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We're a little crazy, about science!

Snail Venom and Pain Relief

sea snail venom

There is no pain like nerve pain. Unfortunately my sister and me both know all too well how bad pain can actually get, her especially. After desperately trying everything from morphine derivatives to a combination of calcium and sodium channel blockers we had exhausted all attempts at keeping her pain at bay. That is where the story would’ve ended too, if it wasn’t for the sea snails.

[Loony hint: Sodium and calcium channel blockers help reduce nerve pain by blocking, or partially blocking signals between nerves. To send messages nerves use certain charged particles, namely calcium or sodium. Blocking those signals can reduce pain. Calcium channel blockers are typically used in people with heart problems, but is also used to treat pain.]

When all seemed lost for my sister we found hope from a chronic pain specialist who offered a different approach to manage the pain, sea snail venom. As it turns out the venom from marine cone snails– used to immobilize prey– contain different peptides [which are just chains of amino acids] called conotoxins, some of which can be used as painkillers in mammals.

A recent study published in The Journal of General Physiology offers some insight into the mechanisms which give pain relief, at least in one particular conotoxin, Vc1.1. The findings help explain the pain relieving powers of this toxin and could [ideally] lead to synthetic forms of Vc1.1 to treat certain types of neuropathic pain in humans.

For those of you who didn’t click the link, neuropathic pain is some of the most painful kind of pain around, it’s hard to treat and even harder to live with. Normally it is associated with an injury, or a dysfunction in the nervous system –such as a birth defect, or in the case of my sister an autoimmune disease, in which the body attacks parts of itself mistaking those parts for foreign invaders.

Neuropathic pain is associated with changes in the transmission of signals between neurons, a process that depends on several types of voltage-gated calcium channels [VGCCs]. However, given the importance of these VGCCs in mediating normal neurotransmission [things as simple as feeling or something more complex like regulating heartbeat], using them as a pharmacological target against neuropathic pain can potentially lead to undesirable side effects and unfortunately typically do. 

This is where it gets a little technical. In previous studies, it was found that Vc1.1 acted against neuropathic pain in mice; they found that, rather than acting directly to block VGCCs, Vc1.1 acts through a different receptor GABA type B [GABABR].

It’s not important to understand the function per see, just that when Vc1.1 acts on the GABA type B receptors it inhibits the N-type [Cav 2.2] channels– a type of calcium channel. In other words it doesn’t block the calcium channel directly [like parking a car in a parking spot blocks that spot] it blocks it through a different mechanism [like closing the garage door to block the parking spot, even if the spot itself is technically open].

This new study shows that Vc1.1 [sea snail venom] also acts on another, not very well understood  channel, R-type [Cav.2.3] channels– another type of calcium channel. R-type calcium channels have been implicated in pain signaling, but their function hasn’t been understood. The new findings may not only help solve the mystery of the R-type calcium channels, but identify them as targets for pain relieving conotoxins.

As for my sister, prialt [or ziconotide] has changed her life. There are some hiccups, after all this is sea snail venom so the side effect list is very long. What will the future hold? Well ideally we will develop a synthetic version that will be more targeted, therefore eliminating or minimizing the side effects.

Know all your different calcium channels? You probably want the full study, which you can find — here!

Source:
Berecki G., McArthur J.R., Cuny H., Clark R.J. & Adams D.J. (2014). Differential Cav2.1 and Cav2.3 channel inhibition by baclofen and alpha-conotoxin Vc1.1 via GABAB receptor activation, The Journal of General Physiology, 143 (4) 465-479. DOI:

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