Opioid inhibition of Ih via adenylyl cyclase

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Abstract

Opioids are coupled through G proteins to both ion channels and adenylyl cyclase. This study describes opioid modulation of the voltage-dependent cation channel, Ih, in cultured guinea pig nodose ganglion neurons. Forskolin, PGE2, and cAMP analogs shifted the voltage dependence of activation of Ih to more depolarized potentials and increased the inward current at -60 mV. Opioids had no effect on In alone, but reversed the effect of forskolin on Ih. This action of opioids was blocked by naloxone. Opioids had no effect on In in the presence of CAMP analogs, suggesting that modulation occurs at the level of adenylyl cyclase. The shift in the voltage dependence of Ih by agents that induce inflammation (i.e., PGE2), is one potential mechanism to mediate an increased excitability. Opioid inhibition of adenylyl cyclase and subsequent inhibition of In may be a mechanism by which opioids inhibit primary afferent excitability and relieve pain.

Original languageEnglish (US)
Pages (from-to)179-186
Number of pages8
JournalNeuron
Volume13
Issue number1
DOIs
StatePublished - 1994

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Adenylyl Cyclases
Opioid Analgesics
Colforsin
Dinoprostone
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
Nodose Ganglion
Naloxone
Inhibition (Psychology)
Ion Channels
GTP-Binding Proteins
Guinea Pigs
Inflammation
Neurons
Pain

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Opioid inhibition of Ih via adenylyl cyclase. / Ingram, Susan; Williams, John.

In: Neuron, Vol. 13, No. 1, 1994, p. 179-186.

Research output: Contribution to journalArticle

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