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J Neurophysiol (April 1, 2003). 10.1152/jn.00748.2002
Submitted on Submitted 3 September 2002; accepted in final form 29 November 2002
Department of Physiology, University of Kentucky Medical Center, Lexington, Kentucky 40536
Gu, Qihai,
Kevin Kwong, and
Lu-Yuan Lee.
Ca2+ Transient Evoked by Chemical Stimulation Is
Enhanced by PGE2 in Vagal Sensory Neurons: Role of cAMP/PKA
Signaling Pathway. J. Neurophysiol. 89: 1985-1993, 2003. 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
107 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 × 107 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
(106 M; 5 min), an activator of adenylyl
cyclase, and 8-(4-chlorophenylthio)adenosine-3'-5'-cyclic monophosphate
(CPT-cAMP; 3 × 106 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; 105 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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