Effect of chronic antidepressant treatment on transcription factor binding activity in rat hippocampus and frontal cortex

  title={Effect of chronic antidepressant treatment on transcription factor binding activity in rat hippocampus and frontal cortex},
  author={Diana Frechilla and Ana Otano and Joaquı́n Del Rı́o},
  journal={Progress in Neuro-Psychopharmacology and Biological Psychiatry},

Identification and expression of frizzled-3 protein in rat frontal cortex after antidepressant and electroconvulsive treatment.

The full-length nucleotide sequence of rat frizzled-3 protein (Frz3) cDNA was determined and it was demonstrated that chronic treatment with two different classes of antidepressants reduced Frz3 mRNA expression significantly in rat frontal cortex.

Pharmacologically Diverse Antidepressants Rapidly Activate Brain-Derived Neurotrophic Factor Receptor TrkB and Induce Phospholipase-Cγ Signaling Pathways in Mouse Brain

The data suggest that rapid activation of the TrkB neurotrophin receptor and PLCγ1 signaling is a common mechanism for all antidepressant drugs.

Selective Phosphorylation of Nuclear CREB by Fluoxetine is Linked to Activation of CaM Kinase IV and MAP Kinase Cascades

The results show that FLX exerts a more marked effect on CREB phosphorylation and suggest that CaMKIV and MAP kinase cascades are involved in this effect.



Chronic antidepressant administration increases the expression of cAMP response element binding protein (CREB) in rat hippocampus

  • M. NibuyaE. NestlerR. Duman
  • Biology, Psychology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1996
Findings indicate that upregulation of CREB is a common action of chronic antidepressant treatments that may lead to regulation of specific target genes, such as BDNF and trkB, and to the long-term effects of these treatments on brain function.

Antidepressants increase glucocorticoid and mineralocorticoid receptor mRNA expression in rat hippocampus in vivo.

Examining whether acute or chronic treatment with antidepressant drugs, which potentiate endogenous monoamines by inhibiting their reuptake, affect hippocampal GR and MR mRNA expression in vivo finds that antidepressant drug administration elevates MR and GR mRNA Expression in hippocampus, but not parietal cortex, in a time-dependent manner.

Regulation of β1‐Adrenergic Receptor mRNA and Ligand Binding by Antidepressant Treatments and Norepinephrine Depletion in Rat Frontal Cortex

The results demonstrate that β1AR mRNA and ligand binding are regulated in parallel by ECS treatment but that levels of receptor mRNA areregulated in a complex manner by imipramine or 6‐OHDA treatments, not predicted by changes in ligandbinding.

Regulation of BDNF and trkB mRNA in rat brain by chronic electroconvulsive seizure and antidepressant drug treatments

The enhanced induction and prolonged expression of BDNF in response to chronic ECS and antidepressant drug treatments could promote neuronal survival, and protect neurons from the damaging effects of stress.

5-HT2A Receptor-Mediated Regulation of Brain-Derived Neurotrophic Factor mRNA in the Hippocampus and the Neocortex

The results of this study raise the possibility that regulation of BDNF expression by hallucinogenic 5-HT2Areceptor agonists leads to adaptations of synaptic strength in the hippocampus and the neocortex that may mediate some of the acute and long-term behavioral effects of these agents.

Regulation of c‐Fos and NGF1‐A by antidepressant treatments

The results demonstrate that ECS‐ and tranylcypromine induction of c‐Fos is mediated by activation of several different neurotransmitter receptors, but that the exact pharmacological profile is different for each treatment and brain region.

Repeated ECS differentially affects rat brain 5-HT1A and 5-HT2A receptor expression

It is demonstrated that in the rat, repeated ECS produces anatomically and molecularly discrete effects on 5-HT1A and5-HT2A receptor gene expression, which may be relevant to the therapeutic effect of repeated E CS in depression.

Antidepressant-Like Effect of Brain-derived Neurotrophic Factor (BDNF)