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Week 2 Flashcards

1
Q

Why do we need to understand synaptic plasticity?

A

Get indication of underlying mechanism of learning and memory

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2
Q

What topology does glutamate receptor subunit have?

A

Tetrameric complexes with the helix region forming the pore

Pore = analogues to voltage gates ion channels

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3
Q

Once glutamates receptor have been identified on the molecular level

A

Possible to investigate where in the brain it is expressed

Investigate the different combinations to subunits that come together to form functioning ion channels

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4
Q

What are majority of AMPA receptors

A

In the CNS

Main mediators of fast, excitatory, glutamatergic transmission in the brain

Receptors that are heteromers

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5
Q

What does AMPA receptors comprise?

A

GluR2 subunits

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6
Q

AMPA receptors that have the GluR2 subunits

A

Impermeable to calcium in neurons

GluR2 subunits - form majority of these receptors in the brain

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7
Q

In the absence of GluR2

A

AMPA receptors are permeable to sodium, potassium and calcium

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8
Q

What is predominant in the forebrain?

A
  1. GluR2 and GluR1

With low levels of GluR3 and GluR4

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9
Q

What does AMPA receptors mediate at most excitatory synapse in the CNS?

A
  1. Mediate postsynaptic depolarisation as a consequence of a net influx of sodium ions
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10
Q

What are the 2 different techniques to investigate the expression of GluR1 subunits in the rat brain?

A
  1. MRNA in-situ hybridisation

2. Immunohistochemistry

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11
Q

Who was the first person to describe neurons in the brain using very primitive microscopy methods?

A
  1. Purkinje

2. See cell bodies of neurons because there was no staining techniques

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12
Q

What technique enables you to visualise the entire neurons?

A
  1. Golgi staining
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13
Q

What can antibodies be used for in the cerebellar cortex?

A
  1. Visualise the actual proteins GluR1 subunits in the dendrite in the molecular layer of cerebellar cortex
  2. Cannot see axons because the axons are not expressing the protein
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14
Q

Where doesn’t the messenger RNA go beyond?

A

The cell body

Only visualising the cells expressing the gene

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15
Q

What evidence show that kainate receptors are found?

A
  1. Pre and post synaptically in synapses in many regions of the brain
  2. Pre- and postsynaptic localisation
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16
Q

What is not uniquely associated with nervous system?

A

Ionotropic glutamate receptors

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17
Q

What structure is different from the ACH/GABA/Glycine type receptors?

A

The ionotropic glutamate receptors

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18
Q

Nicotinic ACH/GABA/Glycine family

A

Evolved completely independently from inotropic glutamate receptors as mediators or inhibitory of synaptic transmission

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19
Q

What are homologous of ACH/GABA/glycine receptors?

A

Prokaryotic

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20
Q

Where has ionotropic glutamate receptors been found?

A

Outside the animal kingdom

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21
Q

What is the most intensively studied plant species?

A

Arabidopsis

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22
Q

What is important to recognise when studying the brain?

A

Often we are dealing with genes mediating neurotransmission which have homologous in completely different organisms that doesn’t have nervous system

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23
Q

What are some examples of genes in Arabidopsis that mediate responses to light?

A
  1. Clade I - GLR1.1
  2. Clade II - GLR2.1
  3. Clade III - GLR 3.1
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24
Q

What primitive plant can fairly live in watery environment?

A

Mosses

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25
Q

What has Glutamate receptor like (GLR) family have been implicated in?

A
  1. Defence against pathogens
  2. Reproduction
  3. Control of stomata aperture
  4. Light signal
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26
Q

What are the GLR genes?

A
  1. GLR1

2. GLR2

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27
Q

What does the GLR1 and GLR2 cause?

A
  1. Failure of sperm cells to target the female reproductive organs
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28
Q

What do GLR genes encode?

A

Non-selective Ca2+ permeable channels that can regulate cytoplasmic Ca2+

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29
Q

Why has ionotropic glutamate receptors been conserved throughout plant evolution?

