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AP-1 controls the p11-dependent antidepressant response.

Revathy U Chottekalapanda1, Salina Kalik2, Jodi Gresack2

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Selective serotonin reuptake inhibitors (SSRIs) activate a specific gene program, AP-1, crucial for antidepressant effects. This pathway links neuronal remodeling and plasticity to mood disorder treatment.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Selective serotonin reuptake inhibitors (SSRIs) are primary treatments for mood disorders.
  • The precise molecular mechanisms underlying SSRI therapeutic effects remain largely unknown.
  • SSRIs are believed to work by increasing brain serotonin and promoting neuroadaptive changes.

Purpose of the Study:

  • To elucidate the specific gene expression programs modulated by SSRIs.
  • To identify the molecular pathways linking SSRI treatment to neuroplasticity and antidepressant response.
  • To investigate the role of the activator protein-1 (AP-1) complex in SSRI action.

Main Methods:

  • Analysis of gene expression programs activated by chronic SSRI treatment.
  • Identification of the AP-1 complex (c-Fos and c-Jun) as a key regulator.
  • In vivo studies to assess the necessity of AP-1 function for antidepressant effects.
  • Investigation of upstream signaling cascades (MAPK, PI3K, JNK) involving BDNF and FGF2.

Main Results:

  • A specific transcriptional program regulated by the AP-1 complex is activated before the chronic SSRI response onset.
  • AP-1 modulates the expression of neuronal remodeling genes, such as S100a10 (p11), connecting plasticity to antidepressant action.
  • AP-1 function was found to be essential for the antidepressant effect in vivo.
  • Neurotrophic factors BDNF and FGF2, via MAPK, PI3K, and JNK pathways, regulate AP-1 function.

Conclusions:

  • A sequential molecular network is proposed for the antidepressant response, initiated by AP-1 activation.
  • This network links SSRI-induced neurochemical changes to neuronal remodeling and therapeutic benefits.
  • Targeting this AP-1 mediated pathway offers potential strategies to enhance or accelerate antidepressant responses by promoting neuroplasticity.