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Am J Physiol Gastrointest Liver Physiol 282: G1002-G1008, 2002; doi:10.1152/ajpgi.00313.2001
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Vol. 282, Issue 6, G1002-G1008, June 2002

Characterization of CCKA receptor affinity states and Ca2+ signal transduction in vagal nodose ganglia

Tim O. Lankisch, Yasuhiro Tsunoda, Yuanxu Lu, and Chung Owyang

Gastroenterology Research Unit, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan 48109

CCKA receptors are present on vagal afferent fibers. The objectives of this study were to identify the presence of high- and low-affinity CCKA receptors on nodose ganglia and to characterize the intracellular calcium signal transduction activated by CCK. Stimulation of acutely isolated nodose ganglion cells from rats with 1 nM CCK-8 primarily evoked a Ca2+ transient followed by a sustained Ca2+ plateau (45% of cells responded), whereas 10 pM CCK-8 evoked Ca2+ oscillations (37% of cells responded). CCK-OPE, a high-affinity agonist and low-affinity antagonist of CCKA receptors, primarily elicited Ca2+ oscillations (29% of cells responded). CCK-OPE inhibited the Ca2+ transient induced by 1 nM CCK-8 but not by carbachol and high K+. This result suggests the presence of high- and low-affinity states of CCKA receptors on nodose ganglia. We further demonstrated that nicardipine (10 µM) but not omega -conotoxins GVIA and MVIIC (10-100 nM) abolished Ca2+ signaling induced by CCK-8, indicating that an L-type voltage-dependent Ca2+ channel and not an N- or Q-type Ca2+ channel is coupled to CCKA receptors. In a separate study, we showed that the G protein activator NaF (10 mM) elicited a Ca2+ transient and inhibited CCK-8-evoked Ca2+ signaling, indicative of G protein(s) involvement in CCKA receptor activity. The Gq protein antagonist Gp antagonist-2A (10 µM) also abolished the action of CCK-8. This study indicates that CCKA receptors exist in both high- and low-affinity states in the nodose ganglia. Activation of high-affinity CCKA receptors elicits Ca2+ oscillations, whereas stimulation of low-affinity CCKA receptors evokes a sustained Ca2+ plateau. These Ca2+-signaling modes are mediated through the L-type Ca2+ channel and involve the participation of Gq protein.

cholecystokinin; cholecystokinin A receptors; Ca2+ signaling


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