Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Brain PD > week 5 part 1 > Flashcards

week 5 part 1 Flashcards

1
Q

Why should we bother about NMDARs?

A

They are involved in mental neuropathaological conditiosn

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

What are examples of neuropathological conditions?

A
  1. Epilepsy
  2. Drugs
  3. Pain
  4. NMDAR receptors as roles in schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the completed model for the documented hypothesis ?

A

Schizophrenia

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

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

What was glutamate known as?

A

MSG,
Ve-tsin
E621

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are NMDAR receptors?

A

Glutamate channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What was NMDAR receptors used as ?

A

Additive to many foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What was glutamate first proposed as?

A

A neurotransmitter by a Japanese scientists

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

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

A

Monosodium glutamate source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What did Hayashi do?

A

He applied glutamate to the brain of animals

Glutamate was pestered in humans in those days

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What did Jeff Watkins in 1950 do?

A

did his experiment with the first glutamate receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can a discovery get lost?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where was depolarisation by glutamate seen?

A

many tissues also tissues which contained inhibitory neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How did Jeff Watkins contribute?

A

synthesising NMDA by testing glutamate and synthesising NMDAR antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When is there no current passing through the receptor?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When is the receptor blocked?

A

When the receptor is challenged with glutamate and glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what can GluR1 subunit have?

A

6 slice variants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how many GluR3 subunits are there?

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How many GluR2 subunts have?

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does GluN2 subunits have?

A

Glutamate binding sites

thats where glutamate binds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where does GluN1 subunits bind?

A

Glycine and also GluN3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the types of NMDA receptors?

A
  1. Conventional NMDA receptors

2. Unconventional NMDARs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is conventional NMDA receptors?

A

contain 2 GluN1 subunits and 2 GluN2 subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are unconventional NMDARs?
Incorporate GluN3 subunits in additions to either GluN1 or also GluN2 and less is known about them
26
What can NMDARs be?
either di-heteromeric or Tri-heteromeric
27
What is di-heteromeric?
Incorporating up to 2 types of different sub-units
28
when does the composition of the pharmacological of receptor change
When the functional properties of the receptors change too
29
What is not enough to provide a receptor function?
Application of a single agonist
30
How does the decay dynamics of the receptors differ?
Dramatically dependent on the subunit which is expressed
31
What are the advantage of tri-heteromeric receptors?
There is a variety of the receptor types which can provide differential depolarising stimuli, some of which are very short and some long
32
What are the reasons for these differences?
the affinity of GluN2 subunits to glutamate differs significantly between GluN2 subunits
33
What does GluN2D subunit bind to with very high affinity?
Glutamate
34
What binds to glutamate with less affinity?
GluN2A subunits
35
why is the mechanism simple?
Agonists stay bound or not bound provided by the different current provided by the receptors
36
What can calcium signals with different lengths activate?
Different types of secondary messengers in the cells expressing these receptors
37
What subunits pass more current at -40mv than 2A?
2C and 2D
38
What brain regions expresses GluN1?
1. Hippocampus 2. Cerebellar 3. Cortical structures of olfactory bulb
39
What mimics the expression of GluN1?
GluN2A
40
What is expressed in GluN2B
1. cortical structures 2. Hippocampus not expressed in the cerebelum
41
What is expressed in the cerebellum?
GluN2C
42
When is expression of GluN1 seen?
Duration of the brain from P0 to adulthood
43
What is not expressed at P0 but they start to be expressed as the brain matures?
Glun2A
44
When are N2D expressed?
Early in development in deep sub-cortical nuclei remains diffusely expressed in adulthood of different parts of the brain
45
What was the significance of the findings of LTP?
The high frequency activation of axonal bundle could lead to enhancement of transmission between neurons when tested later on with low frequency stimulation
46
What is the mechanism of learning and memory?
Strengthening the connections
47
Why is the hippocampal slice preparation from the brain practical?
They have conserved pathway and perforant pathway coming from the entorhinal cortex
48
what are done to different glutamate receptors?
Differentially expressed in different paths of the hippocampus e.g. kainite receptors
49
Where are kainite receptors expressed?
mossy fibres and not expressed in the schaffer collaterals in CA1
50
Where are NMDAR expressed?
throughout the hippocampus
51
What did collingridge study?
NMDAR in plasticity took an antagonist AP5 which can block most NMDAR at 5 concentration
52
what could lead to depression of synaptic transmission?
long application of NMDA
53
what did Morris do?
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
What prolonged depression of synaptic transmission?
1Hz for 15 minutes
55
what can production of LTD be blocked by?
AP5
56
What underlies learning and memory?
Bi-directional regulation of synaptic plasticity
57
When can enhancing learning and memory be beneficial in?
Different types of diseases
58
What can regulation of NMDAR be beneficial in?
Pathological cases e.g. epilepsy/stroke
59
How can NMDAR be targeted?
Directly or indirectly
60
Indirectly: NMDAR function
Affecting the function of other receptors
61
Directly:NMDAR function
Affecting glycine/glutamate binding or by blocking receptor prore
62
How can both indirect and direct effects by achieved by?
1. receptor (and subunit) 2. specific agonists 3. Antagonist and allosteric modulators
63
How are GABA B expressed?
pre-synaptically
64
what does inhibitory transmission provide?
indirect modulation of NMDAR responses by modulating the ability of mg2+ to be relieved depending on membrane potential
65
AMPA positive allosteric modulators
- 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
What has been shown to potentiate NMDA receptor responses?
Group 1 Brass activation
67
What is there inter-relationship between?
NMDA and metabotropic glutmate receptor activation provides potentiation to both species
68
What is in the clinic?
Memantine and ketamine
69
How long can we stall STP for?
up to 6 hours provide enhancement of signal for very long time
70
What is compound UBP-145 potent in?
Blocking 2D than 2A and 2B
71
What does 3 Micromolar of AP5 block?
LTP preserve STP ∇ These was mimicked by 2A referring compounds
72
What did RO affect?
STP | reduced it without affecting LTP
73
What are involved in LTP but also involved in STP1
GluN2A and 2B
74
What is STP1?
The part of STP which is insensitive to 2B and 2D antagonist
75
What is STP2 very sensitive to?
2B/2D antagonist
76
What does ketamine replicate the effects of?
Glun2D antagonist
77
Why do we need STP?
To remember for a shorter period of time
78
What can STP be targeted by?
Ketamine GluN2D antagonist
79
What does UBP684 compound do?
Increases channel opening
80
What does application of UBP684 increase
affinity of GluN2A channel to glutamate
81
What is UBP684?
1. not very soluble | 2. It could not be used to test neurotransmission in slices but it was very potent
82
What is UBP709?
* 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
When is LTD not expressed
1. Adults | 2. Aged rats
84
what goes down with age?
Ability of rats to express LTD
85
What is UBP714?
∇ 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
What does ventral hippocampus show?
less plasticity than those dorsal hippocampus
87
What is the advantage of using allosteric modulators?
differentially change the expression of different types of plasticity
88
What does GluN1-3 bind to?
Glycine
89
What does different sliced variants of GluN1 give?
Receptors of differential conductance
90
What can provide depolarisations in the tissue?
Inhibition of GluN1 in NMDAR which doesnt bind NMDA

Brain PD (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions