9. Control Of Cytosolic Ca2+ Flashcards Preview

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Flashcards in 9. Control Of Cytosolic Ca2+ Deck (12):
1

What are some disadvantages of the large inward gradient of calcium?

It is energy expensive to maintain, Ca2+ overload is easy with slight loss of regulation and can lead to cell death.

2

How is the large inward gradient of calcium set up and maintained?

Relative impermeability of plasma membrane - regulated by open/close state of ion channels.
Expulsion of Ca2+ across the plasma membrane using:
-Ca2+ATPase: high affinity, low capacity. [Ca2+]i increases, Ca2+ binds to cal modules, Ca2+-cal modules binds Ca2+ATPase, Ca2+ATPase removes Ca2+.
- Na+/Ca2+ exchanger: low affinity, high capacity. [Na+] gradient used as driving force. Anti porter is electrogenic and works best at resting membrane potential.
- Ca2+ buffers. They limit Ca2+ diffusion, diffusion depends on concentration of binding molecules and their level of saturation.

3

What are trigger proteins?

Some proteins bind Ca2+ and alter function. They regulate free [Ca2+].

4

How is [Ca2+]i elevated and returned to basal levels?

- Ca2+ influx across the plasma membrane.
A) voltage operated Ca2+ channels: regulated by voltage and undergo conformational changes so calcium can diffus in down the concentration gradient.
B) ionotropic receptors: binding of the ligand (calcium) causes conformational change so channel opens and exposed the pore and Ca+ can move through.
- Ca2+ is released from rapidly releasable intracellular stores, like the endoplasmic reticulum. SERCA pump allow entry of calcium into th endoplasmic reticulum, it then acts as a store that can be released via release channels.
- Non-rapidly releasable stores, like mitochondria.

5

How is Ca2+ release from endoplasmic reticulum mediated?

Via G protein coupled receptors, G protein released from the ligand binding to GPCR reacts with PIP2 and is cleaved into IP3 which opens the IP2 receptor to allow exit of Ca2+ from the stores.
Also by use of Ca2+ induced Ca2+ release (CICR). Ca2+ influx from the VOCC acts on the CICR to allow more release from the stores of Ca2+.

6

Where does the Ca2+ that acts on Ca2+ induced Ca2+ release channels come from?

VOCCs, ionotropic receptors and intracellular stores.

7

What are the landmark features of cardiac action potentials?

0 - upstroke because of Na+ channels opening and Na+ moving in
1 - brief repolarisation as K+ and Cl- move out
2 - plateau as Ca2+ moves in via VOCC and K+ out
3 - rapid repolarisation as K+ moves out
4- stable

8

How do mitochondria uptake Ca2+?

Via uni porters - low affinity, high capacity.

9

What is the role of mitochondrial Ca2+ uptake?

Ca2+ buffering - regulate pattern and extent of Ca2+ signalling.
Stimulation of mitochondrial metabolism - match energy demand and supply.
Role in cell death - apoptosis.

10

How do [Ca2+]i return to normal?

Terminate signal
Ca2+ removal
Ca2+ store refilling.

11

How do Ca2+ stores refill?

There is a depleted signal, so the capacitative or store-operated channel (SOC).

12

What are some advantages of the large inward gradient of calcium?

Changes in [Ca2+]i occur rapidly with little movement of Ca2+, this means little has to be done to restore normal resting condition.