Calcium Channels and Pain Part V. (ziconotide) J. McGivern and S. McDonough

This is a further review of material provided to painonline by McGivern and McDonough. We thank them deeply for their input. For what it is worth, they are experts on sodium channels as well, but we review only their publications on calcium channels. And once again, we are glad a company such as Amgen has this caliber of researchers on board.

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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.

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Calcium Channels and Pain, Part II, (The alpha-1 subunits are the basic componnents of channels) J. McGivern and S. McDonough

Thanks once again to McGivern and McDonough for providing the materials on which this series is based. The culprits in central pain, the calcium ion channels (complicated pores) in the membrane of the neuron, are further described here. For simplicity’s sake, it may help to think of a channel as a very long lens shaped tubule, containing angles and many series of shutters, in which the leaves of the shutters open and close in sequence to “squeeze” calcium through the neuronal membrane, with other structures able to slow or increase the calcium flow by keeping the leaves of the shutters in wider or narrower position.

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