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Membrane Transport And Cell Signalling > Cell Signalling > Flashcards

Cell Signalling Flashcards

1
Q

What are inotropic receptors

A

Receptor which binds to an agonist which is an ion channel

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2
Q

What is a metabotropic receptor

A

A receptor that binds a ligand which triggers a cascade of reactions

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3
Q

What are the forces that effect the opening of an ion channel

A

Chemical gradient and electrical gradient

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4
Q

What is the reverse potential

A

The point at which the forces are equal = no movement of ions

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5
Q

What is the resting membrane potential

A

The average of resting potentials of the open ion channels

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6
Q

Which receptors are non specific cation channels

A

Glutamate and Ach receptors

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7
Q

What are non specific cation channels

A

Not specific to ions and have a reversal potential close to 0

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8
Q

Where are Ach receptors found

A

NMJ in muscle cells
Between pre and post synaptic cells in the ANS

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9
Q

What ions are Ach receptors permeable to

A

Na+, K+, Ca2+

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10
Q

What part of the Ach receptor allows it to bind to Ach

A

Alpha subunit - each Ach molecule can bind 2 receptors

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11
Q

Name an Ach antagonist and how it works

A

Alpha-bungarotoxin
Blocks the ability of the nerve to control the muscles
Causes paralysis

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12
Q

What receptors have a pentameric structure

A

GABA glycine and nicotinic Ach receptors

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13
Q

What is the importance of the amino acids that line the pore of the receptors

A

They dictate if they let through anions or cations

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14
Q

What is the importance of the lock an key mechanism on receptors

A

Affect wha can bind/modulate the activity of the receptors

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15
Q

Why are GABA and glycine receptors inhibitory

A

Ecl is close to Em and below the action potential threshold -> prevents action potentials from happening

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16
Q

Why is subunit composition important

A

Subtle variations can affect the receptor properties e.g sensitivity to ligands

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17
Q

What do GABA-R subunit composition dictate

A

Receptor properties, dynamic variations and cell surface distribution

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18
Q

How does the location of the delta subunit in GABA-R relate to its functions

A

Placed outside of the cell and doesn’t contact much GABA
Monitors the ambient level and persistently open if GABA present

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19
Q

How does the location of the beta subunit in GABA-R relate to its functions

A

At the synapse and come in contact w lots of GABA
Open at precise moments and quickly close

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20
Q

Describe purinergic receptors

A

Excitatory receptors w ATP as their ligand
Permeable to cations
Expressed in the brain

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21
Q

What is glutamate

A

A principal excitatory neurotransmitter in vertebrate nervous systems

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22
Q

Describe ionotropic glutamate receptors

A

The ion channel is the receptor
Lined w negatively charged amino acid subunits
Allows cation to pass through to generate an excitatory subunit

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23
Q

What are the 3 main classes of glutathione receptors that are defined by man made agonists

A

AMPA, NMDA, kainate receptors

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24
Q

Which agonists activate all 3 classes of glutamate receptors

A

Glutamate and kainate

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25
Q

Where are AMPARs and NMDARs usually co-localised

A

At synapses where they mediate fast chemical synaptic transmission

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26
Q

Why are AMPARs and NMDARs needed at the presynaptic terminal

A

To act as auto receptors -> glutamate binds on the presynaptic site

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27
Q

Describe the structure of iGluRs

A

Have 4 subunits and 3 transmembrane domains (TM1, TM3, TM4) with a re-entrant loop (TM2)

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28
Q

What is the importance of the extracellular domain in iGluRs

A

Create the glutamate binding site

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29
Q

What is the importance of the transmembrane loops in iGluRs

A

Create the shape of the pore
Important for various intracellular processes

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30
Q

Where does glutamate bind on iGluRs

A

Between the S and S2 extracellular domains
Each subunit can bind 1 molecule

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31
Q

What subunits make up AMPARs

A

GluA1 - GluA4
Variants of the same protein that bind together to form the receptor

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32
Q

What mutations can the AMPARs subunits undergo

A

Alternative splicing and RNA editing

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33
Q

What channels can the AMPARs form

A

Homomeric; 1 type of subunit
Heteromeric; mix of subunits

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34
Q

Why is the GluA2 subunit important in AMPARs

A

It determines the current/voltage curve
Dictates the reversal potential and affects Ca2+ permeability

