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Reversal of hyperactive higher-order thalamus attenuates defensiveness in a mouse model of PTSD.

Kaiwen XiHaoxiang XiaoXin HuangZiduo YuanMingyue LiuHonghui MaoHaiying LiuGuaiguai MaZishuo ChengYuqiao XieYang LiuDayun FengWenting WangBaolin GuoSheng-Xi Wu
Published in: Science advances (2023)
Posttraumatic stress disorder (PTSD) is a highly prevalent and debilitating psychiatric disease often accompanied by severe defensive behaviors, preventing individuals from integrating into society. However, the neural mechanisms of defensiveness in PTSD remain largely unknown. Here, we identified that the higher-order thalamus, the posteromedial complex of the thalamus (PoM), was overactivated in a mouse model of PTSD, and suppressing PoM activity alleviated excessive defensive behaviors. Moreover, we found that diminished thalamic inhibition derived from the thalamic reticular nucleus was the major cause of thalamic hyperactivity in PTSD mice. Overloaded thalamic innervation to the downstream cortical area, frontal association cortex, drove abnormal defensiveness. Overall, our study revealed that the malfunction of the higher-order thalamus mediates defensive behaviors and highlighted the thalamocortical circuit as a potential target for treating PTSD-related overreactivity symptoms.
Keyphrases
  • posttraumatic stress disorder
  • deep brain stimulation
  • mouse model
  • social support
  • signaling pathway
  • depressive symptoms
  • single cell
  • type diabetes
  • early onset
  • weight gain
  • working memory
  • body mass index