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Developmental and early-life stress-induced effects on 5-HT3R-expressing interneurons within auditory cortex.

James T Moore1,2, Matthew J Sunthimer1,2, Ethan White1

  • 1Hearing Research Group, Department of Biomedical Sciences, Northeast Ohio Medical University, Rootstown, OH, USA.

Neurobiology of Stress
|January 21, 2026
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Summary

Early life stress (ELS) alters auditory cortex development by affecting specific interneuron populations. ELS increases the density and serotonin receptor expression in VIP and NDNF cells, potentially causing sensory processing deficits.

Keywords:
5-HT3RAdversityAuditory cortexCritical periodDevelopmentEarly-life stressInhibitionLayer 1Serotonin

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Area of Science:

  • Neuroscience
  • Developmental Neuroscience
  • Cellular Neuroscience

Background:

  • Early life stress (ELS) is a significant risk factor for neuropsychiatric disorders.
  • ELS during critical developmental periods can lead to lasting sensory processing deficits.
  • The auditory cortex (ACx) is particularly vulnerable during its critical period for auditory processing development.

Purpose of the Study:

  • To investigate how ELS affects the development of specific interneuron populations in the primary auditory cortex.
  • To examine the role of serotonergic interneurons (5-HT3R) in mediating the effects of ELS on ACx plasticity.
  • To quantify changes in VIP and NDNF interneuron densities and Htr3a gene expression under ELS conditions.

Main Methods:

  • Multiplex fluorescent in situ hybridization was used to quantify gene expression and cell densities.
  • The study focused on VIP and NDNF interneuron subpopulations in the primary auditory cortex.
  • Experiments involved comparing animals exposed to ELS with age-matched controls during the ACx critical period.

Main Results:

  • Cell densities of NDNF and VIP interneurons decreased during normal ACx development.
  • ELS led to the maintenance of elevated densities of these interneurons compared to controls.
  • Htr3a expression in VIP neurons was developmentally upregulated and further increased by ELS.

Conclusions:

  • ELS disrupts the normal developmental trajectory of VIP and NDNF interneurons in the auditory cortex.
  • Stress-induced alterations in these serotonergic interneurons may underlie auditory processing deficits.
  • These findings highlight potential mechanisms linking ELS to long-term sensory processing impairments.