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Articles in PresS, published online ahead of print August 1, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00050.2002
Submitted on January 28, 2002
Accepted on July 26, 2002
1 Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman, WA, USA
* To whom correspondence should be addressed. E-mail: simasko{at}vetmed.wsu.edu.
Imaging fluorescent measurements with fura-2 were used to examine cytosolic calcium signals induced by sulfated cholecystokinin octapeptide (CCK-8) in dissociated vagal afferent neurons from adult rat nodose ganglia. We found that 40% (184/465) of the neurons responded to CCK-8 with a transient increase in cytosolic calcium. The threshold concentration of CCK-8 for inducing the response varied from 0.01 nM to 100 nM. In most neurons (13/16) the response was eliminated by removing extracellular calcium. Depleting intracellular calcium stores with thapsigargin slightly augmented the response. Most neurons were unresponsive to nonsulfated CCK-8. The response was eliminated by the CCK-A receptor antagonist lorglumide. Low concentrations of JMV-180 had no effect, however high concentrations of JMV-180 reduced responses to CCK-8. These results demonstrate that CCK acts at the low affinity site of the CCK-A receptor to trigger the entry of extracellular calcium into vagal afferent neurons. Increased cytosolic calcium may participate in acute activation of vagal afferent neurons, or it may initiate long-term changes, which modulate future neuronal responses to sensory stimuli.
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