This article draws attention to one of the more interesting analgesic agents for possible therapy.

Kim et al, in Oct 2005 Brain Research have shed new light on anandamide.

Anandamide is the ethanol amide of arachidonic acid. You already know from the many articles here that arachidonic acid is the precursor of the prostaglandins, which play a role in pain. This modified arachidonic acid is manufactured by the body. It seems to be another case where modification of one peptide or protein inactivates the original product. This is seen in the way GABA inhibits Glutamate, its close cousin.

Anandamide acts at least on the sodium channels, but not in all states. Anandamide is what we call an endogenous cannabinoid, which means it is made in the body and acts on the channels where cannabis acts. There are two cannabis channels CB1 and CB2 and anandamide acts at both of them. It also acts at the vanilloid 1 receptor, which is also known as the Transient Receptor Potential Vanilloid receptor, or TRPV-1.

A neuron is typically polarized with the outside negative relative to the inside. When the relative negativity is really large, it is hard for the neuron to fire an action potential. Around -80 millivolts, we begin to speak of an “inactivated” neuron, it is just too negative to want to fire. When the voltage gets very unlikely to fire, we call it a “resting” neuron. Anandamide works on inactive neurons, but it seems to have little effect on resting neurons. Kim et al used tetradotoxin to try to see which sodium channels were reached by anandamide, and found that both TTX sensitive and TTX resistant channels showed similar effects under the influence of anandamide. Currently, this protein is being considered of possible benefit for peripheral neuropathic pain but NOT for central pain. However, as the molecules are tinkered with, we may come up with something that acts in the central nervous system. Be patient. Help is coming.