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Brain PD > week 5 part 1 > Flashcards

week 5 part 1 Flashcards

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1
Q

Why should we bother about NMDARs?

A

They are involved in mental neuropathaological conditiosn

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2
Q

What are examples of neuropathological conditions?

A
  1. Epilepsy
  2. Drugs
  3. Pain
  4. NMDAR receptors as roles in schizophrenia
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3
Q

What is the completed model for the documented hypothesis ?

A

Schizophrenia

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4
Q

What are NMDAR antagonist receptors in clinical trial for?

A

Treatment of depression especially resistance treatment for depression showing beneficial effects which is similar to electrical therapy

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5
Q

What was glutamate known as?

A

MSG,
Ve-tsin
E621

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6
Q

What are NMDAR receptors?

A

Glutamate channels

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7
Q

What was NMDAR receptors used as ?

A

Additive to many foods

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8
Q

What was glutamate first proposed as?

A

A neurotransmitter by a Japanese scientists

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9
Q

in the 2nd world war where did glutamate come from?

A

Monosodium glutamate source

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10
Q

What did Hayashi do?

A

He applied glutamate to the brain of animals

Glutamate was pestered in humans in those days

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11
Q

What did Hayashi et al found out?

A

==> They found out that an electrical convulsions could be evoked by glutamate applications and that was different from application of specific chloride

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12
Q

What did Jeff Watkins in 1950 do?

A

did his experiment with the first glutamate receptor antagonist

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13
Q

How can a discovery get lost?

A

if you publish it in a language which is not listed by other people

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14
Q

Where was depolarisation by glutamate seen?

A

many tissues also tissues which contained inhibitory neurotransmitter

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15
Q

How did Jeff Watkins contribute?

A

synthesising NMDA by testing glutamate and synthesising NMDAR antagonist

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16
Q

When is there no current passing through the receptor?

A

If there is a negative membrane potential in the presence of mg2+

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17
Q

When is the receptor blocked?

A

When the receptor is challenged with glutamate and glycine

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18
Q

what can GluR1 subunit have?

A

6 slice variants

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19
Q

how many GluR3 subunits are there?

A

2

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20
Q

How many GluR2 subunts have?

A

4

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21
Q

What does GluN2 subunits have?

A

Glutamate binding sites

thats where glutamate binds

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22
Q

Where does GluN1 subunits bind?

A

Glycine and also GluN3

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23
Q

What are the types of NMDA receptors?

A
  1. Conventional NMDA receptors

2. Unconventional NMDARs

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24
Q

What is conventional NMDA receptors?

A

contain 2 GluN1 subunits and 2 GluN2 subunits

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25
Q

What are unconventional NMDARs?

A

Incorporate GluN3 subunits in additions to either GluN1 or also GluN2 and less is known about them

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26
Q

What can NMDARs be?

A

either di-heteromeric or Tri-heteromeric

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27
Q

What is di-heteromeric?

A

Incorporating up to 2 types of different sub-units

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28
Q

when does the composition of the pharmacological of receptor change

A

When the functional properties of the receptors change too

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29
Q

What is not enough to provide a receptor function?

A

Application of a single agonist

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30
Q

How does the decay dynamics of the receptors differ?

A

Dramatically dependent on the subunit which is expressed

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31
Q

What are the advantage of tri-heteromeric receptors?

A

There is a variety of the receptor types which can provide differential depolarising stimuli, some of which are very short and some long

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32
Q

What are the reasons for these differences?

A

the affinity of GluN2 subunits to glutamate differs significantly between GluN2 subunits

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33
Q

What does GluN2D subunit bind to with very high affinity?

A

Glutamate

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34
Q

What binds to glutamate with less affinity?

A

GluN2A subunits

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35
Q

why is the mechanism simple?

A

Agonists stay bound or not bound provided by the different current provided by the receptors

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36
Q

What can calcium signals with different lengths activate?

A

Different types of secondary messengers in the cells expressing these receptors

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37
Q

What subunits pass more current at -40mv than 2A?

A

2C and 2D

38
Q

What brain regions expresses GluN1?

A
  1. Hippocampus
  2. Cerebellar
  3. Cortical structures of olfactory bulb
39
Q

What mimics the expression of GluN1?

A

GluN2A

40
Q

What is expressed in GluN2B

A
  1. cortical structures
  2. Hippocampus

not expressed in the cerebelum

41
Q

What is expressed in the cerebellum?

A

GluN2C

42
Q

When is expression of GluN1 seen?

A

Duration of the brain from P0 to adulthood

43
Q

What is not expressed at P0 but they start to be expressed as the brain matures?

A

Glun2A

44
Q

When are N2D expressed?

A

Early in development in deep sub-cortical nuclei

remains diffusely expressed in adulthood of different parts of the brain

45
Q

What was the significance of the findings of LTP?

A

The high frequency activation of axonal bundle could lead to enhancement of transmission between neurons when tested later on with low frequency stimulation

46
Q

What is the mechanism of learning and memory?