A

Mediate cell-to-cell communication during sexual reproduction

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30
Q

What fam origins of ionotropic glutamate receptors be traced back to?

A

Prokaryotic world

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31
Q

What disease is linked to glutamate receptors?

A
  1. Rasmussen’s encephalitis
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32
Q

What is Rasmussen’s encephalitis?

A

A disease that is characterised by seizures in children (<10)

Only in one half of the cortex

Typically blind on one side

Post mortem shows inflammation on affected side of the brain

Treatment: remove the cortical brain tissue on affected side

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33
Q

What is the disease caused by?

A

Autoantibodies to GluR3

Antibodies to the ligand-binding domain

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34
Q

What shares similarity with bacterial GluRs (GluR0)

A

Ligand binding domain

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35
Q

How does Rasmussen’s encephalitis develop?

A

When antibodies to bacterial GluRs cross the blood brain barrier and interact with GluR3s in the brain

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36
Q

What is permeable to calcium ions?

A

NMDA receptors

37
Q

What are NMDA channels blocked by?

A

Magnesium when the membrane potential is at resting state

38
Q

What can magnesium ion blockade of channel achieved by?

A

Membrane depolarisation

39
Q

What is NMDA receptors thought to be?

A
  1. Ligand gated ion channel

2. Voltage regulated channels

40
Q

What does maximal activation of NMDA receptors require?

A

Presence of extracellular glycine

41
Q

What is glycine?

A

Inhibitory neurotransmitter in the spinal cord

Acts in its own receptors e.g. ligand gated chloride channels

42
Q

In the brain, what does glycine act as?

A

Co-activator is the NMDA receptors

43
Q

What is used to study NMDA receptors?

A

Patch clamping method

44
Q

What are all 3 receptor subtypes activated by?

45
Q

What is the role of NMDA?

A

Selective activation of only NMDA type receptors

46
Q

What receptor is not influenced by glycine?

47
Q

What is glycine able to selectively potentiate?

A

The action of the agonist of NMDA or glutamate on NMDA type receptors

48
Q

Properties of NMDA receptors (graph)

A

Measuring currents in response to a ligand at different membrane potentials

49
Q

What does comparing the two graphs illustrate?

A

How magnesium is affecting the activity of channel in more negative membrane potential which is around resting potential

50
Q

What is the discussion of the graph?

A
  1. The contribution of magnesium ions particularly how they affect activation of receptors in the more negative membrane potential
  2. The contribution of glycine ions as a terminal of the channels
51
Q

What was the first glutamate receptor to be discovered at all?

A

AMPA receptors

Cloning technique

52
Q

What was the first NMDA receptor identified?

53
Q

What was first cloned and sequences in 1991?

A
  1. NMDAR1

2. GRIN1

54
Q

What was the 6 other NMDA receptor subunit identified?

A 
NMDAR2A
NMDAR2B
NMDAR2C
NMDAR2D
NMDAR3A
NMDAR3B
55
Q

What shares sequence similarity with non-NMDA receptors suggesting common evolutionary origin?

A

NMDAR1

GRIN1

56
Q

What comes into dentate gyrus?

A

Perforant fibre

57
Q

Where are granule cells located?

A

Dentate gyrus

Project to CA3

58
Q

Where does CA3 pyramidal cells project to?

A

CA1 region

Form synapses there

59
Q

Where does CA1 pyramidal cells project out to?

A

Hippocampus and back to the cortex

60
Q

Who discovered LTP?

A

Bliss + Lomo

Performed experiments on rabbits

Electrophysiological experiments

61
Q

What did Bliss and Lomo do?

A

Apply electrical stimulus in the presynaptic pathway and record the EPSP post-synaptically

Then they did experiment where they applied high frequency stimulus in succession

62
Q

Large magnitude post-synaptically

A
  1. Large EPSP

2. More glutamate released

63
Q

Activity in a particular pathway

A

Strengthening of the synapse

64
Q

What was most experiment done on LTP

A

Delivering presynaptic stimulus to the Schaffer collaterals (axons of the CA3 pyramidal cells)

Record from CA1 pyramidal cells with electrodes

65
Q

What are the 2 pathways?

