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ESA 2 SK > MR 5 Ligand gated channels and control of intracellular calcium conc > Flashcards

MR 5 Ligand gated channels and control of intracellular calcium conc Flashcards

1
Q

What ion channels can be seen in the nerve terminal?

A

Na+, K+, Ca2+

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2
Q

What happens when an action potential reaches the nerve terminal?

A

Depolarisation opens voltage gated calcium channels
Ca2+ influx down conc grad
Increased intracellular [Ca2+] causes release of neurotransmitter

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3
Q

What is the basic structure of calcium channels similar to?

A

Sodium channels

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4
Q

What is a common calcium channel, where is it found and what blocks it?

A

L type
Muscle, neurones, lung
Dihydropyridines(DHP) e.g Nifedipine

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5
Q

What is fast synaptic transmission?

A

Where receptor is also ion channel

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6
Q

Describe transmitter release (e.g acetyl choline)

A 
Ca2+ enters through Ca2+ channels
Ca2+ binds to synaptotagmin
Vesicle brought close to membrane
Snare complex makes fusion pore
Transmitter released through this pore
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7
Q

What are the two types of blockers of nicotinic receptors?

A

Competitive blcokers- bind at molecular recognition site for Ach
Depolarising blockers- cause a maintained depolarisation at post-junctional membrane. Adjacent Na+ channels will not be activated due to accomodation e.g Succinylcholine

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8
Q

What is succinylcholine used for?

A

To induce paralysis for operations

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9
Q

Describe Myasthenia Gravis

A

Autoimmune disease targeting nicotinic Ach receptors
Patients suffer drooping eyelids, profound weakness increasing with exercise.
Caused by antibodies directed against NAchrRs on postsynaptic membrane of skeletal muscle
Endplate potentials reduced in amplitude leading to muscle weakness and fatigue

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10
Q

What is Myasthenia gravis treated with?

A

Ach-esterase inhibitors so Ach spends longer in synaptic cleft

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11
Q

What causes the end plate potential?

A

Activation of nAchR by Ach activating adjacent Na+ channels causing depolarisation

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12
Q

What are minature end plate potentials caused be and what is their amplitude compared to end plate potentials?

A

Minature potentials caused by the spontaneous release of vesicles (about 1 per sec).
1mV as opposed to 10mV

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13
Q

Why do muscarinic Ach receptors create a slower response that nictotinic Ach receptors?

A

Because nAchR is a ligand channel while mAchR are coupled to G-proteins

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14
Q

Why is it important to control intracellular calcium levels?

A

Many cellular processes calcium sensitive

Ca2+ cant be metabolised so has to be regulated by moving Ca2+ in and out of cytoplasm

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15
Q

What cellular processes are calcium sensitive?

A

Fertilisation, secretion, neurotransmission, metabolism, contraction, learning and memory, apoptosis, necrosis

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16
Q

What are the resting calcium concentrations inside and outside cells?

A

Extracellular- 1-2mM
Intracellular- 0.1uM
the large gradient is energy expensive

17
Q

What are the advantages and disadvantages of the large calcium gradient?

A

+ changes in [Ca2+]in occur rapidly with little movement

- Ca2+ overload can lead to loss of regulation and cell death

18
Q

What does the calcium gradient rely on?

A

The relative impermeability of the plasma membrane
Ability to expel Ca2+ across membrane using Ca2+ATPase ans Na+Ca2+ exchanger
Ca2+ buffers
Both rapidly releasable and non-rapidly releasable intracellular Ca2+ stores

19
Q

Describe the action of Ca2+ATPase

A 
High affinity, low capacity
Intracellular [Ca2+] rises
Ca2+ binds to calmodulin (binding trigger protein)
Calmodulin-Ca2+ binds to ATPase
Ca2+ removed from cell
ATP is hydrolysed in this process
20
Q

Describe the action of Na+/Ca2+ exchanger

A

Low affinity, high capacity
Na+ grad set up by Na+/K+ATPase used
3Na+ in per 1Ca2+ out
Electrogenic and works best at RMP

21
Q

What are Ca2+ buffers?

A

These limit diffusion through ATP and Ca2+ binding proteins like parvalbumin, calreticulin, calbindin and calsequestin. Diffusion depends on concentration of binding molecules and level of their saturation
Many other proteins also bind Ca2+, altering their function e.g calmodulin

22
Q

How is intracellular calcium increased?

A

Influx across plasma membrane (VOCCs, receptor operated ion channels)
Release from rapidly releasable stores (GPCRs, CICR)
Release from non-rapidly releasable stores

23
Q

Where is calcium stored within cells?

A

Sarco/Endoplasmic reticulum and mitochondria

24
Q

How is calcium moved into the sarco/endoplasmic reticulum?

A

Via Sarco/Endoplasmic Reticulum ATPase (SERCA) using ATP then binds to proteins like calsequestrin

25
Q

How do GPCRs facilitate calcium release from the SR/ER

A

Ligand binds to GPCR on cell membrane
Activates G-alpha-q sub unit
This binds to PIP2 triggering IP3 release
IP3 binds to IP3 receptor on SR/ER triggering calcium release down conc grad

26
Q

What is Ca2+ induced Ca2+ release?

A

Ca2+ binds to ryanodine receptor on SR/ER triggering calcium release down conc grad

27
Q

Where is CICR of particular importance?

A

Cardiac myocytes where Ca2+ influx through VOCCs after depolarisation and binds to ryanodine receptor causing explosive calcium release from stores

28
Q

When is Ca2+ taken into mitochondria?

A

When Ca2+ conc high as a protective mechanism

29
Q

Why do mitochondria take up Ca2+?

A

To aid in buffering, regulating signalling, stimulation of ATP production

30
Q

How do mitochondria participate in normal Ca2+ signalling?

A

through microdomains- areas of cytoplasm with higher Ca2+ conc due to proximity to a channel

31
Q

What do mitochondria use to take up calcium?

A

Ca2+ uniporter driven using respiration

32
Q

What does a return to basal Ca2+ levels require?

A

Termination of signal
Ca2+ removal
Ca2+ store refiling

33
Q

What channels increase calcium when intracellular sotres are depleted?

A

Store Operated Channels (SOCs) allow Ca2+ in through plasma membrane to then be taken into SR/ER via SERCA

ESA 2 SK (35 decks)

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