Who is the culprit who tortures humans, who does bad things to good people, who reduces mankind to its lowest condition, actually presaging hell, as it were? Pain is the dark side of the force, the diabolical extinguisher of hope and happiness. It was perhaps meant to protect us from injury, but going rogue, it is anything but a friend. Existing theory points to the ion channels which permit impulses to travel along nerves via what has been called an “action potential”:, which is a sort of current flow achieved by ions of sodium and calcium moving across the nerve membrane.
Just when TRPV1 ion channel was taking all the blame, it turns out that that particular calcium ion channel might have an accomplice. The putative stalking horse goes by the name of TRPA 1 or ankyrin 1.
The transient receptor ion channels are potent activators of pain neurons. While TRPV1 has gotten most of the attention, now studies suggest another channel might well be a co conspirator. In this field, those seeking relief, the disappointed guinea pigs of pain, know not to be overenthusiastic or to start counting our chickens, but at least the new work shows researchers are still investigating. Pain research is not totally dead. Not everyone thinks anticonvulsants are all that a patient in a pain crisis unresponsive to opiates could possibly desire.
Just to make you suitably confused, investigators have reported that a new drug, ADM-09, results in “calcium-mediated binding of the carnosine residue and disulphide-bridge-forming of the lipoic acid residue accounts for the observed persistent blocking or TRPA1. Feel better? Okay, not yet, but somehow just knowing the whole business of basic pain research has not gone away entirely, that scientific gobbledygook can help keep the spirits up. That phraseology just used to snow you actually means ADM_09 is an effective antagonist of the nociceptive sensor channel..”
Or, in other words, if we could block TRPA-1 we might be able to block pain.
This was reported in:
A TRPA1 antagonist reverts oxaliplatin-induced neuropathic pain.