A

Strengthening the connections

47
Q

Why is the hippocampal slice preparation from the brain practical?

A

They have conserved pathway and perforant pathway coming from the entorhinal cortex

48
Q

what are done to different glutamate receptors?

A

Differentially expressed in different paths of the hippocampus e.g. kainite receptors

49
Q

Where are kainite receptors expressed?

A

mossy fibres and not expressed in the schaffer collaterals in CA1

50
Q

Where are NMDAR expressed?

A

throughout the hippocampus

51
Q

What did collingridge study?

A

NMDAR in plasticity

took an antagonist AP5 which can block most NMDAR at 5 concentration

52
Q

what could lead to depression of synaptic transmission?

A

long application of NMDA

53
Q

what did Morris do?

A

took AP5 injected into rats and could show that rats when suddenly not able to perform well in the so called Morris water maze

54
Q

What prolonged depression of synaptic transmission?

A

1Hz for 15 minutes

55
Q

what can production of LTD be blocked by?

A

AP5

56
Q

What underlies learning and memory?

A

Bi-directional regulation of synaptic plasticity

57
Q

When can enhancing learning and memory be beneficial in?

A

Different types of diseases

58
Q

What can regulation of NMDAR be beneficial in?

A

Pathological cases e.g. epilepsy/stroke

59
Q

How can NMDAR be targeted?

A

Directly or indirectly

60
Q

Indirectly: NMDAR function

A

Affecting the function of other receptors

61
Q

Directly:NMDAR function

A

Affecting glycine/glutamate binding or by blocking receptor prore

62
Q

How can both indirect and direct effects by achieved by?

A
  1. receptor (and subunit)
  2. specific agonists
  3. Antagonist and allosteric modulators
63
Q

How are GABA B expressed?

A

pre-synaptically

64
Q

what does inhibitory transmission provide?

A

indirect modulation of NMDAR responses by modulating the ability of mg2+ to be relieved depending on membrane potential

65
Q

AMPA positive allosteric modulators

A
  • They can provide a greater depolarisation by greater activation of AMPA receptors
  • AMPA receptors would modulate NMDAR transmission by changing the ability of mg2+ to be relieved
  • They will be producing greater EPSP
66
Q

What has been shown to potentiate NMDA receptor responses?

A

Group 1

Brass activation

67
Q

What is there inter-relationship between?

A

NMDA and metabotropic glutmate receptor activation

provides potentiation to both species

68
Q

What is in the clinic?

A

Memantine and ketamine

69
Q

How long can we stall STP for?

A

up to 6 hours

provide enhancement of signal for very long time

70
Q

What is compound UBP-145 potent in?

A

Blocking 2D than 2A and 2B

71
Q

What does 3 Micromolar of AP5 block?

A

LTP

preserve STP
∇ These was mimicked by 2A referring compounds

72
Q

What did RO affect?

A

STP

reduced it without affecting LTP

73
Q

What are involved in LTP but also involved in STP1

A

GluN2A and 2B

74
Q

What is STP1?

A

The part of STP which is insensitive to 2B and 2D antagonist

75
Q

What is STP2 very sensitive to?

A

2B/2D antagonist

76
Q

What does ketamine replicate the effects of?

A

Glun2D antagonist

77
Q

Why do we need STP?

A

To remember for a shorter period of time

78
Q

What can STP be targeted by?

A

Ketamine

GluN2D antagonist

79
Q

What does UBP684 compound do?

A

Increases channel opening

80
Q

What does application of UBP684 increase

A

affinity of GluN2A channel to glutamate

81
Q

What is UBP684?

A
  1. not very soluble

2. It could not be used to test neurotransmission in slices but it was very potent

82
Q

What is UBP709?

A
  • It is more soluble
  • It can potentiate responses to glutamate and glycine across all subunits
  • It is a PAM of glutamate receptors subunits – potentiates them all to a similar degree
  • It prolongs the current in a reversal way and hippocampus slice prep it can enhance induction of LTD
  • It down regulated LTP induction and shifted the ability of slices to show LTD and LTP in favour of LTD
83
Q

When is LTD not expressed

A
  1. Adults

2. Aged rats

84
Q

what goes down with age?

A

Ability of rats to express LTD

85
Q

What is UBP714?

A

∇ Can potentiate 2A and 2B receptors more than 2D receptors
∇ 2D subunits are more involved in STP
∇ Subunits 2A and 2B are involved in LTP
∇ 714 Compound blocked LTD
∇ Induce LTP which is induced by sub-threshold stimulation
∇ 714 can potentiate LTP and reduce LTD

86
Q

What does ventral hippocampus show?

A

less plasticity than those dorsal hippocampus

87
Q

What is the advantage of using allosteric modulators?

A

differentially change the expression of different types of plasticity

88
Q

What does GluN1-3 bind to?

A

Glycine

89
Q

What does different sliced variants of GluN1 give?

A

Receptors of differential conductance

90
Q

What can provide depolarisations in the tissue?

A

Inhibition of GluN1 in NMDAR which doesnt bind NMDA

Brain PD (15 decks)

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