Trace amines reduce GABA(B) receptor-mediated presynaptic inhibition at GABAergic synapses of the rat substantia nigra pars compacta

Brain Res. 2005 Nov 16;1062(1-2):175-8. doi: 10.1016/j.brainres.2005.09.009. Epub 2005 Nov 2.

Abstract

Trace amines (TAs) act in the mammalian brain through amphetamine-like effects and as endogenous agonists of specific receptors. We now show that tyramine and beta-phenylethylamine, in the presence of specific dopamine (DA) receptor antagonists, inhibit the GABA(B)-dependent presynaptic inhibition of GABAergic inputs to midbrain DA neurons. Our results further extend the role of TAs as neuromodulators and propose a novel mechanism by which they modulate DA neurons.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Biogenic Monoamines / metabolism*
  • Dopamine / metabolism
  • GABA Agonists / metabolism
  • Neural Inhibition / physiology*
  • Neurotransmitter Agents / metabolism*
  • Organ Culture Techniques
  • Patch-Clamp Techniques
  • Presynaptic Terminals / metabolism
  • Rats
  • Rats, Wistar
  • Receptors, GABA-B / metabolism*
  • Statistics, Nonparametric
  • Substantia Nigra / cytology
  • Substantia Nigra / metabolism*

Substances

  • Biogenic Monoamines
  • GABA Agonists
  • Neurotransmitter Agents
  • Receptors, GABA-B
  • Dopamine