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<p>Stress can disrupt menstrual cycles, impair fertility and cause reproductive disfunction. The posterodorsal medial amygdala (MePD) integrates stress signals and regulates the gonadotropin-releasing hormone (GnRH) pulse generator through a dense network of GABA and Urocortin-3 (UCN3) neurons, yet the mechanisms underlying the circuitry remain poorly understood. Here, we combine in vivo mini-endoscopic calcium imaging, optogenetics, clustering analysis, and computational modeling to investigate the MePD circuitry in female mice. We uncover two anti-correlated GABA subpopulations in the MePD that are involved in the response to restraint stress and UCN3 neuron stimulation. Computational modeling suggests that mutual inhibition between these GABA groups drives their anti-correlated activity and predicts how these interactions shape downstream responses to stimulation of GABA and UCN3 neurons. In vivo optogenetics confirms that GABA neurons are critical for transmitting UCN3 signals to regulate luteinizing hormone (LH) pulse frequency. Together, our findings reveal amygdala GABAergic circuit mechanisms that mediate stress effects on reproductive health, linking emotional processing and neuroendocrine control.</p>

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The role of amygdala GABA neurons in controlling stress and reproduction in female mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月10日

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  • Junru Yu,
  • Saeed Farjami,
  • Kateryna Nechyporenko,
  • Xiao Feng Li,
  • Hafsa Yaseen,
  • Yanyan Lin,
  • Jinbin Ye,
  • Owen Hollings,
  • Ross de Burgh,
  • Baban Singh,
  • Kevin T. O’Byrne,
  • Krasimira Tsaneva-Atanasova,
  • Margaritis Voliotis

摘要

Stress can disrupt menstrual cycles, impair fertility and cause reproductive disfunction. The posterodorsal medial amygdala (MePD) integrates stress signals and regulates the gonadotropin-releasing hormone (GnRH) pulse generator through a dense network of GABA and Urocortin-3 (UCN3) neurons, yet the mechanisms underlying the circuitry remain poorly understood. Here, we combine in vivo mini-endoscopic calcium imaging, optogenetics, clustering analysis, and computational modeling to investigate the MePD circuitry in female mice. We uncover two anti-correlated GABA subpopulations in the MePD that are involved in the response to restraint stress and UCN3 neuron stimulation. Computational modeling suggests that mutual inhibition between these GABA groups drives their anti-correlated activity and predicts how these interactions shape downstream responses to stimulation of GABA and UCN3 neurons. In vivo optogenetics confirms that GABA neurons are critical for transmitting UCN3 signals to regulate luteinizing hormone (LH) pulse frequency. Together, our findings reveal amygdala GABAergic circuit mechanisms that mediate stress effects on reproductive health, linking emotional processing and neuroendocrine control.