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35
Q

What are the AMPARs splice variants

A

2 exon; flip and flop which can affect receptor kinetics

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36
Q

What determines the rate of AMPARs desensitisation to glutamate

A

The subunit composition and flip/flop variant

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37
Q

Which subunit is affected by flip and how

A

The GluA4 subunit
Flip variant lengthens time the receptor is open

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38
Q

Describe how the AMPAR becomes desensitised to glutamate

A

When glutamate is maintained at receptor it doesn’t maintain current
The ion channel close even though glutamate is bound

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39
Q

Which subunits of AMPAR are permeable to Ca2+

A

GluA1 and GluA3

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40
Q

Why are many AMPARs impermeable to Ca2+

A

They contain a GluA2 channel

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41
Q

How can GluA2s permeability to Ca2+ be altered

A

Glutamine at the pore is flipped to arginine

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42
Q

What dictates the functionality of NMDARs

A

Mg2+
Drawn in by the negative field which depolarises cell
Negative field now has less influence so Mg2+ forced out
Leaves the pore open

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43
Q

Compare the I vs V relationship for AMPARs and NMDARs

A

AMPAR; linear relationship
NMDAR; non linear relationship

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44
Q

How is the NMDAR conditional

A

Requires the presence of glutamate and for the cell to depolarise

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45
Q

What is the purpose of phosphoinositide signalling

A

To keep [cystolic Ca2+] low to prevent Ca2+ and excess phosphates bonding to form a precipitate

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46
Q

How does the Ca-ATPase pump work

A

Pumps Ca2+ out of the cell using energy from ATP -> ADP hydrolysis against Ca2+ conc gradient

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47
Q

What is the Ca-ATPase in the plasma membrane called

A

PMCA

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48
Q

What is the Ca-ATPase in the ER called

A

SERCA

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49
Q

What does the SERCA pump do

A

Pump Ca2+ from the cytosol into the ER or the SR in a muscle cell

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50
Q

How does the Na/Ca exchanger work

A

Removes Ca2+ from the cell by exchanging them for Na+
Uses inward Na+ gradient generated by Na/K pump

51
Q

Why is the mitochondria important in maintaining a low cystolic Ca2+ conc

A

Take up Ca2+ when the SERCA and PMCA become saturated

52
Q

Describe the function of calmodulin

A

Sensor protein which undergoes conformational change when bound to Ca2+
Trigger downstream physiological responses

53
Q

What is the function of buffer proteins

A

Bind to Ca2+ and act as aa sponge to bring down cytosolic [Ca2+]

54
Q

Why does the cell need a range of mechanisms to bring down cystolic [Ca2+]

A

So the cells can remove the ions over a wide range of [Ca2+]

55
Q

Where are IP3Rs and RyRs located

A

On the membrane of ER/SR

56
Q

What is the secondary messenger for IP3Rs

A

IP3 and Ca2+

57
Q

What is the secondary messenger for RyRs

A

Ca2+

58
Q

What are the 3 types of Ca2+ signals

A

Elementary events
Global Ca2+ wave intracellular
Global wave Ca2+ intercellular

59
Q

Describe an elementary Ca2+ event

A

Very small and doesn’t take up the entire cell
Ca2+ rise is highly located in the cell

60
Q

Describe a global Ca2+ wave intracellular

A

Ca2+ waves happens in part of the cell and makes it way a cross the whole cell

61
Q

Describe a global Ca2+ wave intercellular

A

The Ca2+ wave doesn’t stop at the boundary of the cell it propagates across the mono layer of cells

62
Q

Describe how a signal binding to a GCPR causes Ca2+ release from the ER/SR

A

Signal binds GCPR -> activates phospholipase C-beta
Clips PIP2 molecule -> DAG and IP3
IP3 released into cytosol and diffuses to IP3R on ER/SR
Opens channel to release Ca2+ from ER/SR

63
Q

What happens to DAG when it’s produced from PIP2

A

Stuck in the plasma membrane and tries to find PKC its target protein

64
Q

Why does DAG remain in the plasma membrane

A

Due to its hydrophobic fatty acid chains

65
Q

How does a Ca2+ signal present itself

A

Series of spikes that will persist as long as a the hormone is present

66
Q

What effect will doubling the [hormone] on the Ca2+ spikes

A

Amplitude remains constant
Frequency will increase

67
Q

Describe CICR

A

Ca2+ released from the ER stimulates further Ca2+ release from neighbouring IP3Rs
Feeds forward to release more Ca2+

