CALCIUM CHANNELS AND PAIN, PART IV. (CaV2.2 is the channel of the capsaicin TRPV-1 receptor) J. McGivern and S. McDonough

We continue with a review of information supplied by McGivern and McDonough. Once again, we thank them for their kind support.We attempt to use nociceptin as an example of why pain blockers outside the opioid pathways are desirable. We attempt to explain why this is relevant and necessary in the hunt for the paths of central pain. We especially encourage your reading about bypassing of the cord by various routes of the autonomic nervous system and why N-type calcium channel chemistry hints at a role for the autonomic system/visceral afferents and compares opiate counterfeiters (NOF/Q) in CP. As before, we acknowledge the input by McGivern and McDonough, cited above.

N-type calcium channels encoded by the CaV2.2 gene are expressed ONLY in neurons. Furthermore, they are expressed in all parts of the neuron. A signal which has passed through a synapse, hits the incoming part of a neuron, passes through the cell body, degrades in strength, and then if powerful enough sets off an action potential or spike in the transmitter segment which is right at the beginning of the axon. N-type calcium channels are there all the way.

The behavior of conscious nerves seems more or less intuitive, but when we get to the autonomics (unconscious nervous system), things get very freaky. You would not guess what happens. Central pain provides one of the most persuasive evidences that the unconscious nervous system not only interfaces with and can