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The Journal of Neurophysiology Vol. 81 No. 6 June 1999, pp. 2612-2619
Copyright ©1999 by the American Physiological Society
Institut für Physiologie und Experimentelle Pathophysiologie, Friedrich Alexander University, D91054 Erlangen-Nuremberg, Germany
Kress, M. and
S. Guenther.
Role of [Ca2+]i in the ATP-Induced Heat
Sensitization Process of Rat Nociceptive Neurons. J. Neurophysiol. 81: 2612-2619, 1999.
Role of [Ca2+]i in the ATP-induced heat
sensitization process of rat nociceptive neurons. In inflamed
tissue, nociceptors show increased sensitivity to noxious heat, which
may account for heat hyperalgesia. In unmyelinated nociceptive
afferents in rat skin in vitro, a drop of heat threshold and an
increase in heat responses were induced by experimental elevation of
intracellular calcium ([Ca2+]i) levels with
the calcium ionophore ionomycin (10 µM). Similar results were
obtained in experiments employing [Ca2+]i
release from preloaded "caged calcium" (NITR-5/AM) via UV
photolysis. In both cases, sensitization was prevented by preventing
rises in [Ca2+]i with the membrane-permeant
calcium chelator BAPTA-AM (1 mM). No pronounced change of mechanical
sensitivity was observed. Heat-induced membrane currents
(Iheat) were investigated with patch-clamp
recordings, and simultaneous calcium measurements were performed in
small sensory neurons isolated from adult rat dorsal root ganglia
(DRG). Ionomycin-induced rises in [Ca2+]i
resulted in reversible sensitization of
Iheat. In the same subset of DRG neurons,
the endogenous algogen ATP (100 µM) was used to elevate
[Ca2+]i, which again resulted in significant
sensitization of Iheat. In correlative
recordings from the skin-nerve preparation, ATP induced heat
sensitization of nociceptors, which again could be blocked by
preincubation with BAPTA-AM. Rises in [Ca2+]i
in response to inflammatory mediators, e.g., ATP, thus appear to play a
central role in plastic changes of nociceptors, which may account for
hypersensitivity of inflamed tissue.
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M. Tominaga, M. Wada, and M. Masu From the Cover: Potentiation of capsaicin receptor activity by metabotropic ATP receptors as a possible mechanism for ATP-evoked pain and hyperalgesia PNAS, June 5, 2001; 98(12): 6951 - 6956. [Abstract] [Full Text] [PDF]
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