Depolarization-evoked release of glutamate, aspartate and gamma-aminobutyric acid from rat dorsal spinal cord slices does not originate from capsaicin-sensitive neurons

Brain Res. 1991 Aug 2;555(2):332-4. doi: 10.1016/0006-8993(91)90360-8.

Abstract

A release of endogenous glutamate (Glu), aspartate (Asp) and gamma-aminobutyric acid (GABA) from rat dorsal spinal cord slices was evoked by a 60 mM K(+)-depolarization (calcium dependent) and by 50 microM veratridine (tetrodotoxin sensitive) indicating a neuronal exocytosis mechanism. No release of the 3 amino acids investigated was obtained with the selective C-fiber excitant capsaicin (1 microM) and after impairment of afferent C-fibers the amount of amino acids released by K(+)-depolarization or veratridine was not reduced. These results suggest that amino acids may be exclusively transmitters of capsaicin-insensitive nerve structures in the rat dorsal spinal cord.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aspartic Acid / metabolism*
  • Capsaicin / pharmacology*
  • Glutamates / metabolism*
  • Glutamic Acid
  • Immunohistochemistry
  • Neuromuscular Depolarizing Agents / pharmacology*
  • Neurons / drug effects
  • Neurons / metabolism*
  • Potassium / pharmacology
  • Rats
  • Rats, Inbred Strains
  • Spinal Cord / metabolism*
  • Tetrodotoxin / pharmacology
  • Veratridine / pharmacology
  • gamma-Aminobutyric Acid / metabolism*

Substances

  • Glutamates
  • Neuromuscular Depolarizing Agents
  • Aspartic Acid
  • Glutamic Acid
  • Tetrodotoxin
  • gamma-Aminobutyric Acid
  • Veratridine
  • Potassium
  • Capsaicin