Memory And Learning Flashcards

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1
Q

What are the two stages of learning and memory?

A
  1. The acquisition of a short term memory
  2. The consolidation of a long term memory
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2
Q

What is physical modification of the brain because by?

A

Incoming sensory information

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3
Q

Define memory consolidation

A

Is the process by which some experiences, held temporarily by transient modifications of neurons, are selected for permanent storage in long term memory

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4
Q

Describe the flow of sensory information into long term memory

A

Sensory experience - (memory acquisition) - short term memory - (memory consolidation) - long term

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5
Q

What is the IT area involved in?

A

Visual area and an area involved with memory

Lesions = propagnosia

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6
Q

Define prospagnosia

A

A selective amnesia for familiar faces that can result from damage to the infertemporal cortex in humans

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7
Q

What is stimulus activity?

A

Response with a barrage of action potentials to the presentation of some but not all stimuli

Example, IT neurons

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8
Q

Define distributed memory

A

The concept that memories are encoded by widespread synaptic modifications of many neurons, not by a single synapse or cell

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9
Q

What is graceful degradation

A

The slow removal of neuronal networks

Representations tend to blend together as neurons are lost, such that one memory gets confused with another

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10
Q

What was found on studies about snail memory storage ?

A

Simple forms of learning were accompanied by changes in the strength of synaptic transmission between sensory neurons and motor neurons

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11
Q

What brain region is critical for memory formation?

A

Hippocampus

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12
Q

What are the two thin sheets of neurons in the hippocampus?

A
  1. Ammon’s horn
    • CA3 and CA1
  2. Dentate’s GYRUS
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13
Q

Describe the trisynaptic circuit

A
  1. Entorhinal cortex - dentate gyrus (perforant path) synapses
  2. DENTATE GYRUS - CA3 (mossy fibre) synapses
  3. CA3 - CA1 (Schaffer collateral) synapses
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14
Q

Define tetanus

A

A brief burst of high-frequency stimulation (typical 50-100 stimuli at a rate of 100/sec)

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15
Q

Define input specificity

A

A property of synapse plasticity that ensure that modifications induced by stimulation of one input onto a neuron do not spread to other unstimulated so puts on the same neuron

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16
Q

What does tetanus cause?

A

A modification of the stimulated synapses so they are more effective

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17
Q

What are the remarkable features of plasticity?

A
  1. Induced by brief tetanus
  2. Longevity
18
Q

What is a requirement for LTP?

A

Synapses are active at the same time that the postsynaptic CA1 neuron is strongly depolarised

19
Q

What is necessary for depolarisation with tetanus require?

A
  1. Synapses must be stimulated at frequencies high enough to cause temporal summation of EPSPs.
  2. Enough synapses must be active simultaneously to cause significant spatial summation of EPSPs.
20
Q

How are excitatory synaptic transmission in the hippocampus mediated?

A

Glutamate through the NMDA receptor due to the release of Ca2+ as it signals when presynaptic and postsynaptic elements are active at the same time

21
Q

How is LTP inducted inhibited?

A

Rises in Ca2+ as it activates two protein kinases: protein kinase C and calcium-calmodulin-dependent protein kinase (CaMKII), which cause phosphorylation of the AMPA receptors to increase ionic conduction of the channel or the insertion of new AMPA receptors

22
Q

Define BCM theory

A

A theory proposing that synapses are bidirectionally modifiable. Synaptic potentiation results when presynaptic activity correlates with a strong postsynaptic response, and synaptic depression results when presynaptic activity correlates with a weak post synaptic response.

23
Q

What is a key assumption of the BCM theory?

A

That synapses will undergo synaptic weakening instead of LTP when they are active at the same time the postsynaptic cell is only weakly depolarised by other inputs.

24
Q

Define long term depression

A

A long lasting decrease in the effectiveness of synaptic transmission that follows certain types of conditioning stimulation

25
Q

What two rules govern bidirectional plasticity?

A
  1. Synaptic transmission occurring at the same time as a strong depolarisation of the post synaptic neuron causes LTP of the active synapses
  2. Synaptic transmission occurring at the same time as a weak or modest depolarisation of the post synaptic neuron causes LTD of the active synapses.
26
Q

Define spike timing-dependent plasticity

A

Bidirectional modification of synaptic strength induced by varying the relative timing of the presynaptic and postsynaptic spikes

27
Q

At the Schaffer collateral - CA1 synapse, describe the two distinct forms of homosynaptic LTD.

A
  1. Activation of the NMDA receptor
  2. Activation of the G-coupled metabotrophic glutamate receptors
28
Q

What is the difference between LTP and LTD?

A

LTP is putting phosphate groups on

LTD is taking them off

LTP and LTD appear to reflect the bidirectional regulation of both the phosphorylation and the number of postsynaptic AMPA receptors

29
Q

Define metaplasticity

A

Activity dependent modification of the rules of synaptic plasticity

30
Q

When is LTP and LTD favoured?

A

LTP - more NR2B-containing receptors are expressed at the synapse

LTD - more NR2A- containing receptors are expressed

31
Q

When are NR2A levels high andNR2B levels low?

A

High cortical activity

32
Q

Describe denervation supersensitivity

A

Widespread response of neurons to the loss of synaptic input

33
Q

Define synaptic scaling

A

A cell wide adjustment of synaptic strengths in response to a change in the average firing rate of the post synaptic neuron

34
Q

Why is phosphorylation as a long term memory consolidation mechanism an issue?

A
  1. Not permanent
  2. Protein molecules are not permanent
35
Q

What induces LTP in CA1

A

Entry of calcium into the postsynaptic cell and the activation of CaMKII

36
Q

Describe the structure of CaMKIII

A

Ten subunits arranged in a rosette pattern

Each unit has two parts attached like a hinge. Two parts are the catalytic region (phosphorylation ) and regulatory region.

37
Q

How does regulation of CaMKIII occur

A

When hinge is closed, there is no available second messenger and the catalytic region is covered by the regulatory region. Open when second messenger present. Removal = closed

After LTP, hinge stays slightly open and continues phosphorylation.

38
Q

Define molecular switch hypothesis

A

The idea that protein kinases can be switched on by auto phosphorylation to a state in which they no longer require the presence of a specific second messenger to be active. Such persistently active kinases may hold the memory of an episode of strong synaptic activation.

39
Q

What is the role of ZIP

A

Inhibits protein kinase m zeta resulting in erasing LTP and memories established many days prior.

Cause dephosphorylation - erasing memory trace

40
Q

What are the two forms of CREB?

A

CREB-2: represses gene expression when it binds to CRE

CREB-1: activates transcription, but on,y when it is phosphorylated by protein kinase A.