Norepinephrine-independent regulation of GRII mRNA in vivo by a tricyclic antidepressant

S. Paul Rossby, Irena Nalepa, Mei Huang, Charles Perrin, Alvin M. Burt, Dennis E. Schmidt, David D. Gillespie, Fridolin Sulser*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

59 Scopus citations


Desipramine (DMI), a tricyclic antidepressant drug used in the treatment of depression, has been shown to increase steady-state levels of glucocorticoid receptor type II (GRII) mRNA in vitro and in vivo. To determine whether this effect is secondary to norepinephrine (NE) reuptake inhibition i.e., increases in synaptic NE induced by DMI, GRII mRNA levels were assayed in rat hippocampus following neurotoxic lesioning of NE neurons with DSP4. Chronic DMI treatment significantly increased GRII mRNA levels to the same degree in lesioned and non-lesioned animals. In contrast to DMI, the non-tricyclic antidepressant fluoxetine had no effect on GRII mRNA. These results provide evidence which demonstrates that a tricyclic antidepressant can regulate steady-state mRNA levels in vivo by a mechanism which is independent of its effects on synaptic monoamine levels.

Original languageEnglish (US)
Pages (from-to)79-82
Number of pages4
JournalBrain research
Issue number1-2
StatePublished - Jul 31 1995


  • DSP4 lesion
  • Desipramine
  • Fluoxetine
  • Glucocorticoid receptor mRNA
  • Hippocampus

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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