4.7 Article

The Slack Channel Regulates Anxiety-Like Behaviors via Basolateral Amygdala Glutamatergic Projections to Ventral Hippocampus

期刊

JOURNAL OF NEUROSCIENCE
卷 42, 期 14, 页码 3049-3064

出版社

SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2027-21.2022

关键词

anxiety; basolateral amygdala; corticosterone; Slack channel; ventral hippocampus

资金

  1. Important Project of Natural Science in Colleges and Universities in Jiangsu Province [14KJA320002]
  2. Jiangsu Specially Appointed Professorship
  3. Natural Science Foundation of China (NSFC) [81471314, 81671090]
  4. Natural Science Foundation of Jiangsu Province [SBK201502515]
  5. Xuzhou Science and Technology Program [KC19036, KC16H0230]
  6. NSFC [31671212]
  7. Priority Academic Program Development of Jiangsu Higher Education Institutions [BL201402]
  8. Jiangsu Provincial Special Program of Medical Science [BL201402]
  9. Postgraduate Research & Practice Innovation Program of Jiangsu Province [KYCX21_2708]
  10. College Students Innovation and Entrepreneurship Training Program [201510313034Y, 201810313017Z]

向作者/读者索取更多资源

Anxiety disorders are mental disorders characterized by anxiety and fear, and their molecular basis is still unclear. The study reveals the role of Slack channels in controlling anxious behaviors by decreasing the excitability of BLA-vHPC glutamatergic projections. This provides a potential target for anxiolytic therapies.
Anxiety disorders are a series of mental disorders characterized by anxiety and fear, but the molecular basis of these disorders remains unclear. In the present study, we find that the global Slack KO male mice exhibit anxious behaviors, whereas the Slack Y777H male mice manifest anxiolytic behaviors. The expression of Slack channels is rich in basolateral amygdala (BLA) glutamatergic neurons and downregulated in chronic corticosterone-treated mice. In addition, electrophysiological data show enhanced excitability of BLA glutamatergic neurons in the Slack KO mice and decreased excitability of these neurons in the Slack Y777H mice. Furthermore, the Slack channel deletion in BLA glutamatergic neurons is sufficient to result in enhanced avoidance behaviors, whereas Kcntl gene expression in the BLA or BLA-ventral hippocampus (vHPC) glutamatergic projections reverses anxious behaviors of the Slack KO mice. Our study identifies the role of the Slack channel in controlling anxious behaviors by decreasing the excitability of BLA-vHPC glutamatergic projections, providing a potential target for anxiolytic therapies.

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