Hormonal and non-hormonal regulation of glutamine synthetase in the developing neural retina

Rena Gorovits, Aline Yakir, Lyle E. Fox, Lily Vardimon*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


Two isoforms of the glucocorticoid receptor, with apparent molecular mass of 90 and 95 kDa, are expressed in embryonic chicken neural retina. The 95-kDa receptor represents a hyperphosphorylated form of the 90-kDa receptor. Activation of the glucocorticoid receptor by cortisol results in a dose-dependent increase in receptor phosphorylation, translocation of receptor molecules into the nucleus and a decline in the total amount of the receptor. Activation of the glucocorticoid receptor can also be observed in the developing retinal tissue in ovo. At late embryonic ages, when the systemic level of glucocorticoids increases, a substantial quantity of receptor molecules becomes translocated into the nucleus, the relative level of the 95-kDa isoform increases, and the total amount of receptor declines. Activation of the receptor molecules in ovo correlates directly with an increase in transcription of the glucocorticoid-inducible gene, glutamine synthetase. The close correlation between the increase in systemic glucocorticoids, activation of glucocorticoid receptor molecules and induction of glutamine synthetase gene transcription suggests that glucocorticoids are directly involved in the developmental control of glutamine synthetase expression. Long-term organ culturing of embryonic retinal tissue in the absence of hormone results in an increase in glutamine synthetase expression. This increase, which is only 5 to 10% of that observed in ovo, is not mediated by activated receptor molecules and represents a mechanism for non-hormonal regulation of glutamine synthetase.

Original languageAmerican English
Pages (from-to)321-329
Number of pages9
JournalMolecular Brain Research
Issue number1-2
StatePublished - 31 Dec 1996
Externally publishedYes

Bibliographical note

Funding Information:
We are grateful to Dr. H.M. Westphal for the anti-GR mAbs. This work was supported by the Israeli Ministry of Science and Arts and by Grant FY95-0531 from the March of Dimes Birth Defects Foundation.


  • Glucocorticoid receptor
  • Glutamine synthetase
  • Neural retina
  • Neuronal cell death


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