Ca2+ transient evoked by chemical stimulation is enhanced by PGE2 in vagal sensory neurons: Role of cAMP/PKA signaling pathway

Qihai Gu, Kevin Kwong, Lu Yuan Lee

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68 Scopus citations


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 (3 × 10-8 to 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 (3 × 10-7 M; 5 min), the peak of this capsaicin-evoked Ca2+ transient was increased by almost fourfold, 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 8-(4-chlorophenylthio)adenosine-3′-5′-cyclic monophosphate (CPT-cAMP; 3 × 10-6 M, 10 min), a membrane-permeable cAMP analogue. Furthermore, the potentiating effects of PGE2, forskolin, and CPT-cAMP were abolished by N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (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.

Original languageEnglish
Pages (from-to)1985-1993
Number of pages9
JournalJournal of Neurophysiology
Issue number4
StatePublished - Apr 1 2003

ASJC Scopus subject areas

  • General Neuroscience
  • Physiology


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