68
Q

What are the 2 components to a Ca2+ signal

A

Temporal (spike) and spatial (wave)

69
Q

Describe how a Ca2+ spike and wave are linked

A

When spike begins = initiation of Ca2+ propagation
Midway through spike = mid propagation halfway through the cell
Peak = whole cell is full of Ca2+

70
Q

What buffers/prevents the diffusion of Ca2+ through the cell

A

Buffered by binding to buffer proteins = no wave/spike

71
Q

What needs to happen to generate a Ca2+ wave/spike

A

CICR needs to overcome the buffer proteins momentarily to generate wave/spikes

72
Q

What needs to take place for the falling phase of the Ca2+ spike

A

IP3Rs stop releasing Ca2+ to allow the off mechanisms to remove Ca2+

73
Q

What happens in between Ca2+ spikes

A

Cell at rest and off mechanisms relax which allow the cell to produce another Ca2+ spike

74
Q

What is the suggested stimulus for RyRs

A

CADPR

75
Q

Why is IP3 required for CICR to be triggered

A

To sensitise the receptor and Ca2+ for CICR

76
Q

How does RyRs differ from IP3Rs

A

RyRs don’t need cADPR to sensitise the receptor in order to behave as a CICR channel
IP3Rs need IP3 to be able to behave as a CICR channel

77
Q

Why do RyRs and IP3Rs require ATP

A

As aa safety mechanism

78
Q

How does ATP work as aa safety mechanism for RyRs and IP3Rs

A

If cell has plenty energy then there will be ATP present
If low ATP - site wont be occupied on receptor so no movement of Ca2+
= no Ca2+ signalling

79
Q

What is a Ca2+ puff

A

When Ca2+ is released from a cluster of 10 IP3Rs

80
Q

What is a Ca2+ spark

A

When Ca2+ is released from a cluster of 10 RyRs

81
Q

What is an abortive Ca2+ wave

A

When the wave is borderline before intermediate/high level of hormones
Wave only propagates across part of the cell not the full wave

82
Q

How are puffs and sparks forerunners for a Ca2+

A

Sensitise the IP3R so that if the hormone stimulus increases, the channels can produce a CICR

83
Q

What is a Ca2+ blip

A

A fundamental event released as a result from only 1 IP3R

84
Q

What is a quark

A

A fundamental event released as a result from only 1 RyR

85
Q

How can a Ca2+ dependent response be triggered i.e wave not necessary

A

Ca2+ spark in muscle -> Sr releases Ca2+ near membrane
Spark close to the Ca2+ activated K+ channel
Activates the channel = cell hyperpolarisation = muscle relaxation

86
Q

How does a global Ca2+ effect differ to aa spark in muscle cells

A

Global = contraction
Spark = relaxation

87
Q

How can a Ca2+ wave propagate though cells

A

IP3 and Ca2+ are needed to diffuse through gap junctions

88
Q

How do the cilia of different cells coordinate a response

A

Through Ca2+ intracellular wave events

89
Q

Describe a cell specific calcium signalsome

A

Defines the precise isoforms of each component that is any given cell

90
Q

What are the 2 types of remodelling signalsomes undergo

A

Phenotype and genotypes remodelling

91
Q

What is phenotypic remodelling of a signalsome

A

when the component become phosphorylated which can change its activity

92
Q

What is genotypic remodelling of a signalsome

A

Somatic mutations in single cells alter activity of a component and are passes on from one generation to the next via germline mutations

93
Q

Describe how phenotypic remodelling allows the heart to have stronger/larger contractions

A

CAMP dependent reversible phosphorylation of key Ca2+ signalling components
= enables more Ca2+ to enter the cell and more pumped out to generate larger Ca2+ signals

94
Q

What drives liver regeneration

A

Down regulation of key Ca2+ signalling components

95
Q

How does Alzheimer’s disease affect memory

A

Extracellular plaque deposits of beta amyloid peptide which aggravates outside of nervous cells to disrupt synaptic transmission

96
Q

How does APP and beta amyloid affect the cytosolic Ca2+ levels

A

Up regulation of Ca2+ signalling
Beta amyloid oligomers increase Ca2+ entry via the NMDAR
APP increase Ca2+ release from stores

