Term
How do ligand gated channels sorta work? |
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Definition
A ligand binds inducing conformational change opening channel |
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Term
How long does it take for a ligand gated channel to open? |
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Definition
Like no time at all. milliseconds? |
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Term
Are ligand gated channels specific to specific ions? |
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Definition
NO, they let all the stuff just flowwww |
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Term
Can you get an action potential caused by a ligand gated channel? |
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Definition
yes, they can depolarize the membrane causing action potential |
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Term
What do excitatory ligand gated channels do? |
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Definition
They get horny. Actually...they usually have stuff flow into the cell. This depolarizes and causes action potential |
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Term
What do inhibitory ligand gated channels do? |
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Definition
They let K+ out usually, or bring alotta Cl- in. This hyperPOlarizes the membrane, inhibiting action potential.
However, a point he wants us to know here is that Cl- doesn't actually alter the Vm, it somehow decreases membrane resistance--making it harder for the cell to depolarize |
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Term
What are the two major families of ligand gated channels? |
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Definition
Cys-loop and glutamate receptors |
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Term
What are two famous examples of Cys-loop channels and what do they do? |
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Definition
nicotinic acetylcholine receptor--nonselective cation channel which depolarizes the membrane (and gets attacked in myasthenia gravis); and GABA receptor--brings in Cl-, inhibiting action potential |
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Term
What does glutamate receptor do? |
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Definition
It mediates fast synaptic activity in the brain. There are NMDA type and AMPA type. Activated by excitatory neurotransmitter, glutamate. |
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Term
What is special about the Cys-loop receptor? |
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Definition
There is this large extracellular loop at the N-terminus that has cysteine bonds. |
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Term
How are cys loop channels opened? |
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Definition
each cys-loop receptor has two binding sites for ligand. each must be bound for the thing to open |
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Term
What type of ions do nicotinic acetylcholine receptors select for, and how? |
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Definition
they select for cations by having a bunch of negatively charged residues on the outside |
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Term
Do nicotinic acetylcholine channels get rid of hydration spheres like other types of channels? |
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Definition
No, the hydration spheres can fit in |
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Term
How does the nicotinic acetylcholine receptor gate work? |
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Definition
When the ligands are unbound, there is a hydrophobic region which swings in towards the channel--blocking it. When the ligands are bound, conformational change forces the hydrophobic segments to swing out, opening gate. |
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Term
Which type of GABA receptor is ligand gated? |
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Definition
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Term
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Definition
gamma-aminobutyric acid (a neurotransmitter) |
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Term
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Definition
mediates fast inhibitory transmission in the brain |
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Term
What do GABA receptors' channels select for, and how do they do this? |
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Definition
They are for Cl-, and they do this by having positive residues around the pore |
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Term
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Definition
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Term
Why are glutamate receptors considered differently from all the cys-loop ones? |
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Definition
These guys have a very different structure |
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Term
What is the pore structure of Glutamate receptor channel? |
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Definition
There is a little P-loop like thing |
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Term
What are the two types of glutamate receptors and what are they selective for? |
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Definition
AMPA is selective for Na+ and K+. NMDA is selective for Ca2+ |
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Term
How are glutamate receptors opened? |
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Definition
glutamate binds. NMDA also requires glycine and it needs to get extracellular Mg+ away (by having hyperdepolarization) |
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Term
How does this all happen at a synapse? |
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Definition
Glutamate is released by presynaptic neuron. Receptors are on postsynaptic neuron. they bind AMPA and NMDA glutamate receptors, but only the AMPA open (because Mg+ is bound to the NMDA). The AMPA start depolarizing the cell by letting in Na+ and K+. This depolarization eventually kicks out the Mg+ from the NMDA because the cell is less negative. Then (assuming glycine is also bound) the NMDA ones will open.
Ca2+ now flows into the postsynaptic neuron through the NMDA channels, activating enzymes and producing long-lasting changes in the efficiency of communication between the presynaptic and postsynaptic neuron that are thought to underlie the formation of memories. |
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