Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology & Physiology 1 > Receptor Mechanisms I, II & III > Flashcards

Receptor Mechanisms I, II & III Flashcards

1
Q

What is the significance of receptors?

A

Without receptors the cells can’t produce any biological responses

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

Where is Ach produced?

A

Motor nerve produces ACh and stores it in vesicles

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

How are different biological responses produced via same chemicals?

A

The same chemical can produce carious biological responses in different tissues depending on the receptor mechanism

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

What hormones cause blood vessels to constrict?

A

NA, angiotensin II and thromboxane all stimulate different receptors but all constrict blood vessels

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

How does the β₁ adrenoceptor cause an increase in heart rate?

A
  1. Nor Adrenaline binds to β₁ adrenoceptor
  2. Increases adenyl cyclase activity
  3. cAMP levels increased
  4. PKA phosphorylates Ca2+ channel, activated by cAMP
  5. Greater influx of Ca2+
  6. Increased pacemaker, contraction increases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the effect of the activation of Growth Factor receptors?

A

Causes the activation of a receptor kinase leading to the activation of multiple signalling pathways

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

In biological terms what is a ligand?

A

A chemical activator

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

How is the JAK/STAT signalling pathway activated?

A

By growth hormones

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

How does an Insulin receptor differ from other Receptor Kinases?

A

Receptor kinases consist of a single transmembrane domain

Insulin consists of 2 (2a and 2b)

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

How is the Neuromuscular synapse adapted for fast responses in skeletal muscle?

A
  • short distance between nerve and muscle for Ach to
    cross
  • Abundance of Ach receptors on postsynaptic
    membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Summarise the Enzyme linked signal transduction pathway

A

PATHWAY: Enzyme linked

TRANSDUCTION MECHANISM: Conformational change &
phosphorylation of G
protein

EFFECTOR: Proteins with SH2 domain

INACTIVATION: Phosphatase

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

What is the effect of Ach on blood vessels?

A

Although Ach contracts skeletal muscles, it relaxes blood vessels using the same type of M3 receptors

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

Describe the structure of an insulin receptor

A

Consists of 2a and 2b subunits linked by disulphide bridges

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

Describe the structure of a Ligand gated ion channel

A

Has a ligand binding site
Aqueous pathway present
5 proteins make up LGIC (pentameter protein)
form cavity in middle - ionic pathway
- each protein has 4 transmembrane domains
- each LGIC made up of (5x4) 20 proteins/domains

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

What is the effect of stimulated β₁ adrenoceptor?

A
  • increases force of contraction

- increases contraction rate

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

Describe the structure of GPCR

A
  • 7 transmembrane domains
  • consists of 1 protein only
    On 1st TM domain an α subunit (different to LIGC) is bound to a GDP molecule as well as ɣβ subunits joined at the top

G-proteins = αɣβ

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

What is the function of RAS?

A

Involved in transmitting signals within cells by activating GDP –> GTP via GTPase activity
Causes: Growth
Differentiation
Cell Motility

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

Name the 2 GABA receptors that cause hyperpolarisation

A
  • GABAₐ receptors (Cl-)
  • Glycine receptors (Cl-)
    these receptors have a different TM domain #2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the function of Phospholipase C enzyme?

A

Digests phospholipids especially Phosphotidylinositol biphosphate (PIP₂)
PIP₂ -> IP₃ + DAG
Phosphatidylinositol biphosphate –> Inositol triphosphate + Diacylglycerol

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

What is the effect of an activated Ligand gated ion channel?

A

The direct opening of an ion channel upon binding with an agonist
- super fast response

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

Summarise the Inositol P pathway

A

PATHWAY: Inositol P

TRANSDUCTION MECHANISM: Conformational change in
G protein

EFFECTOR: Phospholipase C

INACTIVATION: GTPase phosphorylation

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

What are the types of muscarinic AchR in humans?

A

In adults - δ 𝜺
In foetal - ɣ α
In neonatal - α β only

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

Where are insulin receptors found?

A

Act on liver and muscles to reduce blood glucose levels via tyrosine kinase activity

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

Outline the process of Tyrosine Kinase Receptor Activation

A
  • Activation of tyrosine kinase receptors activates multiple
    pathways
  1. Dimerisation causes phosphorylation of tyrosine motifs
  2. Phosphorylated motifs recognised by other proteins
    (e. g. GRB-2 recognises SH2 domain)
  3. Undergoes conformational change
  4. Causing interactions with KASGEF protien
  5. KASGEF activates KAS and recongises SH3 domain
  6. This activates proteins which interact with PIP₂ on
    membrane
  7. PIP₂ phosphorylated –> PIP₃
  8. PIP₃ recognised by other kinases (e.g. PDK-1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Explain how the transmembrane domains in LGIC contribute to the overall structure

A

The TM domains contain hydrophobic amino acids that contribute to the aqueous pathway
specifically TM domain #2 amino acids make up the ionic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is an action potential generated?