97
Q

What happens to APP once it has been metabolised

A

Makes its way to the nucleus to act as a TF and increase the txn of RyRs and decrease txn of calbindin

98
Q

How does APP result in amyloid dependent Ca2+ signalling

A

Increase Ca2+ leak through RyR into cytosol
Decrease in Ca2+ buffering
= [Ca2+] in nervous cells

99
Q

How are memories formed

A

Triggered by a strong Ca2+ signal through NMDAR through the LTP
Initially enter temporary memory store but are consolidated into the permanent memory store at night

100
Q

How does Ca2+ erase the temporary memory store

A

Broader raise of Ca2+ but at a lower signal triggers LTD
Erases temporal memory store so it is ready to receive new temporary memories

101
Q

How does Alzheimer’s affect memory

A

Increased level of resting Ca2+ so there is still LTP during the day but there is persistent activation of LTD
= erasing of temporary memory store before it can be consolidated to permanent store

102
Q

How can vitamin D potentially reverse Ca2+ dependent neuro-degeneration

A

Increases the expression of plasma membrane ATPase and Na/Ca+ exchanger
Increases [calbindin]
= decrease in resting cytosolic [Ca2+]

103
Q

How does positive feedback make it hard to perceive the primary cause of Alzheimer’s

A

Amyloid stimulates an increase in Ca2+ which can stimulate APP which also increases Ca2+

104
Q

What is Brody myopathy

A

Skeletal muscle genetic disorder characterised by stiffness and cramp

105
Q

What causes Brody myopathy

A

Mutation in SERCA1pump therefore can’t pump out all the Ca2 back into SR
Impedes relaxation

106
Q

What are the 2 types of adenylyl cyclase

A

Plasma membrane form
Soluble form

107
Q

How is the membrane bound from of adenylyl cyclase activated

A

By the alpha s subunit on GPCR which causes a conformational change
Allows the catalytic subunits to come together

108
Q

What is the reaction to form cAMP

A

ATP -> cAMP and pyrophosphate via adenylyl cyclase

109
Q

How can forskolin activate all isoforms

A

Bypasses receptor - GCPR complex and binds directly to adenylyl cyclase

110
Q

What is the role of PDEs

A

To breakdown cAMP and some can breakdown cGMP

111
Q

Why are PDEs important

A

Can affect the duration of cAMP rise and how the cAMP level can rise
Alerts the spatial localisation of the cAMP signal

112
Q

What are the 3 off mechanisms for cAMP signalling

A

PDEs
Inhibit cAMP production
CAMP removal

113
Q

How can cAMP production be inhibited

A

Some GCPR agonist activate the Gai to reduce AC activity by binding to AC

114
Q

How can cAMP be removed from the cell

A

MRP transporters that pump cAMP out of the cell

115
Q

What affect does cAMP removal have on the signal

A

Affects the duration and amplitude of signal
Can impact on spatial aspects

116
Q

What suggests that cAMP signalling is compartmentalised to micro domains and are agonist specific

A

Different agonists increase cAMP levels but produce different response in same cell
Some agonists produce cAMP dependent responses but do not change global cAMP levels

117
Q

How can cAMP signalling be compartmentalised

A

AKAPs bind to PKA and have a target domain which allows them to be brung closer to their substrates
Help assemble signalsomes

118
Q

What are the 2 forms of PKA

A

Type 1 and type 2

119
Q

Describe type 1 PKA

A

Inactive PKAA binds to cAMP binding domains which releases the catalytic domain to phosphorylate other molecules

120
Q

Describe type 2 PKA

A

Bind to AKAPS via docking domain but catalytic domain isn’t released
AKAPS bring PKA closer to the substrate

121
Q

Where are beta adrenergic receptors located in a muscle cell and why

A

Localised near the T tubule where all the excitatory contraction machinery is located

122
Q

Why do prostanoid receptors excitation not lead to a contraction

A

Localised in different regions and phosphorylate metabolism enzymes not contraction machinery

123
Q

What leads to PKA dependent phosphorylation of key Ca2+ components in a muscle cell

A

Beta adrenergic stimulation -> increased elevations in cAMP

124
Q

Ha

A

Membrane Transport And Cell Signalling (4 decks)

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