Activation of adenosine A1 and A2 receptors differentially modulates calcium channels and glycinergic synaptic transmission in rat brainstem

Neuron. 1994 Dec;13(6):1439-46. doi: 10.1016/0896-6273(94)90429-4.

Abstract

Multiple types of calcium channels are responsible for calcium influx that triggers transmitter release in the mammalian CNS. To test the contribution of each calcium channel type on synaptic modulation, we recorded calcium currents from somata of presynaptic interneurons and unitary glycinergic postsynaptic currents in the rat brainstem. In interneuron somata, A1 receptor activation inhibited predominantly N-type (omega-conotoxin GVIA-sensitive) and, to a lesser extent, P-type (omega-agatoxin IVA-sensitive) channels. At the presynaptic terminal, N- and P-type channels mediated synaptic transmission. omega-CgTx occluded synaptic inhibition by A1 receptor activation, suggesting that synaptic inhibition was mediated predominantly by N-type channel inhibition. A2 receptor activation facilitated synaptic transmission, probably through potentiation of P-type channels at the presynaptic terminal.

Publication types

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

MeSH terms

  • Adenosine / pharmacology*
  • Animals
  • Brain Stem / physiology*
  • Calcium Channels / physiology*
  • Glycine / physiology*
  • Interneurons / physiology
  • Ion Channel Gating
  • Nerve Endings / physiology
  • Peptides / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Purinergic P1 / physiology*
  • Spider Venoms / pharmacology
  • Synapses / physiology
  • Synaptic Transmission
  • omega-Agatoxin IVA
  • omega-Conotoxin GVIA

Substances

  • Calcium Channels
  • Peptides
  • Receptors, Purinergic P1
  • Spider Venoms
  • omega-Agatoxin IVA
  • omega-Conotoxin GVIA
  • Adenosine
  • Glycine