A
  1. Ach binds to LIGC
  2. Kink formed in LIGC
  3. Causes influx of Na+/Ca2+
  4. Cell depolarised
  5. Excitatory junction potential produced (EJP)
  6. Causes voltage gated ion channels to open
  7. action potential produced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens when RAS is activated?

A
  • RAS bound to GDP when inactive
  • When activated, GDP replaced by GTP by GUanine
    nucleotide Exchange Factor (GEF)
  • GTPase activity occurs
  • causing slow dephosphorylation aided by GTPase
    Activating Proteins (GAP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Explain how a cell becomes hyperpolarised

A

GABA receptors cause anions to move into cell
inhibitory neurotransmitters brought in causing hyperpolarisation
2 GABA bind causing a kink in receptor, allowing Cl- to enter cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Outline how Ach binds to M3 to contract skeletal muscle

A
  1. Ach binds to GPCR M3 receptors
  2. Activates G₉ α subunit
  3. Increases Phospholipase C activity
  4. More Ca2+ channels open - greater influx
  5. Increased smooth muscle contraction
30
Q

Give an example of receptor failure

A

Myasthesia Gravis
- autoimmune disease where muscarinic nAchR are
degraded
- α1 subunits are targeted by antibodies secreted by the
body
(neuronal AchR are unaffected)

31
Q

How are the phosphorylated tyrosine residues recognised?

A

Phosphotyrosine and their surrounding amino acids are recognised by SH2 domains on other proteins, allowing them to bind and undergo further activation

32
Q

What happens when an agonist binds to a GPCR?

A
  1. GDP molecule replaced by GTP
  2. causes α subunit to dissociate from ɣβ
  3. α subunit interacts with specific enzyme to cause desired effect
  4. GTP hydrolysed back to GDP
  5. α subunit reassociated with ɣβ
33
Q

Name some examples of Growth Factor receptors

A
  • Tyrosine Receptors Kinase
    (e.g. Insulin, Epidermal growth factor & Platelet Derived
    Growth Factor Receptors)
  • JAK/STAT
    (e. g. Growth hormone, and Interferon receptors)
  • Serine Threonine Receptor Kinase
    (e. g. TGFβ)
34
Q

How do LIGC produce fast responses?

A

When an agonist binds to its receptor, an instantaneous molecular kink is formed

  • ionic pathway is opened
  • allowing ions to flow through
35
Q

How does the M2 AchR cause a decrease in heart rate?

A
  1. AcH binds to GPCR
  2. Activates G₁ α subunit
  3. Reduces adenyl cyclase activity
  4. Decreased cAMP levels
  5. Less influx of Ca2+
  6. Reduces pacemaker - heart rate decreased
36
Q

How does the G₁ α subunit effect levels of cAMP?

A

G₁ α subunit in GPCR inhibits adenyl cyclase, so cAMP levels reduced

37
Q

Explain how RAS activity regulated?

A
  1. Activated GTPase leads to removal of phosphates
    from GTP => GDP
  2. Complex of RAS-RAF breaks down becoming
    inactivated
  3. Inactive form waits to be reactivated
38
Q

Which receptors cause depolarisation?

A
  • Nicotinic receptors (Na+/Ca2+)

- 5HT3 receptors (Na+/Ca2+)

39
Q

How does Ach binding to M3 cause blood vessels to relax but smooth muscle to contract?

A

Ach relaxes smooth muscle in blood vessels as the M3 receptors are present on the epithelial cells and not on the muscle itself

40
Q

What is the effect of G₉ α subunit interacting with Ach on GPCR?

A
  1. Activated G₉ α subunit activates phospholipase C (PLC)
  2. PLC breaks a PIP₂ bond splitting it into IP3 and DAG
  3. IP₃ binds to its receptor on ER - causing influx of Ca2+
    in cytosol
  4. Ca2+ in cytosol bind to Protein Kinase C activating
    more PKC and DAG
  5. PKC used for protein phosphorylation causing smooth
    muscle to contract
41
Q

Describe the structure of growth factor receptors

A

Predominantly single transmembrane domain receptors

42
Q

Where are the different types of nAchR?

A

N1/Nm - in skeletal muscle end plates

N2/Nn - in autonomic ganglia in the brain

43
Q

How is heart rate increased?

A

Via stimulation of the GPCR, β₁ adrenoceptor

44
Q

How does Ach cause a decrease in heart rate?

A

Stimulation of muscarinic AchR M2 in the heart causes decreased contraction and force
as Ach is released from the Parasympathetic Vagus nerve on SAN and AVN cells
causing a decreased heart rate

45
Q

What processes do enzyme linked receptors help regulate?

