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4
Q

types of learning

A
  • Non-associative learning: habituation, sensitisation
  • Associative learning
  • Imprinting
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5
Q

types of learning and LTM

A

non-declarative (procedural)

declarative

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6
Q

non-declarative learning

A
  • Conditioning
  • Priming
  • Skill learning
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7
Q

declarative memory

A
  • Knowledge of facts (semantic memories)

- Episodic memories (what happened when and where)

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8
Q

duration of memory

A
  • Short-term (STM)
  • Long-term (LTM)
  • Middle-term/Intermediate
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9
Q

hypothesised memory processes - encoding, consolidation and retrieval

A
  • Incoming info
  • Sensory buffers (e.g. iconic memory)
  • STM/WM
  • Consolidation
  • LTM
  • Retrieval –> STM –> Perf
  • Loss
    DIAGRAM
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10
Q

where are memories stored in the brain?

A
  • Karl Lashley’s search for the memory ‚engrams’ (1929, 1950)
  • Lesion studies with rats
  • Lashley concluded that memory is not located in particular area of the rat cortex
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11
Q

Hebb synapse

A
  • Santiago Ramón y Cajal (1893) first proposed the idea that the site of contact between neurons could play a role in memory formation.
  • Foster & Sherrington (1897) termed these sites ‘synapses’ (Charles Sherrington - nobel prize laureat 1932).
  • “When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased.”
  • Furthermore, Hebb emphasised that there are likely to be many Hebb synapses in distributed networks
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12
Q

synaptic plasticity - what does change?

A

Assume presynaptic Neuron A very often transmit a signal that is 10 Hz (10 spikes per second) causing an EPSP in the postsynaptic Neuron B that is enough to transmit a signal by B.

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13
Q

how can the dynamics of signal transmission be altered?

A

by changing synapse efficiency over time

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14
Q

what might change in neuron A? (might need to look at slides)

A
  • Temporal filtering (change in selectivity for the frequency range of spikes arriving in the axon terminal)
  • Gain control (change in the amount of neurotransmitter that is released for a given signal)
  • Presynaptic facilitation or depression
  • Increased ntm, membrane size and/ sensitivity and pre- and post synapse size = increases PSP
  • Something could also change in neuron B
  • Evidence from studies that investigated mechanisms of associative learning
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15
Q

memory engrams - physiological and anatomical changes in the brain

A

Kandel and his team made important discoveries measuring changes in pre- and postsynaptic cells during learning and memory

developed mechanistic models of synaptic plasticity which are widely used in neuroscience and medicine.

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16
Q

habituation

A

Response weakens with repeated stimulus presentation due to repetition but not due to adaptation of senses or fatigue

Not an extinction of associations acquired through learning.

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17
Q

dishabituation - siphon example

A

The repeated tactile stimulation of the siphon leads to a reduced gill withdrawal response

The response is reinstated after stimulation by a different stimulus (dishabituation).

18
Q

the abdomen ganglion of Aplysia

A

L7 - one of the motor neurons that innervates gill muscles and controls gill withdrawal

19
Q

presynaptic depression as a form of synaptic plasticity - siphon example

A
  • When the siphon is first stim by squirt water, Aplysia retracts gill, protecting it in case animal under attack
  • Reflect mediated by sensory neurons synapsing directly upon motor neurons that withdraw gill
  • Many sensory and motor neurons
  • If siphon squirted repeatedly over hr, animal soon habituates to stimulus
  • No longer retracts gill
    ST habituation results as sensory neurons release less ntm on motor neurons
  • If siphon squirted repeatedly over days, animal habituates faster each day and eventually shows almost no response
  • LT habituation due to retraction of some synaptic terminals from sensory neurons onto motor neurons
20
Q

what is LTM formation characterised by?

A

Structural changes in neurons

21
Q

what is another type of non-associative learning?

A

sensitisation

when a strong tail shock precedes the tactile stimulation, the gill response is much stronger

22
Q

presynaptic facilitation

A
  • Changes involving interneuron modulation

- Interneuron modulation causes increased transmitter release = increases PSP

23
Q

other synaptic changes that may store memories

A

The neural mechanisms underlying associative learning, i.e. classical (also called pavlovian) conditioning have been studied in Aplysia, Drosophila melanogaster (fruit fly) and Apis mellifera (honeybees)

24
Q

associative learning - classical conditioning learning tasks

A
  • When a dog receives food, it starts to salivate (UR - unconditioned response).
  • Pavlov noticed that his experimental dogs were already salivating before given food.
  • If a sound (CS) always shortly precedes food (US), then a dog will learn that sound predicts food and will start to salivate on hearing the sound (CR)
  • Coincidence of US and CS determine learning outcome
25
Q

structural changes in hippocampus associated with extensive spatial learning and route following

