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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Pharmacology

Background:

  • Selective serotonin reuptake inhibitors (SSRIs) are widely used antidepressants.
  • SSRIs paradoxically increase anxiety and depression risk when used during perinatal periods.
  • The underlying developmental mechanisms for these long-term effects remain unknown.

Purpose of the Study:

  • To investigate the developmental role of the serotonin transporter (SERT) in prefrontal cortex (PFC) circuits.
  • To elucidate the impact of early-life SSRI exposure on neural circuit development and adult behavior.
  • To identify specific PFC descending circuits targeted by antidepressants during development.

Main Methods:

  • Examined transient Slc6a4/SERT expression in mouse PFC layer 5-6 pyramidal neurons during early postnatal development (P0-P10).
  • Investigated PFC-SERT+ neuron synaptic connections with dorsal raphe nucleus (DRN) serotonin and GABA neurons.
  • Utilized complete and cortex-specific SERT ablation, early-life fluoxetine exposure, and pharmacogenetic manipulation of PFC-SERT+ neuron activity.

Main Results:

  • Developmental SERT expression in PFC neurons influences the maturation of PFC-to-DRN glutamatergic synapses.
  • SERT ablation or early fluoxetine exposure led to PFC-to-DRN hyperinnervation and anxiety/depressive-like behaviors.
  • Pharmacogenetic modulation of PFC-SERT+ neuron activity bidirectionally altered stress-related behaviors.

Conclusions:

  • Developmental SERT expression in specific PFC neurons is critical for regulating the maturation of PFC-to-DRN circuits.
  • Early-life SSRI exposure can disrupt these circuits, leading to long-term behavioral alterations and increased stress vulnerability.
  • These findings identify key developmental targets of SSRIs and offer insights into the basis of perinatal antidepressant side effects.