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Neuropharmacology > Lecture 9 > Flashcards

Lecture 9 Flashcards

1
Q

What are the adenine nucleotide signalling molecules?

A
  • ATP, ADP
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2
Q

What are the adenine nucleoside signalling molecules?

A

Adenosine

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3
Q

What are the stages of purine receptor activation?

A

1) purine synthesis and release 2) extracellular conversions 3) receptor activation

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4
Q

How is adenosine synthesised and released?

A

1) ATP is hydrolysed= AMP 2) AMP is hydrolysed and converted into adenosine via adenosine kinase - ADK can phosphorylate adenosine to from AMP then later ATP

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5
Q

How do purines leave the presynaptic terminal?

A
  • leakage (tissue damage) - exocytosis - adenosine transporter
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6
Q

How are purines packaged into vesicles?

A
  • VNUT (vesicular nucleotide transporter) - requires Na+ concentration gradient generated by ATP
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7
Q

What is the role of nucleotidases in the extracellular space?

A
  • limit ATP signalling - can give rise to other signalling molecules e.g. ADP and adenosine
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8
Q

What is the role of the adenosine transporter?

A
  • equilibrated transporter - operates on concentration gradients - high extracellular adenosine concentration= removed from extracellular space
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9
Q

What receptors does ATP target?

A
  • P2X (ligand gated ion-channels) - P2Y (GPCRs)
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10
Q

What receptor does ADP target?

A

P2Y (GPCRs)

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11
Q

What receptor does adenosine target?

A

P1 (GPCRs)

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12
Q

What are the subtypes of the P2X receptor?

A

P2x1 to 7

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13
Q

What are the subtypes of the P2Y receptor?

A
  • P2Y1, 12, 13 (ADP) - P2Y2, 11 (ATP)
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14
Q

What are the subtypes of the P1 receptor?

A

P1A1, A2A, A2B, A3

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15
Q

What are some effects of antagonists at the P1 receptor?

A
  • cognitive disease - neurodegeneration - asthma/cough - diabetes - diarrhoea
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16
Q

What are some effects of agonists at the P1 receptor?

A
  • sleep disorder - stroke - respirator disorders - cystic fibrosis - cancer - cardiac and kidney ischaemia
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17
Q

What does alpha, beta, methylene-ATP do?

A
  • desensitises P2X receptors - increased concentration decreases number of excitatory junction potentials at NEJ
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18
Q

Is the spontaneous release of ATP inhibited by alpha, beta methylene-ATP?

19
Q

What is the role of varicosities in purine release?

A

The release of ATP means it can be converted to adenosine which inactivates receptors stimulated by ATP= fine parasympathetic control

20
Q

What are areas in the brain where P2X-mediated synaptic transmission has been identified?

A
  • medial habenula - hippocampus The use of nicotinic or glutamate antagonists has little effects in these regions
21
Q

What is the structure of the P2X receptors?

22
Q

How does purinergic signalling in pain pathways achieve analgesia?

A
  • P2X antagonists (blocks ATP release from tumour, endothelial and merkel cells) - A1 agonists
23
Q

What do antagonists at the P2X3 receptor treat?

A
  • chronic cough - tissue damage releases ATP activating P2X3 receptors - AF-219 (Gefapixant)= significant decrease in chronic cough
24
Q

What is associated with P2X7 activation?

A

Pain and cell death

25
What prevents P2X7 desensitisation?
- palmitoylation - P2X7 receptor stays in an open state= consistent ion conduction
26
What G protein does P2Y1-11 bind to?
G alpha q
27
What G proteins do P2Y-11 bind to?
- G alpha s - G alpha q
28
What G protein does P2Y12-14 bind to?
G alpha i/o
29
What is the effect of P2Y12 activation?
Platelet aggregation
30
What are antagonists of the P2Y12 receptor used for?
- inhibits process of platelet aggregation leading to artherscleortic plaques - reduces risk of stroke, pulmonary embolus and heart attack - e.g. clopidogrel, ticlopidine
31
What are the functions of the A1 receptor?
- bradycardia - antinociception - reduction of parasympathetic and sympathetic activity - neuronal hyperpolarisation - ischemic preconditioning
32
What are the functions of the A2A receptor?
- inhibition of platelet aggregation - vasodilation - protection against ischemic damage - wound healing
33
What are the functions of the A2B receptor?
Relaxation of smooth muscle in vasculature and intestine
34
What are the functions of the A3 receptor?
- enhancement of mediator release from mast cells - preconditioning
35
How does adenosine act as a cardiac 'retaliatory metabolite'?
- energy supplier e.g. coronary dilation, insulin sensitivity - regulates energy demand e.g. heart rate, adrenergic modulation
36
How is adenosine used to treat supraventricular tachycardia?
- slows heart rate- regulates rhythm
37
What is the role of adenosine during seizure activity?
Elevated concentrations of adenosine suppress further seizure activity in the hippocampus= anticonvulsant
38
Why is there certainty that it is adenosine that suppresses seizure activity and not ATP?
- ATP sensor does not detect a signal during seizures - ATP is being converted to adenosine to sustain metabolic demands of the seizure activity
39
What happens when you use an adenosine A1 receptor antagonist?
Induces seizure activity in typically non-epileptic tissue e.g. CPT
40
How is adenosine kinase linked with seizure activity?
- increased concentration of ADK reduces extracellular adenosine= facilitates seizure activity - ADK inhibition increases extracellular adenosine= reduces seizure activity e.g. IODO
41
Where is ADK primarily located?
Astrocytes
42
What is the role of astrocytes in seizure activity?
- severe epilepsy= astrocyte proliferation - increased ADK presence e.g. via kainic acid
43
When you have both an ADK inhibitor and an A1 antagonist together, would you expect there to be seizure activity?
Yes
44
Would a genetic ADK deficiency increase or decrease the risk of seizure activity?
Decrease

Neuropharmacology (15 decks)

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