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<p>Innate escape behaviors, while not requiring prior learning, are shaped by an animal’s learned experiences, such as previous exposure. Here, we found that learned threat experience in mice enhances flight behaviors, which is linked to increased activation of cholecystokinin-expressing neurons in the dorsal premammillary nucleus (PMd<sup>CCK</sup> neurons), a population that controls circa-strike escape responses. This heightened activity coincides with reduced inhibition from parvalbumin-expressing GABAergic neurons in the ventral tegmental nucleus of Gudden (VTg<sup>PV</sup>), which typically suppress PMd<sup>CCK</sup> activity and escape behaviors. Furthermore, threat memory prompts a prefrontal projection to stimulate the release of endocannabinoids, inhibiting the axon terminals of VTg<sup>PV</sup> neurons. The necessity of this endocannabinoid-mediated disinhibition for the observed enhancement in flight behaviors is confirmed through genetic deletion or pharmacological blockade of endocannabinoid receptors on VTg<sup>PV</sup> neurons. Thus, our study uncovers a neural mechanism by which experience amplifies innate escape behaviors, highlighting the crucial role of endocannabinoids.</p>

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Endocannabinoids disinhibit the ventral tegmental nucleus of Gudden to dorsal premammillary nucleus pathway to enhance escape behavior following learned threat experience

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月27日

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  • Ruikai Chai,
  • Nawen Wang,
  • Jinlu Nie,
  • Zongyi Xu,
  • Shuqian Zhang,
  • Suixin Deng,
  • Rongxin Wang,
  • Mu Li,
  • Xinyi Gao,
  • Ruijie Geng,
  • Haibin Li,
  • Lei Li,
  • Hebi Wu,
  • Zhiming Li,
  • Tian-Lin Cheng,
  • Xiao-Hong Xu,
  • Yousheng Shu,
  • Huilin Hong,
  • Xiao Huang,
  • Weisheng Wang

摘要

Innate escape behaviors, while not requiring prior learning, are shaped by an animal’s learned experiences, such as previous exposure. Here, we found that learned threat experience in mice enhances flight behaviors, which is linked to increased activation of cholecystokinin-expressing neurons in the dorsal premammillary nucleus (PMdCCK neurons), a population that controls circa-strike escape responses. This heightened activity coincides with reduced inhibition from parvalbumin-expressing GABAergic neurons in the ventral tegmental nucleus of Gudden (VTgPV), which typically suppress PMdCCK activity and escape behaviors. Furthermore, threat memory prompts a prefrontal projection to stimulate the release of endocannabinoids, inhibiting the axon terminals of VTgPV neurons. The necessity of this endocannabinoid-mediated disinhibition for the observed enhancement in flight behaviors is confirmed through genetic deletion or pharmacological blockade of endocannabinoid receptors on VTgPV neurons. Thus, our study uncovers a neural mechanism by which experience amplifies innate escape behaviors, highlighting the crucial role of endocannabinoids.