A
  • London taxi drivers have larger hippocampi (Maguire et al. 2000 PNAS).
  • Compared to bus drivers have had greater gray matter volume in mid-posterior hippocampi and less volume in anterior hippocampi
26
Q

hippocampus lesions prior to training

A

don’t specifically impair working/reference memory, but spatial task

  • All rats showed the same escape latency in the second phase of the experiment - cue-based navigation.
  • Reversal to hidden platform in third phase - rats with hippocampal lesions performed poorly again.
  • Lesions after training have less strong effects.
  • Hippocampus is not involved in permanent memory storage. - used in learning
27
Q

the hippocampus is involved in spatial memory formation - the 3 main pathways

A
  1. Perforant pathway
  2. Mossy fibre pathway (dentate gyrus to CA3 pyramidal cells)
  3. Schaffer collateral pathway (CA3 to CA1 pyramidal cells)
    - Ntm - glutamate
    - Can take slices from hippocampus that preserve a functioning network.
    - Easy to keep alive and to perform recordings on.
28
Q
  1. perforant pathway
A

(input from entorhinal cortex)

29
Q
  1. mossy fibre pathway
A

(dentate gyrus to CA3 pyramidal cells)

30
Q
  1. Schaffer collateral pathway
A

(CA3 to CA1 pyramidal cells)

31
Q

LTP (long term potentiation) - enhancement of synaptic transmission when both neurons fire

A
  • Per Andersson (1966), University of Oslo, found that in the perforant pathway of the hippocampus of anesthesised rabbits that during repetitive stimulation an additional strong depolarisation with many fast pulses during few seconds (tetanus) caused an increase in neuronal firing of the postsynaptic cell.
  • In his lab, Bliss & Lømo (1973) continued that work and discovered LTP demonstrating that frequency potentiations can be long-lasting.
  • LTP has been found in the other hippocampus pathways too
32
Q

ionotropic receptors in CA1 pyramidal neurons

A
  • AMPA receptors are ionotropic receptors (ligand-gated ion channels
  • AMPA receptors open if glutamate binds to them. When open Na+ flow into the postsynaptic neuron.
  • The synapse is excitatory, because the influx of Na+ depolarises the membrane (EPSPs).
33
Q

what do CA1 neurons have?

A

2 glutamate receptors in dendrites

  • NMDA receptors are both ligand and voltage gated.
  • When the cell is at rest they are blocked by Mg2+.
  • Binding of the neurotransmitter glutamate is necessary but on its own not sufficient to open them
34
Q

what do NMDA receptors act as

A

coincidence detectors

35
Q

when do NMDA receptors open?

A
  1. Binding of glutamate
  2. Membrane depolarises above threshold expelling the Mg2+ plug
    - This leads to an influx of Ca2+ ions into the postsynaptic cell, which also contributes to the EPSP.
36
Q

changes at a synapse - more receptors for stronger EPSPs

A
  • In the dendritic spine there are vesicles that contain AMPA receptors in the membrane
  • If the NMDA receptor opens, it lets in Ca2+ from the synaptic cleft
  • Ca2+ activates proteins that make those vesicles bind with the cell membrane in the synaptic cleft
  • There are then more AMPA receptors in active zone, so more Na+ will enter each time the neurotransmitter is released
  • The increased number of AMPA receptors in the cell membrane will last several hours
37
Q

why is NMDA receptor a substrate for associative learning?

A
  • It is found in neuronal pathways required for associative learning
  • It is activated when two events happen together
38
Q

strongest LTM effect

A
  • Growth of new dendritic spines with synapses
  • High influx of Ca2+ activates intracellular enzymes, protein kinases. Of those, PKA, PKC and CaMKII (calcium-calmodulin dependent protein kinase II) activates transcription factor CREB (cAMP response element binding protein).
  • CREB targets many genes that are required for growing new dendritic spines and synapses.
39
Q

LTP can be induced in hippocampal slices - mice need hippocampus for spatial learning - what is missing to establish causal link?

A

Show that mice cannot learn without NMDA receptors in hippocampus

40
Q

is hippocampal LTP mechanism underlying spatial learning?

A
  • Increasing evidence from various studies suggest this.
  • AP5 (also APV) treatment (amino-5-phosphonovaleric acid) is a selective NMDA receptor antagonist, which blocks them.
  • AP5 treatment of hippocampus cells suppresses LTP.
  • Pharmacological experiments with AP5 in mice show that treatment groups do not learn the spatial task.
41
Q

NMDA receptor knockout mice - using genetic tools to study brain functions

A

LTP is absent in NMDA knockouts and normal in wild-type animals and controls (also knock-outs, but with intact NMDA receptors)

42
Q

neural plasticity - from behaviour to genes

A
  • Key evidence from research that links synaptic plasticity to properties of neural networks and changes in behaviour.
  • Integration of different levels of research (behavioural, network and cellular) is important for finding more answers.

PSY1202 Introduction to biological psychology (23 decks)

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