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<p>Hypertension, a chronic condition, has affected &gt; 1 billion people worldwide and is linked to a heightened risk of anxiety disorders. Despite this association, the exact mechanisms underlying the connections between hypertension and anxiety disorders remain largely elusive. In this research, we observed that systolic blood pressure (SBP) increased in mice subcutaneously administered with angiotensin II (Ang II) alongside signs of heightened anxiety. Furthermore, immunofluorescence and electrophysiological analyses revealed that Ang II enhanced neuronal activity and altered the synaptic activities of ventral CA1 (vCA1) neurons. Meanwhile, in vivo recordings showed that these neurons in Ang II-treated mice were significantly more responsive to anxiety-inducing stimuli. Additionally, chemogenetic inhibition of neural activity in vCA1 effectively alleviated anxiety-like behavior in the treated animal. Moreover, the expression of the serotonin receptor 5-HT<sub>1A</sub> receptor (5-HT<sub>1A</sub>R) in vCA1 was suppressed under hypertension. Activating these receptors with the agonist 8-OH-DPAT effectively modified neuronal excitability and reduced anxiety-related behavior in mice. These findings elucidate the critical role of vCA1 neural activity and 5-HT<sub>1A</sub>R dysregulation in hypertension-associated anxiety, highlighting potential therapeutic targets for managing this condition.</p>

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Targeting the 5-HT1A receptor in the ventral hippocampus alleviates anxiety-like behavior in mice with angiotensin II-induced hypertension

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月6日

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  • Wenjun Chen,
  • Zhoucai Luo,
  • Mingfeng Huang,
  • Xiaoqi Zheng,
  • Nating Xiong,
  • Caiyan Gan,
  • Jianlin Wu

摘要

Hypertension, a chronic condition, has affected > 1 billion people worldwide and is linked to a heightened risk of anxiety disorders. Despite this association, the exact mechanisms underlying the connections between hypertension and anxiety disorders remain largely elusive. In this research, we observed that systolic blood pressure (SBP) increased in mice subcutaneously administered with angiotensin II (Ang II) alongside signs of heightened anxiety. Furthermore, immunofluorescence and electrophysiological analyses revealed that Ang II enhanced neuronal activity and altered the synaptic activities of ventral CA1 (vCA1) neurons. Meanwhile, in vivo recordings showed that these neurons in Ang II-treated mice were significantly more responsive to anxiety-inducing stimuli. Additionally, chemogenetic inhibition of neural activity in vCA1 effectively alleviated anxiety-like behavior in the treated animal. Moreover, the expression of the serotonin receptor 5-HT1A receptor (5-HT1AR) in vCA1 was suppressed under hypertension. Activating these receptors with the agonist 8-OH-DPAT effectively modified neuronal excitability and reduced anxiety-related behavior in mice. These findings elucidate the critical role of vCA1 neural activity and 5-HT1AR dysregulation in hypertension-associated anxiety, highlighting potential therapeutic targets for managing this condition.