A
  1. Single stimuli being delivered

2. High frequency stimulus is being delivered

66
Q

Pathway 1

A

Active

High frequency stimulation is delivered

Potentiation

Increase in magnitude of EPSP

Sustained for a long time

67
Q

What is associativity?

A

If you have high frequency stimulation in pathway 1 and pair it with weak stimulation of pathway 2

Strengthening of both synapses

68
Q

What can high frequency stimulation in one pathway influence?

A

Adjacent synapse provided there is some activity in pathway 2

Synapse onto the same postsynaptic cell

69
Q

What is required for LTP to occur?

A

Both pre- and postsynaptic activity

70
Q

What are the molecular mechanism of LTP?

A
  1. Excitatory synaptic transmission in the hippocampus is mediated by AMPA-type glutamate receptors
  2. Single-pulse stimulus to Schaffer collaterals causes release of glutamate, triggering a AMPA-receptor-mediated EPSP in CA1 pyramidal cell
  3. Pyramidal cells also express NMDA receptors but these are not activated by a single-pulse stimulus because EPSP is not sufficient to relieve them of magnesium block
  4. A high-frequency stimulus to Schaffer collaterals causes release of glutamate, triggering a large AMPA -receptor mediated EPSP in CA1 pyramidal cell
  5. Elevation of post-synaptic calcium is the trigger for LTP
71
Q

How is glutamate released?

A

Pre-synaptically

72
Q

What are present in the postsynaptic cell?

A
  1. AMPA receptors

2. NMDA receptors

73
Q

What are critical for LTP to occur?

A

NMDA receptors

74
Q

How do you block NMDA receptors?

A

Antagonist - AP5

75
Q

How does post-synaptic entry of calcium ions trigger LTP?

A
  1. Calcium activates calmodulin
  2. Calcium/calmodulin (CAM) activates CAM-kinase II
  3. CAM-kinase II phosphorylates AMPA receptors
  4. Phosphorylation of AMPA receptors causes increased postsynaptic responsiveness to glutamate
76
Q

What are the consequences of phosphorylation of AMPA receptors?

A
  1. Up-regulation of AMPA receptors on the post-synaptic cells
  2. Increasing the number of AMPA receptors on the post-synaptic membrane
77
Q

More receptors post-synaptically

A

Much larger response to a single stimulus than you’ve done before

78
Q

Phenomonen aspect of LTP

A

Increase in the number of AMPA receptors

79
Q

What are synaptotagmin?

A

Proteins that are important in regulating and mediating calcium dependent neurotransmitter release presynaptically

80
Q

Adenovirus mechanism

A

Knock down gene expression in particular population of neurons

81
Q

What are required for induction of LTP?

A

Synaptotagmin 1 and 7

Facilitates the process by which AMPA receptors are being released onto cell surface

82
Q

What are synaptotagmin involved in?

A
  1. Regulating the fusion of these AMPAR receptors with cell surface
83
Q

CA3-CA1 synapse

A
  1. All of the changes are occurring postsynaptically

2. It is the up-regulation of AMPA receptors as a result of NMDA receptor activation with no changes presynaptically

84
Q

How can you achieve a decrease in synaptic strength?p

A

Low frequency stimulation over sustained period

85
Q

LTP

A
  1. LTP is induced by high frequency stimulation

2. 100Hz stimulation for 1s

86
Q

LTD

A
  1. LTDis induced by low frequency stimulation

2. 5Hz stimulation for 3 min given twice with 3 min interval

87
Q

LTD - opposite effect

A

Reduction in number of AMPAR receptors on the cell surface

88
Q

What are activated in LTD?

A
  1. Phosphatases
  2. Calcinerium PP1
  3. De-phosphorylation of AMPAR
  4. Reduction of cell surface targets
89
Q

What can be changed as a mechanism of LTP?

A

Size of the post-synaptic density

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