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Dopaminergic Projection from Ventral Tegmental Area to Substa
AAV-ChR2 was used for optogenetic manipulation. AAV-hM3Dq was used for chemogenetics manipulation. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Optogenetic  PT-0001 AAV-DIO-ChR2-EYFP
 PT-0002 AAV-retro-DIO-ChR2-mCherry
Chemogenetics  PT-0042 AAV-DIO-hM3Dq-mCherry
CRE Recombinase  PT-2947 AAV-TH-Cre
Feng He, Pei Zhang, Qian Zhang, Guangjian Qi, Hongwei Cai, Tongxia Li, Ming Li, Jiazhen Lu, Jiaen Lin, Jie Ming, Bo Tian
Pub Date: 2021-08-12, DOI: 10.1007/s12035-021-02522-7, Email: [email protected]
Numerous human clinical studies have suggested that decreased locomotor activity is a common symptom of major depressive disorder (MDD), as well as other psychiatric diseases. In MDD, the midbrain ventral tegmental area (VTA) dopamine (DA) neurons are closely related to regulate the information processing of reward, motivation, cognition, and aversion. However, the neural circuit mechanism that underlie the relationship between VTA-DA neurons and MDD-related motor impairments, especially hypolocomotion, is still largely unknown. Herein, we investigate how the VTA-DA neurons contribute to the hypolocomotion performance in chronic social defeat stress (CSDS), a mouse model of depression-relevant neurobehavioral states. The results show that CSDS could affect the spontaneous locomotor activity of mice, but not the grip strength and forced locomotor ability. Chemogenetic activation of VTA-DA neurons alleviated CSDS-induced hypolocomotion. Subsequently, quantitative whole-brain mapping revealed decreased projections from VTA-DA neurons to substantia nigra pars reticulata (SNr) after CSDS treatment. Optogenetic activation of dopaminergic projection from VTA to SNr with the stimulation of phasic firing, but not tonic firing, could significantly increase the locomotor activity of mice. Moreover, chemogenetic activation of VTA-SNr dopaminergic circuit in CSDS mice could also rescued the decline of locomotor activity. Taken together, our data suggest that the VTA-SNr dopaminergic projection mediates CSDS-induced hypolocomotion, which provides a theoretical basis and potential therapeutic target for MDD.

Figure 1. Whole-brain mapping of the outputs of ventral tegmental area (VTA) dopamine neurons in chronic social defeat stress mice.
In this study, the authors have investigated the behavioral adaptations of locomotor activity following CSDS and the role of VTA-DA neurons. Collectively, dopaminergic projections from VTA to SNr appear to mediate CSDS-induced hypolocomotion, and this circuit may be involved in MDD.
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