Implicit Memory Flashcards

1
Q

Know the role of the neostriatum in habit learning in humans

A

In humans, the neostriatum (caudate nucleus and putamen) is essential for the gradual, incremental learning of associations that is characteristic of habit learning.

  • learning related plascticity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The marine snail, Aplysia:
- understand the advantages (4) of studying invertebrate nervous systems

A
  1. Aplysia’s nervous system is relatively simple (10^5 - 10^6 neurons vs 10^12 in humans)
  2. Cell bodies are large (up to 1mm): ideal for electrophys and for identifying the circuits critical for specific types of Learning and memory
  3. Larger neurons are found in the same locations in all aplysia: enables scientists to find them easily
  4. Aplysia capable of several simple forms of learning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Reductionism approach?

A

studying individual parts of a complex system in order to understand the systems functions:

Behaviour → circuits → neurons → synapses → signalling molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

know the experimental paradigms for habituation and sensitization of the gill withdrawal reflex (GWR)

A
  • touching the siphon or shock to the tail both result in gill withdrawal reflex
  • Repeated shocks elicit long-term memory for withdrawal
  • Sensitization of the GWR by applying a noxious stimulus to another part of th body (tail) enhances the withdrawal reflex of both the siphon and the gill
  • Spaced repetition converts short-term memory into LTM in aplysia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

know the synaptic and molecular mechanisms for short- and long-term
habituation and sensitization of the GWR

A
  • Short-term habituation of the GWR is caused by synaptic depression resulting from reduced presynaptic transmitter release
  • STH is caused by reduction of transmitter release at the SN-MN synapse (sensory neuron-motor neuron)
  • Habituation = reduction of reflex when a harmless stimulus is repeated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

know the synaptic and molecular mechanisms for short- and long-term
habituation and sensitization of the GWR

A
  • Long-term habituation correlates with persistently depressed synapses
  • Percentage of sensory neurons making physiologically detectable connections with motor neurons in habituated animals is decreased at 3 points in time after long-term habituation training
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

know the synaptic and molecular mechanisms for short- and long-term
habituation and sensitization of the GWR

A

Short-term sensitization = enhancement of EPSPs recorded from motor neurons

  • Following shock to the tail, a mild touch to the siphon now elicits a powerful GWR = sensitization
  • Interneuron releases serotonin (5-HT)
    • increases transmitter release from sensory nn onto motor nn
    • = presynaptic facilitation → enhancement of GWR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

know the synaptic and molecular mechanisms for short- and long-term
habituation and sensitization of the GWR

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the molecular mechanism of short-term sensitization; which kinases are involved?

A
  • Pathway One
    • serotonin released from facilitating interneuron → G-proteins increase activity of adenylyl cyclase → converts ATP to cAMP
    • cAMP binds and activates PKA
    • PKA phosphorylates K+ channels
    • Prolongs the AP → increasing Ca++ influx → augmenting NT release
  • Pathway 2:
    • serotonin binds to second class of metabotropic receptor that activates Gq → enhances activity of PLC
    • PLC activity → production of diacylglycerol
    • activates PKC
    • phosphorylates presynaptic proteins → mobilization of vesicles containing glutamate from a reserve
    • increases efficiency of NT release
  • TWO KINASES INVOLVED:
    • PKA - closure of K+ channels
    • PK - increase vesicle mobilization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

know the signalling mechanisms, kinases, and proteins involved in long-term sensitization - understand the key roles of PKA and MAPK in long-term sensitization

A
  • PKA acts in the cytosol and nucleus
    • persistently active after its R subunits are degraded by ubiquitin hydrolase
    • phosphorylates other proteins such as CREB, K+ channels and the exocytosis apparatus
  • MAPK acts in the nucleus to promote transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

know the signaling mechanisms, kinases, and proteins involved in long-term sensitization - understand the key roles of PKA and MAPK in long-term sensitization

A

Long-term sensitization involves Nuclear Transcription (CREB-1) and Protein Synthesis

  • Repeated stimulation causes the level of cAMP to rise and persist for several minutes
  • Catalytic subunits can then translocate to the nucleus and recruit MAPK
  • In the nucleus, PKA and MAPK phosphorylate and activate the cAMP response element-binding (CREB) protein and remove the repressive action of CREB-2 (inhibitor of CREB-1)
  • CREB-1 activates several immediate-response genes including a ubiquitin hydrolase necessary for regulated proteolysis of the reg subunit of PKA
  • Cleavage of the inhibitory regulatory subunit results in persistent activity of PKA
  • Persistent phosphorylation of the substrate proteins of PKA
  • Seconde immediate-response gene activated by CREB-1 is C/EBP which acts both as a homodimer and as a heterodimer with activating factor (AF) to activate downstream genes (including elongation factor 1 alpha (EF1alpha) that lead to the growth of new synaptic connections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • understand the structural changes that correlate with long-term habituation & sensitization
A
  • Habituation
    • Fewer pre-synaptic terminals
      • retraction of synapses
  • Sensitization
    • More presynaptic terminals
      • new synapses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

know the experimental paradigm for classical conditioning of the GWR - Unpaired Stimuli

