Induction of Glutamine Synthetase in Rat Astrocytes by Co‐Cultivation with Embryonic Chick Neurons

Abstract

Co-cultivation of confluent rat astrocyte cultures with embryonic chick neurons resulted in induction of glutamine synthetase activity in the astrocytes. This induction of glutamine synthetase in astrocytes by neurons was independent of induction by hydrocortisone and forskolin, but was dependent on the length of co-cultivation and the number of neurons present in the co-culture. Cycloheximide and actinomycin D inhibited the induction of glutamine synthetase in astrocytes by neurons, whereas cytosine arabinoside had no apparent effect. Results suggest that this induction of glutamine synthetase in astrocytes is mediated by cell contact with neurons and may represent a specific neuronal and glial interaction.

Energy Metabolism in Astrocytes and Neurons Treated with Manganese: Relation among Cell-Specific Energy Failure, Glucose Metabolism, and Intercellular Trafficking Using Multinuclear NMR-Spectroscopic Analysis

“…From the manganese-induced accumulation of glutamate in these cells, one might expect an increased flux through GS, but glutamine synthesis remained unchanged and even decreased after brief exposure despite a more than fivefold elevation of [4-13 C]glutamate. Despite cocultivation of astrocytes with neurons stimulating both synthesis and release of glutamine, which is consistent with increased GS messenger RNA and activity (Mearow et al, 1990;Wu et al, 1988), de novo synthesized glutamine was hardly detectable after manganese treatment. These findings are in disagreement with reports of increased GS expression in manganese-exposed rat brain (Zheng et al 1999) and cultured astrocytes (Chen and Liao, 2002).…”

Involvement of a C/EBP-like protein in the acquisition of responsiveness to glucocorticoid hormones during chick neural retina development.

“…In the neural retina, GS is confined to Muller cells, the gliocyte compartment in the retina. The development of glioblasts into mature Muller cells is regulated by neuronal-glial cell-cell interactions (42,43,48,79). Glucocorticoid activation of GS expression is * Corresponding author.…”

Regulation of glial metabolism studied by 13C‐NMR

“…Furthermore, glutamine de novo synthesis, as well as GS mRNA and activity, increased markedly in astrocytes co-cultured with neurons. [122][123][124] It is generally believed that GS is an astrocyte-specific protein. However, GS expression and de novo glutamine synthesis in cultured neurons has also been observed in cultured neurons and synaptosomes.…”

“…The enzyme activites of mME and cME in brain homogenates are 55 and 45%. 120 While the mitochondrial isozyme is expressed in neurons and synaptic terminals 121,122 it is widely accepted that cME is preferentially, if not exclusively, a glial enzyme. 118,120,200 Although cME is reversible, more than 95% of the malate present is converted to pyruvate at physiological concentrations of malate and pyruvate, 201 which is consistent with the cytosolic isozyme accounting for as much as 95% of total ME activity in astrocytes.…”