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1 Department of Physiology, University of Kentucky Medical Center, Lexington, KY, USA
* To whom correspondence should be addressed. E-mail: lylee{at}uky.edu.
The effect of prostaglandin E2 (PGE2) on chemical stimulation-evoked calcium (Ca2+) transient was investigated in isolated vagal sensory neurons of the rat using fura-2-based ratiometric Ca2+ imaging. Application of capsaicin (3x10-8 - 10-7 M; 15 s) caused a rapid surge of intracellular Ca2+ concentration in small- and medium-size neurons; the response was reproducible when >10 min elapsed between two challenges, and was absent in nominally Ca2+-free solution. After pretreatment with PGE2 (3x10-7 M; 5 min), the peak of this capsaicin-evoked Ca2+ transient was increased by almost four-fold, and its duration was also prolonged. This augmented response to capsaicin induced by PGE2 gradually declined, but remained higher than control after 15-min washout. Similarly, PGE2 pretreatment also markedly enhanced the Ca2+ transients induced by other chemical stimulants to C neurons, such as phenylbiguanide (PBG), adenosine 5'-triphosphate (ATP) and KCl. The Ca2+ transients-evoked by PBG, ATP and KCl were potentiated after the pretreatment with PGE2 to 242%, 204% and 163% of their control, respectively. This potentiating effect of PGE2 could be mimicked by forskolin (10-6 M; 5 min), an activator of adenylyl cyclase, and CPT-cAMP (3x10-6 M, 10 min), a membrane permeable cAMP analogue. Furthermore, the potentiating effects of PGE2, forskolin and CPT-cAMP were abolished by H89 (10-5 M; 15 - 20 min), a protein kinase A (PKA) inhibitor. In summary, these results show that PGE2 reversibly potentiates the chemical stimuli-evoked Ca2+ transients in cultured rat vagal sensory neurons, and this potentiating effect is mediated through the cyclic AMP/PKA transduction cascade.
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