Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

physiology, pharmacology and neuroscience > signalling, receptors and pharmacology > Flashcards

signalling, receptors and pharmacology Flashcards

1
Q

how does aspirin exhibit its biological effect?

A

irreversibly inhibits cycooxygenase

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

what is the ligand for the enzyme/receptor cyclooxygenase?

A

arachidonic acid

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

how do ligand-gated ion channels exert their effect as a receptor? give an example of one

A

allow the influx/efflux of ions in order to cause depolarisation/hyperpolarisation to bring about a cellular response
nicotinic acetylcholine receptors

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

how do most receptors with intrinsic enzymatic activity exert their effect as receptor? give an example of one

A

often cause phosphorylation of key amino acids, leading to gene transcription and production of proteins which exert a cellular effect
insulin receptor

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

how do intracellular receptors differ from most of the subtypes of receptors? name an intracellular receptor

A

they can cross the cell membrane

glucocorticoid receptors

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

give 2 examples of EXOGENOUS adrenoceptor ligands

A

isoprenaline

salbutamol

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

what is meant by the statement ‘isoprenaline is a subtype selective adrenoceptor ligand’?

A

acts upon only a few of the 9 adrenoceptors, producing a selective response

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

give an example of an exogenous adrenoceptor antagonist

A

propranolol

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

what is meant by the lock-and-key concept when referring to receptors?

A

the points of hydrophobic, electrostatic and ionic interactions within the flexible 3D landscape of the receptor binding pocket

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

how does a ligand-receptor complex form?

A

the receptor protein transitions between multiple different conformations and the ligand stabilises a particular conformation which brings about a cellular response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what forces is ligand binding governed by?

A

kinetics of association and dissociation

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

what does Emax refer to?

A

the maximum cellular response to a ligand

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

what is EC50? how can it be found from graphical data?

A

the effective concentration of ligand producing 50% of Emax

the midpoint of a sigmoidal curve

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

how can radioligand binding be used to quantify drug-receptor binding?

A

the radioactive form of the agonist/antagonist binds to the cells, allowing equilibrium to form. excess washed off, test
repeat with higher [ligand] until most of the receptor sites are filled

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

what information does radioligand binding provide?

A

how many receptors are present

affinity of the ligand for the receptor

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

define ‘antagonist’

A

possesses affinity for the receptor but lacks the ability to cause receptor activation and therefore cannot bring about a cellular response

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

what is the observed difference when a log of an antagonist response is plotted against the log of an agonist response?

A

right-ward shift in the curve

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

what is meant by the term ‘signal transduction’?

A

the way in which a cell allows a response to be generated from an extracellular signal

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

give an example of a receptor with intrinsic enzymatic activity and explain how it works

A

epidermal growth factor receptor
EGF binds, activating an enzyme which phosphorylates the enzyme itself and other substrates, triggering the cellular response

20
Q

give 2 examples of B2-adrenoceptor agonists

A

salbutamol, salmeterol

21
Q

give two examples of u-opioid receptor agonists

A

morphine, fentanyl

22
Q

give 2 examples of D2- dopamine receptor agonists

A

haloperidol, sulpiride

23
Q

what is the general structure of a GPCR?

A

-single polypeptide chain -7 transmembrane spanning regions -extracellular N-terminal -intracellular C-terminal

24
Q

which two regions of a GPCR can be responsible for ligand binding?

A
  • binding site formed from 2-3 transmembrane domains

- the N-terminal region

25
Q

how do GPCRs respond to ligands?

A

conformational change which allows it to interact with the G protein

26
Q

which change does the GPCR cause to the G protein, causing it to become active?

A

causes GDP to exchange for GTP on the alpha subunit

27
Q

what effect does GTP have on the alpha subunit of a G protein?

A

causes the a-BY complex to dissociate

28
Q

how is G protein signalling terminated?

A

the a-subunit has GTPase activity, which hydrolyses GTP to GDP, this causes the affinity of the a-subunit for the By subunit to increase

29
Q

how does noradrenaline/adrenaline interact with B-adrenoceptors?

A

GPCR interacts with Gs-Protein, causing increased adenylyl cyclase activity

30
Q

how does noradrenaline/adrenaline interact with a2-adrenoceptors?

A

GPCR interacts with Gi-Protein, decreasing adenylyl cyclase activity

31
Q

how does noradrenaline/adrenaline interact with a1-adrenoceptors?

A

GPCR interacts with Gq-protein, increasing phospholipase C activity

32
Q

what is the role of adenylyl cyclase?

A

converts cellular ATP to cyclic AMP

33
Q

what is the role of phospholipase C?

A

converts PIP2 into IP3 and DAG

34
Q

what is the role of phosphoinositide 3-kinase?

A

converts PIP2 into PIP3

35
Q

name some cellular ‘recievers’ of cAMP

A
  • cAMP dependent protein kinase
  • guanine-nucleotide exchange factors
  • cyclic nucleotide gated ion channels
36
Q

which pathways is PKA used for?

A

GPCR pathways involving:
B-adrenoceptors
D1-dopamine receptors
H2-histamine receptors

37
Q

which type of G-protein subtype is responsible for the inhibition of adenylyl cyclase?

A

G-alpha-I

38
Q

how does cAMP activate PKA?

A

cAMP binds to the regulatory domains of PKA, causing the catalytic domains to be released

39
Q

outline agonist-stimulated regulation of phospholipase C

A

agonist binds to GPCR, Gq protein activated and triggers cleavage of PIP2 by PLC, IP3 and DAG released

40
Q

after phospholipase C cleaves PIP2, what happens to IP3?

A

goes into cytoplasm and binds to IP3 receptor on the endoplasmic reticulum, triggering release of calcium

41
Q

name some examples of Gq coupled receptors

A

a1-adrenoreceptors, M1 muscarinic receptors, H1 histamine receptors

42
Q

name some examples of Gi coupled receptors

A

a2-adrenoceptors, D2 dopamine receptors, H2 histamine receptors

43
Q

how is signal amplification achieved by GPCR pathways?

A

enzymes such as adenylyl cyclase and PKA produce many molecules more product

44
Q

when [drug]log is plotted against physiological response and receptor occupancy, what is observed?
what does this suggest?

A

a rightward shift for physiological response.

there are ‘spare receptors’. very little receptor activity is required to achieve near physiological maximum

45
Q

what causes bronchoconstriction of airway smooth muscle?

A

acetylcholine released from post-ganglionic parasympathetic nerve endings

46
Q

which signalling pathway causes positive inotropy in the heart?

A

adrenaline and noradrenaline interact with ventricular b1-receptors via GPCR activation of adenylyl cyclase, and cAMP phosphorylation of L-type voltage gated calcium channels to increase the amount of Ca2+ released

47
Q

how do opiate painkillers relieve pain?

A

binding to u-opioid GPCR, activating Gi protein and causing By subunit to bind to VOOC, reducing influx of Ca2+ and thus reducing NT release

physiology, pharmacology and neuroscience (14 decks)

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