I've checked in Medline now, and it turns out that Platypus venom is very special. It causes immediate intense pain, and pain as well as paralysis can last for days or months. However, the interesting thing is that it also frequently leads to hyperalgesia, which is not typical for venoms in general. Studies indicate that this is due to the Platypus venom acting directly on nociceptors, ie pain receptors. Because of this unique property, it is hypothesised that it may possibly be useful as a painkiller.
Perhaps Craig posted a sad smiley because he thought of the platypuses, should this hypothesis turn out correct? Don't worry, the venom will be synthesised - besides, I am sure you can extract the venom from the spurs without harming the platypus.J Neurophysiol 2001 Mar;85(3):1340-5
Venom from the platypus, Ornithorhynchus anatinus, induces a calcium-dependent current in cultured dorsal root ganglion cells.
de Plater GM, Milburn PJ, Martin RL.
Division of Neuroscience, Australian National University, Canberra, ACT 0200, Australia.
The platypus (Ornithorhynchus anatinus), a uniquely Australian species, is one of the few living venomous mammals. Although envenomation of humans by many vertebrate and invertebrate species results in pain, this is often not the principal symptom of envenomation. However, platypus envenomation results in an immediate excruciating pain that develops into a very long-lasting hyperalgesia. We have previously shown that the venom contains a C-type natriuretic peptide that causes mast cell degranulation, and this probably contributes to the development of the painful response. Now we demonstrate that platypus venom has a potent action on putative nociceptors. Application of the venom to small to medium diameter dorsal root ganglion cells for 10 s resulted in an inward current lasting several minutes when the venom was diluted in buffer at pH 6.1 but not at pH 7.4. The venom itself has a pH of 6.3. The venom activated a current with a linear current-voltage relationship between -100 and -25 mV and with a reversal potential of -11 mV. Ion substitution experiments indicate that the current is a nonspecific cationic current. The response to the venom was blocked by the membrane-permeant Ca(2+)-ATPase inhibitor, thapsigargin, and by the tyrosine- and serine-kinase inhibitor, k252a. Thus the response appears to be dependent on calcium release from intracellular stores. The identity of the venom component(s) that is responsible for the responses we have described is yet to be determined but is probably not the C-type natriuretic peptide or the defensin-like peptides that are present in the venom.
Or, alternatatively, Craig may have referred to the long term pain and hyperalgesia induced by platypus poison, but this is thankfully not a chronic pain condition, it goes into remission spontaneously after some time.
