Seppi
Bluelighter
- Joined
- Feb 22, 2014
- Messages
- 294
Could you explain that simpler please? really trying to understand.
thanks.
I mean most nociceptors are voltage-gated ion channels, not ligand-gated ion channels. The difference between the two is that the voltage-gated ion channel's primary/physiological gating mechanism is membrane voltage instead of ligand binding, which is the primary gating mechanism for ligand-gated ion channels (i.e., they require one or more ligands to be bound to an active site on the receptor in order for the channel to open - most LGICs require 1 ligand, but some like the NMDA receptor require the simultaneous binding of 2 distinct ligands for channel gating); however, like I said before, the function of some of those voltage-gated ion channels can be modulated by the binding of a ligand to a binding site on the ion channel protein.
To rephrase that as simply as possible, I stated that "nociceptor" was a misnomer because the "-ceptor" suffix implies that these proteins, most of which are voltage-gated ion channels, are receptors; but, unlike receptor proteins, a number of voltage-gated ion channels do not possess a ligand binding site. Rather, the gate on these channels simply opens/closes in response to (i.e., these channels are gated by) changes in membrane voltage.
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