The Journal of Neurophysiology Vol. 88 No. 4 October 2002, pp. 1843-1850
Copyright ©2002 by the American Physiological Society

Cellular Mechanisms of Nociception in the Frog

 ¹Institute of Physiology, Academy of Sciences, Prague 4, Vídenská 1083, Czech Republic; and  ²Institute of Neurobiology, Unité Propre de Recherche, San Juan, Puerto Rico 00901

Kuffler, D. P., A. Lyfenko, L. Vyklický, and V. Vlachová. Cellular Mechanisms of Nociception in the Frog. J. Neurophysiol. 88: 1843-1850, 2002. Cellular mechanisms underlying defense reactions induced by noxious heat and acids were studied in frogs (Rana pipiens) by measuring whole cell membrane currents in cultured dorsal root ganglion (DRG) neurons. Seventy-eight of 82 DRG neurons exposed to 3-s ramps of increasing temperature to 48°C exhibited an inward current (I_HEAT) of 490 ± 70 pA at 70 mV. I_HEAT exhibited reversal at ~10 mV with a pronounced outward rectification, suggesting opening of nonselective cation channels. In frogs, in contrast to mammals, I_HEAT was not influenced by capsaicin (5 µM), capsazepine (10 µM), or ruthenium red (10 µM). In a large proportion (~80%) of heat-sensitive DRG neurons, acids produced a large slowly inactivating sodium carried current (I_ACID) with average pH₅₀ 5.7. I_ACID was blocked by 1 mM amiloride (to 22%) and was absent if extracellular Na⁺ was substituted by Cs⁺. Elevating temperature to 38°C increased I_ACID, whereas temperatures >40°C profoundly inhibited it (by 82 ± 2%; n = 42). The inhibition was long-lasting (>30 s) but fully reversible. Phorbol ester myristate acetate (PMA, 1 µM) and forskolin (1 µM) inhibited I_ACID to 37 ± 5% (n = 5) and 78 ± 8% (n = 4), respectively. It is suggested that I_HEAT in frog DRG neurons is carried through capsaicin-insensitive nonselective cation channels distinct from vanilloid receptor in mammals, whereas I_ACID is carried through amiloride-sensitive sodium channels that are strongly inhibited by noxious heat, possibly due to activation of the intracellular messenger systems.