Enhancement of beta-adrenergic responses by Gi-linked receptors in rat hippocampus

Neuron. 1993 Jan;10(1):83-8. doi: 10.1016/0896-6273(93)90244-l.

Abstract

Many excitable cells express a class of neurotransmitter receptors functionally defined by their ability to increase potassium conductance through G proteins of the Gi/G(o) class that directly activate the potassium channels. Biochemical studies have shown that these same receptors can also inhibit forskolin-stimulated adenylyl cyclase, although the functional significance of this effect remains unclear. In this study electrophysiological techniques were used to examine how activation of serotonin and gamma-aminobutyric acid receptors belonging to this class affect beta-adrenergic responses signaled through adenylyl cyclase. Surprisingly, activation of these receptors not only failed to inhibit but actually enhanced beta-adrenergic responses. These observations are consistent with evidence indicating that Gi-linked receptors can enhance the ability of Gs to stimulate certain adenylyl cyclases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenylyl Cyclases / metabolism
  • Animals
  • Baclofen / pharmacology
  • Colforsin / pharmacology
  • Electric Conductivity
  • Electrophysiology
  • GTP-Binding Proteins / physiology*
  • Hippocampus / drug effects
  • Hippocampus / physiology*
  • Male
  • Norepinephrine / pharmacology
  • Potassium Channels / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Adrenergic, beta / physiology*
  • Receptors, GABA-A / physiology
  • Receptors, Serotonin / physiology

Substances

  • Potassium Channels
  • Receptors, Adrenergic, beta
  • Receptors, GABA-A
  • Receptors, Serotonin
  • Colforsin
  • GTP-Binding Proteins
  • Adenylyl Cyclases
  • Baclofen
  • Norepinephrine