Term
| Ligand gated channels open in seconds, how long does it take signal transduction to open channels? |
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Definition
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Term
| How does signal transduction work to open channels? |
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Definition
| well, like membrane delimited stuff can get activated, directly opening a channel. Or, stuff can get phosphorylated and phosphorylate channels, activating them...3rd messengers |
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Term
| So explain how calcium gets released from sarcoplasmic reticulum, and also the ER |
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Definition
| So, IP3 is what binds the ER Ca2+ channels causing release. Ca2+ then gets cytoplasmic and binds receptors on the sarcoplasmic reticulum causing major release. This is like what muscle activity happens (remember Ca2+ binding troponin). This is all from the PLC-->PIP2-->IP3+DAG pathway. |
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Term
| Where is the IP3 receptor found? |
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Definition
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Term
| What is the ca2+ receptor on the sarcoplasmic reticulum called? |
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Definition
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Term
| How does the IP3 receptor essentially work on the ER? |
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Definition
| it basically gets bound by ligand, has conformational change, and releases Ca2+ |
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Term
| What is Ca2+-induced Ca2+ release (CICR)? |
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Definition
The released Ca2+ (from the IP3, or from nicotinic acetylcholine receptors) in turn feeds back to activate nearby ryanodine
receptors, accelerating the rate of release. Since the ryanodine receptor is inhibited by high Ca2+
concentrations, positive feedback is curtailed, preventing excessive and prolonged Ca2+ release. Ca2+
stores are replenished during periods of relaxation. |
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Term
| In addition to making IP3 and Dag, what consequence does activation of the PLC pathway have? |
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Definition
| it depletes PIP2. The consequence of this is that PIP2 can no longer interfere with K+ channel inactivation. (PIP2 is a membrane associated protein which is negative, so it helps the ball and chain of voltage gated K+ channels come in.) SO, K+ channels get inactivated more quickly. |
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Term
| How does ATP regulate insulin release? |
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Definition
So, Ca2+ channels entering pancreatic beta cells causes insulin release. For these Ca2+ channels to open, there needs to be a depolarization (ie the cell needs to become less negative). When ATP is high and ADP is low, KATP channels are inhibited, so the cell gets depolarized, because K+ can't egress and the cell just keeps getting more and more positive. This depolarization (caused by KATP inhibition) causes Ca2+ channels to open and Ca2+ to rush into the cell. Then, shit goes down and insulin is ejaculated (from the b-cell).
WHEN BLOOD GLUCOSE IS HIGH, THERE IS LOTS OF ATP IN THE CELL |
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Term
| How can mutations in the Katp receptor in pancreatic beta cell cause diabetes and other problems? |
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Definition
There are two important subunits of the Katp receptor, SUR1 and Kir6.2.
If they are messed up, you can have permanent depolarization of the cell (because the Katp channel will just be blocked) and then you will have too much insulin release. Then you can get hypoglycemia and hyperinsulinemia.
Alternatively, you can get a hyperactive Katp pore caused by a mutation, so you won't get insulin release and you will get neonatal diabetes! |
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Term
| How is heart rate controlled by an inward rectifier? |
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Definition
These G-protein-regulated inward rectifying K+ channel (GIRK) are really "outward rectifiers" in the sense that they have K+ going out of the cell. This causes hyperpolarization at the end of the cardiac action potential. The channels open, K+ rushes out, and the cell becomes really negative. Then these channels close, and the cell gets back to original Vm.
THE STRONGER THE GIRK, THE MORE HYPERPOLARIZED post-action potential, and therefore THE LONGER IT TAKES BETWEEN ACTION POTENTIALS.
Acetylcholine functions to slow the heart rate by activating GIRK channels. |
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Term
| Relate acetylcholine to the patch clamp stuff and heart rate. |
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Definition
| So, you know that acetylcholine functions with a membrane delimited mechanism, because when you do patch clamp with excision, the K+ channels only work when you add acetylcholine into the pipette. This makes you realize that a gpcr is involved, because the ligand has to bind on the extracellular side. This has to do with gprotein beta-gamma subunits. |
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