A
  • Cell growth
  • Division
  • Differentiation
  • Survival
  • Migration
46
Q

Explain how the LIGC ionic pathway opens up

A

The internal cavity expands due to the binding of 2 agonists to receptors
There are 2 binding sites in the receptor as 2 agonist molecules are required to bind in order to achieve a full opening of LIGC

47
Q

Explain how Ach interacts with the Gₛ α subunit in GPCR

A
  1. Gₛ α subunit activates adenylate cyclase in cell membrane
  2. Adenylate cyclase activates cAMP using ATP
  3. Protein Kinase A (PKA) activated by cAMP
  4. cAMP degraded by phosphodiesterase
  5. cAMP acts as a secondary messenger
48
Q

Explain the effect of insulin binding to its receptor

A
  1. Insulin binds to Insulin receptor
  2. Autophosphorylation of 2b subunits
  3. Activates IRS family of small protein substrates
  4. IRS activates RAS and Phospholipase C
49
Q

What are the symptoms of a pateint with Myasthesia Gravis?

A
  • muscle weakness
  • drooping eyelids
  • fatigue
  • difficulty swallowing/talking
  • difficulty in exertion
50
Q

How are Tyrosine Kinase Receptors activated?

A

Dimerisation brings two receptor molecules together
Allowing phosphorylation of specific tyrosine residues
(not all tyrosine residues can be phosphorylated)

51
Q

How can enzyme linked receptors cause cancer?

A

The inappropriate activation of enzyme linked receptors is associated with disease, particularly cancer

52
Q

How does depolarisation occur?

A

When Ach activates a nicotinic receptor, an influx of (cations) Na+ or Ca2+ ions causes the cell to depolarise - cell is excited

53
Q

Which muscarinic AchR is responsible for decreased heart contraction?

A

The M2 muscarinic AchR containing G₁ α subunit

54
Q

What causes fast muscle contraction?

A

Stimulation of nAchR in skeletal muscle causes muscles to contract quickly

55
Q

What is the consequence of mutated RAS?

A

Mutated RAS is found in 30% of human tumours

56
Q

Why does a healthy membrane potential still fluctuate?

A

Healthy people have a fluctuating membrane potential due to MEPPs ( miniature end plate potentials) as there is always some Ach binding

57
Q

What are the 3 main types of α subunits?

A

Gₛ - stimulates adenyl cyclase
G₁ - inhibits adenyl cyclase
G₉₁₁ - stimulates phospholipase C

58
Q

How are receptor kinases deactivated?

A

Dephosphorylation leads to inactivation

59
Q

What happens when the motor nerve is activated?

A
  1. Depolarisation occurs as Na+ channels open
  2. Causes an influx of Ca2+ ions at postsynaptic membrane
  3. Acetylcholine released in neuromuscular junction
60
Q

Where are G protein coupled receptors found?

A

In muscles - muscarinic receptors

61
Q

Summarise the cAMP signalling pathway

A

PATHWAY: cAMP

TRANSDUCTION MECHANISM: Conformational change in
G protein

EFFECTOR: Adenyl Cyclase

INACTIVATION: GTPase phosphodiesterases

62
Q

Outlie how JAK/STAT signalling pathway occurs

A
  1. JAKs cross phosphorylate eachother on tyrosine
  2. Activated JAKs phosphorylate receptors on tyrosine
  3. STATS dock on phosphotyrosines (phosphorylated by
    JAKs)
  4. STATS dissociate from receptors and dimerise via SH2
    domain
63
Q

How can mutations in key regulatory mechanisms lead to cancer?

A

Over expression of EGF (epidermal growth factor) can cause breast cancer
due to loss of phosphatase activity
and loss of GTPase activity

64
Q

What determines the enzyme the α subunit binds to in an activated GPCR?

A

The specific enzyme the α subunit binds to depends on the type of α subunit present

65
Q

What is RAS?

A

Small G protein family member - related to cAMP Gα subunit

66
Q

How is a slow response produced by AchR?

A

A slow response is produced by G protein coupled receptors that peak in 10-20 seconds

67
Q

Outline how Receptor kinases are inactivated

A
  1. When the receptor is activated, phosphatases are also
    activated
  2. Signalling process sets in motion events that lead to
    signal termination
  3. Small G-proteins have intrinsic GTPase activity occur
  4. Receptor is internalised
68
Q

Give an example where in the body ligand gated ion channels produce fast responses

A

Skeletal muscle contraction

69
Q

Where are GPCR containing G₉ α subunits found?

A

Present in gut lumen as required for smooth muscle contraction for peristalsis
(wave-like muscle contractions to move food along gut)

70
Q

Outline the SMAD- dependent signalling pathway

A
  1. TGF-β binds to Type II TGF-β receptor causing
    dimerisation of the receptor
  2. Dimerisation causes autophosphorylation of
    serine/Threonine kinase domain
  3. Acts as a phosphorylation docking site for SMAD 2 and
    3
  4. Phosphorylated SMAD 2 & 3 recognised by SMAD 4
    which is also phosphorylated
  5. Complex enters nucleus to bind to specific DNA
    regions causing gene transcription

Pharmacology & Physiology 1 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions