| Literature DB >> 30808765 |
Tingting Sun1, Zihua Song1, Yanghua Tian2, Wenbo Tian1, Chunyan Zhu2, Gongjun Ji2, Yudan Luo2, Shi Chen3, Likui Wang3, Yu Mao1,4, Wen Xie5, Hui Zhong5, Fei Zhao6, Min-Hua Luo6, Wenjuan Tao1, Haitao Wang1, Jie Li1, Juan Li1, Jiangning Zhou1, Kai Wang7, Zhi Zhang8.
Abstract
Obsessive-compulsive disorder (OCD) affects ∼1 to 3% of the world's population. However, the neural mechanisms underlying the excessive checking symptoms in OCD are not fully understood. Using viral neuronal tracing in mice, we found that glutamatergic neurons from the basolateral amygdala (BLAGlu) project onto both medial prefrontal cortex glutamate (mPFCGlu) and GABA (mPFCGABA) neurons that locally innervate mPFCGlu neurons. Next, we developed an OCD checking mouse model with quinpirole-induced repetitive checking behaviors. This model demonstrated decreased glutamatergic mPFC microcircuit activity regulated by enhanced BLAGlu inputs. Optical or chemogenetic manipulations of this maladaptive circuitry restored the behavioral response. These findings were verified in a mouse functional magnetic resonance imaging (fMRI) study, in which the BLA-mPFC functional connectivity was increased in OCD mice. Together, these findings define a unique BLAGlu→mPFCGABA→Glu circuit that controls the checking symptoms of OCD.Entities:
Keywords: BLA; OCD checking symptoms; mPFC; neural circuit
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Year: 2019 PMID: 30808765 PMCID: PMC6397577 DOI: 10.1073/pnas.1814292116
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205