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Distinct thalamocortical circuits underlie allodynia induced
AAV-GCaMP6m was used to visualize calcium signals in conscious mice. AAV-hM3Dq and AAV-hM4Di were used for chemogenetics manipulation. AAV-ChR2 and AAV- eNpHR3.0 were used for optogenetic manipulation. (All viruses were packaged by BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Calcium sensors  PT-0283 rAAV-Ef1a-DIO-GCaMP6m-WPRE-pA
CRE Recombinase
 PT-0220 retro-AAV-CaMK2a-Cre-WPRE-pA PT-0136 retro-AAV-hSyn-Cre-WPRE-pA
Chemogenetics  PT-0043 rAAV-Ef1α-DIO-hM4D(Gi)-mCherry-WPRE-pA
 PT-0042 rAAV-Ef1α-DIO-hM3D(Gq)-mCherry-WPRE-pA
 PT-0049 rAAV-CaMK2a-hM3D(Gq)-mCherry-WPRE-pA
Optogenetic  PT-0002 rAAV-Ef1α-DIO-hChR2 (H134R)-mCherry-WPRE-Pa
 PT-0003 rAAV-Ef1α-DIO-eNpHR3.0-EYFP-WPRE-pA
Tracing Helper  PT-0023 rAAV-Ef1α-DIO-RVG-WPRE-pA
Control  rAAV-Ef1α-DIO-EGFP-WPRE-pA
 PT-0013 rAAV-Ef1α-DIO-mCherry-WPRE-pA
 PT-0108 rAAV-CaMK2a-mCherry-WPRE-hGH-pA
 PT-1134 rAAV-DLX5/6-mCherry-WPRE-hGH
RV  RV01002 RV-EnvA-ΔG–DsRed
Xia Zhu, Hao-Di Tang, Wan-Ying Dong, Fang Kang, An Liu, Yu Mao, Wen Xie, Xulai Zhang, Peng Cao, Wenjie Zhou, Haitao Wang, Zahra Farzinpour, Wenjuan Tao, Xiaoyuan Song, Yan Zhang, Tian Xue, Yan Jin, Juan Li, Zhi Zhang
Pub Date: 2021-03-08, DOI: 10.1038/s41593-021-00811-x, Email:
In humans, tissue injury and depression can both cause pain hypersensitivity, but whether this involves distinct circuits remains unknown. Here, we identify two discrete glutamatergic neuronal circuits in male mice: a projection from the posterior thalamic nucleus (POGlu) to primary somatosensory cortex glutamatergic neurons (S1Glu) mediates allodynia from tissue injury, whereas a pathway from the parafascicular thalamic nucleus (PFGlu) to anterior cingulate cortex GABA-containing neurons to glutamatergic neurons (ACCGABA→Glu) mediates allodynia associated with a depression-like state. In vivo calcium imaging and multi-tetrode electrophysiological recordings reveal that POGlu and PFGlu populations undergo different adaptations in the two conditions. Artificial manipulation of each circuit affects allodynia resulting from either tissue injury or depression-like states, but not both. Our study demonstrates that the distinct thalamocortical circuits POGlu→S1Glu and PFGlu→ACCGABA→Glu subserve allodynia associated with tissue injury and depression-like states, respectively, thus providing insights into the circuit basis of pathological pain resulting from different etiologies.

Figure 1. The PFGlu→ACCGABA→Glu circuit controls allodynia induced by depression-like states.
In this study, the authors dissected the functional organization of the posterior thalamic nucleus (PO)→S1 and PF→ACC circuits and explored the principle of the circuit adaptation in a mouse model of allodynia induced by tissue injury and depression-like states. They used in vivo calcium imaging and multi-tetrode electrophysiological recordings to show that these populations undergo different adaptations in the two states.
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