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J Neurophysiol 85: 1340-1345, 2001;
0022-3077/01 $5.00
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The Journal of Neurophysiology Vol. 85 No. 3 March 2001, pp. 1340-1345
Copyright ©2001 by the American Physiological Society

RAPID COMMUNICATION

Venom From the Platypus, Ornithorhynchus anatinus, Induces a Calcium-Dependent Current in Cultured Dorsal Root Ganglion Cells

G. M. de Plater,1,2 P. J. Milburn,2 and R. L. Martin3

 1Division of Neuroscience and  2Division of Biochemistry and Molecular Biology, John Curtin School of Medical Research; and  3Division of Biochemistry and Molecular Biology, The Faculties, Australian National University, Canberra, ACT 0200, Australia

de Plater, G. M., P. J. Milburn, and R. L. Martin. Venom From the Platypus, Ornithorhynchus anatinus, Induces a Calcium-Dependent Current in Cultured Dorsal Root Ganglion Cells. J. Neurophysiol. 85: 1340-1345, 2001. 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 Ca2+-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.






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