Abstract
Using the whole cell patch clamp technique, a population of nociceptors were identified, by virtue of their small size and capsaicin responsivity. Response to capsaicin was increased following treatment with the hyperalgesic prostaglandins, PGE2 and PGI2. Treatment of the cells with the cyclic adenosine monophosphate (cAMP) analogues, 8 bromo cAMP and dibutyryl cAMP, also resulted in an increase in the capsaicin-induced currents. The effects of the cAMP analogues were greater than that produced by prostaglandin treatment. We conclude that PGE2 and PGI2 act directly on nociceptors, with cAMP as second messenger, to sensitize them to noxious stimulation.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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1-Methyl-3-isobutylxanthine / pharmacology
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8-Bromo Cyclic Adenosine Monophosphate / pharmacology
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Animals
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Bucladesine / pharmacology
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Capsaicin / pharmacology*
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Cells, Cultured
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Dinoprostone / pharmacology*
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Epoprostenol / pharmacology*
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Evoked Potentials / drug effects
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Ganglia, Spinal / physiology*
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Membrane Potentials / drug effects
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Neurons / drug effects
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Neurons / physiology*
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Nociceptors / drug effects
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Nociceptors / physiology*
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Rats
Substances
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8-Bromo Cyclic Adenosine Monophosphate
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Bucladesine
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Epoprostenol
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Dinoprostone
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Capsaicin
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1-Methyl-3-isobutylxanthine