Excitatory Amino Acid Neurotransmitters

0.0(0)
studied byStudied by 0 people
full-widthCall with Kai
GameKnowt Play
learnLearn
examPractice Test
spaced repetitionSpaced Repetition
heart puzzleMatch
flashcardsFlashcards
Card Sorting

1/44

encourage image

There's no tags or description

Looks like no tags are added yet.

Study Analytics
Name
Mastery
Learn
Test
Matching
Spaced

No study sessions yet.

45 Terms

1
New cards

Excitatory amino acid neurotransmitters examples (3)

Glutamate, aspartate, homocysteic acid

2
New cards

what do excitatory amino acid neurotransmitters do

Produce an excitatory response in neurons

• i.e., the neuron is more likely to send an action potential

3
New cards

Most important NT for normal brain function

Glutamate (Nearly all excitatory neurons in CNS are glutamatergic)(but remember glutamate are present in all cells!)

4
New cards

Glutamate is synthesised from ______ by what enzyme

Glutamate is synthesised from glutamine by glutaminase

5
New cards

Glutamate that has been released is taken up by what

astrocytes

6
New cards

When glutamate is taken up by astrocytes, it is converted to what by what enzyme

it is converted back to glutamine by glutamine synthetase

<p>it is converted back to glutamine by glutamine synthetase</p>
7
New cards
term image
knowt flashcard image
8
New cards

Antagonists of the NMDA receptor

D-AP5

MK801

Mg2+

<p>D-AP5</p><p>MK801</p><p>Mg<sup>2+</sup></p>
9
New cards

Significance of AMPA receptors & NMDA receptors being on the same membrane generally

The opening of NMDA receptor is reliant on the AMPA receptor

10
New cards

How is the NMDA receptor reliant on the AMPA receptor

knowt flashcard image
11
New cards

slide 64

12
New cards

Link between excitatory amino acid receptors & stroke

It is usually excitatory amino acid receptors that cause the damage associated with strokes

13
New cards

How do excitatory amino acid receptors cause the damage associated with strokes

With the ischemia that comes with the block in blood supply, there is excessive Glu release → causes over-stimulation of NMDA receptors → Excess Ca2+ influx into postsynaptic neurons → Leading to excitotoxic cell death (excitotoxicity)

<p>With the ischemia that comes with the block in blood supply, there is excessive Glu release → causes over-stimulation of NMDA receptors → Excess Ca2+ influx into postsynaptic neurons → Leading to excitotoxic cell death (excitotoxicity)</p>
14
New cards

Explain how the bold part works: With the ischemia that comes with the block in blood supply, there is excessive Glu release → causes over-stimulation of NMDA receptors → Excess Ca2+ influx into postsynaptic neurons → Leading to excitotoxic cell death (excitotoxicity)

Large influx of Ca2+…

  • Can activate proteases (calpains), phospholipases, nitric oxide synthase (NOS), nucleases etc. → Leads to very rapid cell death by necrosis

  • Is spotted & gathered into mitochondria resulting in swelling and eventual rupture of mitochondria → Leads to delayed cell death

15
New cards

NMDA-R antagonists _____ and _____ provide protection in models of ischemia

NMDA-R antagonists D-AP5 and MK801 provide protection in models of ischemia

16
New cards

Take a moment to compartmentalise :)

17
New cards

Give an example of an inhibitory amino acid neurotransmitter

GABA

18
New cards

What do inhibitory amino acid neurotransmitters do

They cause an influx of negatively charged ions such as Cl-

Inside of cell becomes more negative

Hyperpolarisation of post-synaptic cell making it less likely to initiate an action potential

19
New cards

What is the main inhibitory NT in the brain

γ-aminobutyric acid (GABA)

20
New cards

Approx ___% of synapses in brain uses GABA

Approx 33% of synapses in brain uses GABA

21
New cards

Presence of ____ indicates a GABAergic neuron

Presence of GAD indicates a GABAergic neuron

22
New cards

slide 69 diagram

23
New cards

True/False GABA receptors can be Ionotropic & Metabotropic

True

Ionotropic: GABAA and GABAC

Metabotropic: GABAB

24
New cards

slide 71 & 72

25
New cards

How does Presynaptic inhibition work

Inhibitory NT binds to receptors on the presynaptic cell → 

Reduction in depolarisation of the presynaptic nerve terminal → Less Ca2+ influx → Less excitatory NT release

<p>Inhibitory NT binds to receptors on the presynaptic cell →&nbsp;</p><p>Reduction in depolarisation of the presynaptic nerve terminal →&nbsp;Less Ca2+ influx →&nbsp;Less excitatory NT release</p>
26
New cards

slide 74

27
New cards

What are Biogenic amines

Bioactive amine neurotransmitters

28
New cards

What do Biogenic amines do

Implicated in wide range of behaviours

E.g., movement, reward, addiction, depression, sleep

29
New cards

What do Biogenic amines all have in common

knowt flashcard image
30
New cards

slide 78

31
New cards

catecholamine neurotransmitters are all derived from what

They are all derived from tyrosine

32
New cards

Explain the pathway from tyrosine to catecholamine

neurotransmitters such as epinephrine

Tyrosine → DOPA → Dopamine → Norepinephrine → Epinephrine

33
New cards

The rate limiting step in the formation of catecholamine neurotransmitters is controlled by what enzyme

Tyrosine hydroxylase

34
New cards

Where is Tyrosine hydroxylase found

Only found in sympathetic neurons and adrenal chromaffin cells

35
New cards

If a cell has tyrosine hydroxylase, it is known as a what

catecholaminergic cell

36
New cards

slide 82 -91

37
New cards

What are some treatments for Parkinson’s disease

Written in red

<p>Written in red</p>
38
New cards
39
New cards
40
New cards
41
New cards
42
New cards
43
New cards
44
New cards
45
New cards