Modulation of Ca2+ channels by activation of adenosine A1 receptors in rat striatal glutamatergic nerve terminals

Neurosci Lett. 1996 Dec 20;220(3):163-6. doi: 10.1016/s0304-3940(96)13252-3.

Abstract

We determined that activation of adenosine A1 receptors in striatal synaptosomes with 100 nM N6-cyclopentyladenosine (CPA) inhibited both the release of endogenous glutamate and the increase of intracellular free Ca2+ concentration ([Ca2+]i), due to 4-aminopyridine (4-AP) stimulation, by 28 and 19%, respectively. Furthermore, CPA enhanced the inhibition of endogenous glutamate release due to omega-conotoxin GVIA (omega-Cgtx GVIA), omega-Cgtx MVIIC or omega-Cgtx GVIA plus omega-Cgtx MVIIC. Similar effects were observed in the [Ca2+]i signal. The inhibitory effects of CPA and omega-Cgtx GVIA were additive, but the effects of CPA and omega-Cgtx MVIIC were only partially additive. These results suggest that P/Q-type Ca2+ channels and other type(s) of Ca2+ channel(s), coupled to glutamate release, are inhibited subsequently to activation of adenosine A1 receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials / physiology
  • Adenosine / analogs & derivatives
  • Adenosine / pharmacology
  • Animals
  • Biotransformation / physiology
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / metabolism*
  • Drug Interactions
  • Fluorometry
  • Glutamic Acid / metabolism
  • Glutamic Acid / physiology*
  • Male
  • Membrane Potentials / physiology
  • Neostriatum / cytology
  • Neostriatum / metabolism*
  • Presynaptic Terminals / metabolism*
  • Rats
  • Rats, Wistar
  • Receptors, Purinergic P1 / metabolism*

Substances

  • Calcium Channel Blockers
  • Calcium Channels
  • Receptors, Purinergic P1
  • Glutamic Acid
  • N(6)-cyclopentyladenosine
  • Adenosine