A
  • Intracellular electrodes are inserted into the sensory and motor neurons to record spikes and EPSPs respectively
  • UNPAIRED STIMULI:
    • Touching siphon and tail shock are not paired together in time
    • EPSPs show no facilitation before and after training
  • Under these conditions, the size of motor nn EPSP is only weakly facilitated by the tail shock
    • in this example the EPSP actually decreases slightly because, despite the tail shock, repeated unpaired stimulation of the siphon leads to synaptic depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Classical conditioning of the GWR: Paired Stimuli

A
  • siphon is touched immediately prior to shocking the tail
    • the siphon sensory neurons are primed to be more responsive to input from the facilitatory interneurons of the unconditioned pathway
    • Amplifies the response of the conditioned pathway and restricts the amplification to that pathway
  • Recordings of EPSPs in motor nn after training is considerably greater = more vigorous gill withdrawal
    • eg mild touch to siphon now elicits powerful gill withdrawal as the animal has learned to associate a siphon stimulus with a harmful stimulus
    • From persistent increase in transmitter release at both he SN-MN synapses and the neuromuscular synapses in the gill
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the difference between homosynaptic and heterosynaptic plasticity?

A
  • Homosynaptic
    • activity in branch A elicits plasticity only in A
  • Heterosynaptic
    • Activity in branch A elicits plasticity at A and B
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is heterosynaptic plasticity accomplished?

A
  • Experiment:
    • single presynaptic sensory nn that contacts 2 postsynaptic motor neurons (A and B)
    • 5-pulses of serotonin applied to sensory nn synapse with motor neuron A = long term facilitation at these synapses
    • One pulse of serotonin at the motor neuron B synapse = allows it to capure new proteins produced in the cell body in response to the five pules of 5-HT at the other synapse
      • 1-pulse produces short-term facilitation which returns to normal after 24 hours
  • Pairing the 5-pulses at A with 1 pulse at B = Cell B displays long-term fascilitation because:
    • single pulse at B creates a tag = captures proteins synthesized by the sensory neuron
      • SYNAPTIC CAPTURE OF LONG TERM FACILITATION
17
Q

The mammalian amygdala:

  • *- know the experimental procedures for classical fear conditioning**
  • know the neural circuitry for consolidation of fear memory
  • know the cellular and synaptic mechanisms of fear memory
  • understand the roles of PKA and MAPK in fear memory: how do
A
  • Pairs tone with shock
  • If animal remembers the association between the tone and the shock then it will freeze = conditioned fear memory
  • Contextural memory requires hippocampus and amygdala
  • Cued memory requires the amygdala
18
Q

The mammalian amygdala:

  • *- know the experimental procedures for classical fear conditioning : Pairing the CS with US - how to test cued memory**
  • know the neural circuitry for consolidation of fear memory
  • know the cellular and synaptic mechanisms of fear memory
  • understand the roles of PKA and MAPK in fear memory: how do
A

After pairing, animal is moved to changed box - in this example it is peppermint scented and lacks the metallic grid floor for cued memory test (amygdala dependent)

  • see if animal responds to tone
    • record time spent frozen
19
Q

The mammalian amygdala:

  • know the experimental procedures for classical fear conditioning
  • *- know the neural circuitry for consolidation of fear memory**
  • know the cellular and synaptic mechanisms of fear memory
  • understand the roles of PKA and MAPK in fear memory: how do
A
  • Tone is captured by the auditory thalamus → auditory cortex → Lateral nucleus
  • Shock: Somatosensory thalamus → somatosensory cortex → Lateral nucleus
  • Lateral nucleus of the amygdala is the critical site that integrates the CS and the US
  • Lateral nucleus → central nucleus → Fear responses
20
Q

Synaptic potentiation in the _______ occurs during retrieval of cued fear memories

A

Synaptic potentiation in the lateral nucleus of the amygdala occurs during retrieval of cued fear memories

  • tone produces potentiation of EPSE in the LA nucleus
21
Q

The mammalian amygdala:

  • know the experimental procedures for classical fear conditioning
  • know the neural circuitry for consolidation of fear memory
  • *- know the cellular and synaptic mechanisms of fear memory**
  • understand the roles of PKA and MAPK in fear memory: how do they act?
A
  • In the Lateral Nucleus (LA), a tone produces potentiation of EPSP
  • the animal freezes when tone is heard = associative fear memory
  • LTP in the amygdala requires PKA activation
22
Q

The mammalian amygdala:

  • know the experimental procedures for classical fear conditioning
  • know the neural circuitry for consolidation of fear memory
  • know the cellular and synaptic mechanisms of fear memory
  • *- understand the roles of PKA and MAPK in fear memory: how do they act?**
A

PKA and MAPK trigger changes in gene transcription through CREB activation and epigenetic regulation