• N&PD Moderators: Skorpio | thegreenhand

Any other Analgesia Neurotransmitters/Receptors?

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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serotonin can also contribute to the analgesic acion of opioids,see tramadol.Calcium channels action can help with neuropathic pain

Nefopam was supposedly serotonin mediated. My Merck Index is somewhat out of data so I would really need to search to see if it has been studied further. It's been around in the UK for 30+ years. Apparently it has abuse potential! I am amazed. It just made me feel odd..... well, odder than usual.
 
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