neurotransmitter question

[DRfej]

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drugs that bind to the neurotransmitters receptor on hte postsnyaptic membrane without activating them are???

a) receptor collaborators
b) agaonists of the NT
c) antagonist of the NT
d) a mechanism for deactivation

 

[marcusnasland]

I would say c... depending on concentration of antagonist will change effect.

An example could be poison darts (curare) which is an antagonist to acetylcholine... The curare blocks acetylcholine receptors on junctional folds of motor end plate, which stops the action potential from reaching the terminal cisternae, thus we suffer anything from muscle weakness, to paralysis, to cardiac arrest depending on the concentration of curare in the neromuscular junction.

 

[MTD52]

The answer above makes sense, but it seems like it can also be D, because something that binds to the postsynaptic membrane receptor and doesn't activate it could be also be seen as "deactivating" the cell. That being said, if the postsynaptic cell was never activated to begin with, I guess it isn't technically being "deactivated." Seems like the best choice, then, would probably be C, as stated above.

This a pretty poorly worded question IMO.

 

[cyrano]

a) receptor collaborators- No idea what this is
b) agonists of the NT- Opposite of what is right. Agonists perform the same function of opening the channel (activate), but sometimes for different amounts of time. e.g. muscarine in musacrinic Ach receptors or nicotine in nicotinic Ach receptors
c) antagonist of the NT- Bingo! The example of curare is a great one. It bings Ach receptors for a pretty long period of time which does indeed cause muscle weakness. Another example would be bungarotoxin (found in some poisonous snakes) which binds the same receptor but the binding is completely irreversible and results in death because your lung muscles cannot contract so you cannot inhale 🙁
d) a mechanism for deactivation - At first this sounds like a decent answer but upon further review I think we can say it's wrong. Before a drug binds to a channel the channel is closed (almost always). So if a drug binds to a channel and is an antagonist that means it just keeps the channel closed. It's not "deactivating" anything. It's basically just keeping the status quo going (no change in membrane potential). Now keeping the status quo can definitely result in inactivity, but it was not "deactivated" per exactly because you didn't "turn it off".

Now let's flip the system and say we have a hormone going out to close channels. Now an antagonist to this hormone would lock the channel in an open position. Once again we aren't deactivating or changing the action of the channel, instead we are just preventing the affects of the hormone.

 

[BaylorDDS]

The question can be confusing but is not worded poorly. Nerves receive different signals that inhibit them and excite them. So a deactivating mechanism would be another nerve sending an inhibitory signal to the nerve, or a molecule binding to a receptor on the membrane (obviously a different receptor than the NT binds) and sending an inhibitory signal to the nerve.

 

[cyrano]

The question can be confusing but is not worded poorly. Nerves receive different signals that inhibit them and excite them. So a deactivating mechanism would be another nerve sending an inhibitory signal to the nerve, or a molecule binding to a receptor on the membrane (obviously a different receptor than the NT binds) and sending an inhibitory signal to the nerve.

Are you certain that deactivation is synonymous with inhibition? I'm inclined to think otherwise. Inhibition is almost always the activation of certain channels. e.g. The activation of the Ca2+-calmodulin complex dependent chloride channels in the olfactory system that result in adaptation (smell cookies baking at first, but after a while you don't smell them without taking a big whiff of fresh air). This invokes an IPSP that degrades the EPSP which results in the membrane potential dipping below AP producing threshold.