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Related Experiment Videos

Opioids at low concentration decrease openings of K+ channels in sensory ganglion neurons.

S F Fan1, K F Shen, S M Crain

  • 1Department of Neuroscience, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY 10461.

Brain Research
|August 30, 1991
PubMed
Summary
This summary is machine-generated.

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Opioid agonists decrease voltage-sensitive potassium channel activity in dorsal root ganglion neurons. This modulation, mediated by diffusible second messengers, influences action potential duration and sensory neuron excitability.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cell Biology

Background:

  • Opioids affect action potential duration (APD) in dorsal root ganglion (DRG) neurons.
  • Low opioid concentrations prolong APD, while higher concentrations shorten it.

Purpose of the Study:

  • To investigate the mechanisms underlying opioid modulation of DRG neuron excitability.
  • To determine the role of voltage-sensitive potassium channels in opioid effects.

Main Methods:

  • Whole-cell and cell-attached patch voltage-clamp recordings from cultured DRG neurons.
  • Application of mu, delta, and kappa opioid agonists (DAGO, DPDPE, dynorphin) at picomolar to nanomolar concentrations.
  • Use of opioid receptor antagonists (naloxone, diprenorphine) to block opioid effects.

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Main Results:

  • Opioid agonists reversibly decreased voltage-sensitive K+ channel activity in DRG neurons.
  • Naloxone and diprenorphine prevented opioid-induced decreases in K+ channel activity, confirming receptor specificity.
  • Opioid effects on K+ channels occurred even when the channels were in a sealed-off membrane patch, suggesting diffusible second messengers.

Conclusions:

  • Opioid-induced changes in DRG neuron excitability are mediated by diffusible second messengers.
  • Excitatory effects of opioids on sensory neurons involve Gs-linked excitatory opioid receptors and cyclic AMP-dependent ionic channels.