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Flashcards in Calcium & G-coupled Receptors Deck (53)
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In regards to the movement of ions, how an Na+ K+ ATPase functions?

3 Na+ ions out, 2 K+ ions in


Describe, in simple terms, the structure of PKA.

A combination of 4 subunits - 2 r subunits to which cAMP binds, and 2 c subunits which are the catalytic entity


List 3 ion transporters used to remove Ca2+ from the cell. Are these ion transporters passive or active transporters?

Plasma membrane Ca2+ ATPase (PMCA) - active
Smooth Endoplasmic Reticulum Ca2+ ATPase (SERCA) - active
Na+ Ca2+ Exchanger (NCX) - passive (antiporter)


What effect do agonists have on a receptor? In that case, what effect do antagonists have on a receptor?

Agonists activate a receptor - antagonists do not activate a receptor


Describe the structure of a G-protein coupled receptor?

A single polypeptide chain spanning the membrane 7 times - it has an extracellular N-terminus and an intracellular C-terminus


Describe the steps explaining how a substrate may activate a G protein.

The substrate binds the G protein-coupled receptor at either the N-terminus or by burying itself in the membrane of the receptor - this causes a conformational change in the receptor which releases the G protein - this causes the G protein to release GDP and bind GTP


What type of G-protein activates phospholipase C? What does phospholipase C catalyse?

Phospholipase C is actives by a Gq-type G-protein, and catalysts the cleavage of PIP2 to IP3 and DAG


What type of G-protein activates adenylyl cyclase? What type inhibits it?

Adenylyl cyclase is activated by Gs-type G-proteins, and is inhibited by Gi-type G-proteins


What molecules make up a G-protein?

A G-protein contains an alpha, beta, and gamma subunit (is heterotrimeric) - the beta and gamma subunits functionally act as one however


What cation is required for neurotransmitter release?

Ca2+ entry


What is the neuromuscular junction?

The synapse between a nerve and a skeletal muscle fibre (cell)


Are Ca2+ levels higher intracellularly or extracellularly?



What is needed to increase the amount of Ca2+ entry at a nerve terminal?

Increase in frequency (as opposed to amplitude) of action potentials


What is the pore-forming subunit of a voltage-gated Ca2+ channel?

A1 (alpha 1) subunit


How many subunits does a voltage-gated Ca2+'channel have? How does this relate to a voltage-gated Na+ channel?

Both have 4 subunits, and share a very similar structure


What molecules can block L-type Ca2+ channels? Can you give 1 example?

DHP (dihydropyridines) e.g. nifedipine


What type,of Ca2+ channels are found in the heart?

R-type and T-type


How does increased intracellular Ca2+ affect Ca2+ channels?

Increased intracellular Ca2+ channels block the activity of Ca2+ channels


How do voltage-gated Ca2+ channels act in comparison to voltage-gated Na+ channels?

They act in a slower manner


What type of Ca2+ channels are found in skeletal muscle?



What breaks down acetylcholine in the synaptic cleft?



What molecule brings Ca2+ vesicles to the pre-synaptic member ae to be released?



What complex is associated with fusion of the Ca2+ vehicle to form a pore in the pre-synaptic membrane?

The SNARE complex


What molecules does a nicotinic acetylcholine receptor let pass through its pore?

Na+ and K+


How many molecules of acetylcholine are required to induce a conformational change and open a nicotinic acetylcholine receptor?

2 molecules of acetylcholine


If a nicotinic acetylcholine receptor lets through both Na+ and K+, which does Na+ flood into the cell and not K+?

The resting membrane potential of a cell is much closer to the equilibrium potential of K+ - as it is much further from the equilibrium potential of Na+, Na+ floods into the cell in an effort to reach equilibrium, which leads to depolarisation of the cell


State an example of a competitive nicotinic acetylcholine receptor blocker.



How can a competitive blocker of a nicotinic acetylcholine receptor (such as tubocurarine) be overcome?

Increasing the amount of acetylcholine (or the receptors endogenous substrate)


How do depolarising blockers act at nicotinic acetylcholine receptors?

They act to keep nicotinic acetylcholine receptors in a depolarised state, thereby deactivating adjacent Na+ channels meaning an action potential cannot propagate


Can you list an example of a depolarising nicotinic acetylcholine receptor blocker?