Evidence that aspartate aminotransferase activity and ketodicarboxylate carrier function are essential for biosynthesis of transmitter glutamate

J Neurochem. 1988 Jul;51(1):317-20. doi: 10.1111/j.1471-4159.1988.tb04872.x.

Abstract

Based on the selective inhibition of glutamate release in cerebellar granule cells in primary cultures by the aspartate aminotransferase inhibitor, aminooxyacetic acid, and by the ketodicarboxylate carrier inhibitor, phenylsuccinate, a novel model for synthesis of transmitter glutamate is suggested: Glutamate is formed from glutamine in the mitochondrial intramembrane space by phosphate-activated glutaminase, transported across the inner membrane in exchange with aspartate, transaminated in the matrix to alpha-ketoglutarate, which via the ketodicarboxylate carrier is transferred to the cytoplasm, and transaminated to form transmitter glutamate. Such a mechanism would explain the functional role of aspartate aminotransferase in glutamatergic neurons.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aminooxyacetic Acid / pharmacology
  • Animals
  • Aspartate Aminotransferases / antagonists & inhibitors
  • Aspartate Aminotransferases / metabolism*
  • Aspartic Acid / metabolism
  • Calcium Chloride / pharmacology
  • Carrier Proteins / antagonists & inhibitors
  • Carrier Proteins / metabolism*
  • Cells, Cultured
  • Cerebellum / drug effects
  • Cerebellum / enzymology*
  • Cobalt / pharmacology
  • Glutamates / biosynthesis*
  • Glutamic Acid
  • Glutamine / metabolism
  • Mice
  • Succinates / pharmacology

Substances

  • Carrier Proteins
  • Glutamates
  • Succinates
  • Glutamine
  • Aminooxyacetic Acid
  • Aspartic Acid
  • Cobalt
  • Glutamic Acid
  • 2-phenylsuccinate
  • Aspartate Aminotransferases
  • cobaltous chloride
  • Calcium Chloride