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<p>Chronic hypoxia at high altitudes disrupts emotional and metabolic homeostasis. However, the underlying mechanisms remain unclear. Using mice chronically exposed to 11.35% oxygen, we combined three-dimensional motion capture, anxiety-related behavioral tests, brain-wide c-Fos mapping, and metabolic cage recordings. Hypoxic mice showed anxiety-like behavior, altered posture, and spontaneous behavioral distribution, elevated oxygen consumption, carbon dioxide production, and energy expenditure, together with reduced feeding. c-Fos mapping implicated the limbic, prefrontal, hypothalamic, and nucleus accumbens shell (NAcSh) regions in hypoxic adaptation. Selective depolarization of NAcSh dopamine D1 receptor (D1R) neurons alleviated anxiety-like behavior and attenuated hypoxia-associated hypermetabolism while further shifting substrate utilization. Exercise preconditioning also reduced anxiety-like behavior and partially restored NAcSh D1R-related signaling. Together, these findings identify NAcSh D1R-related signaling as a key component of chronic hypoxia adaptation and show that activation of NAcSh D1R neurons is sufficient to attenuate the coupled anxiety-like and metabolic phenotypes.</p>

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Nucleus Accumbens D1 Receptor Neurons Contribute to Emotional and Metabolic Adaptation to Chronic Hypoxia

  • 期刊论文

  • 发表日期：

    2026年7月25日

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  • Yan Chen,
  • Jie Shao,
  • Lu Zhang,
  • Yuchuan Hong,
  • Hao Yang,
  • Shirui Jun,
  • William Weijia Lu,
  • Jie Tu,
  • Guoxin Ni,
  • Fan Yang

摘要

Chronic hypoxia at high altitudes disrupts emotional and metabolic homeostasis. However, the underlying mechanisms remain unclear. Using mice chronically exposed to 11.35% oxygen, we combined three-dimensional motion capture, anxiety-related behavioral tests, brain-wide c-Fos mapping, and metabolic cage recordings. Hypoxic mice showed anxiety-like behavior, altered posture, and spontaneous behavioral distribution, elevated oxygen consumption, carbon dioxide production, and energy expenditure, together with reduced feeding. c-Fos mapping implicated the limbic, prefrontal, hypothalamic, and nucleus accumbens shell (NAcSh) regions in hypoxic adaptation. Selective depolarization of NAcSh dopamine D1 receptor (D1R) neurons alleviated anxiety-like behavior and attenuated hypoxia-associated hypermetabolism while further shifting substrate utilization. Exercise preconditioning also reduced anxiety-like behavior and partially restored NAcSh D1R-related signaling. Together, these findings identify NAcSh D1R-related signaling as a key component of chronic hypoxia adaptation and show that activation of NAcSh D1R neurons is sufficient to attenuate the coupled anxiety-like and metabolic phenotypes.