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Activation of astroglial CB1R mediates cerebral ischemic tole
DREADD viruses were used for chemogenetics manipulation. GFAP-Cre was used for specific CB1R deletion combined with CB1R-floxed mice. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Chemogenetics  PT-0042 AAV2/9-EF1a-DIO-hM3Dq-mCherry-WPRE-pA
 PT-0043 AAV2/9-EF1a-DIO-hM4Di-mCherry-WPRE-pA
CRE Recombinase  PT-0209 AAV2/9-GFAP-Cre-WPRE-pA
Control  PT-0013 AAV2/9-EF1a-DIO-mCherry-WPRE-pA
Cen Yang, Jingjing Liu, Jingyi Wang, Anqi Yin, Zhenhua Jiang, Shuwei Ye, Xue Liu, Xia Zhang, Feng Wang, Lize Xiong
Pub Date: 2021-03-04, DOI: 10.1177/0271678x21994395, Email: [email protected]
There are no effective treatments for stroke. The activation of endogenous protective mechanisms is a promising therapeutic approach, which evokes the intrinsic ability of the brain to protect itself. Accumulated evidence strongly suggests that electroacupuncture (EA) pretreatment induces rapid tolerance to cerebral ischemia. With regard to mechanisms underlying ischemic tolerance induced by EA, many molecules and signaling pathways are involved, such as the endocannabinoid system, although the exact mechanisms have not been fully elucidated. In the current study, we employed mutant mice, neuropharmacology, microdialysis, and virus transfection techniques in a middle cerebral artery occlusion (MCAO) model to explore the cell-specific and brain region-specific mechanisms of EA-induced neuroprotection. EA pretreatment resulted in increased ambient endocannabinoid (eCB) levels and subsequent activation of ischemic penumbral astroglial cannabinoid type 1 receptors (CB1R) which led to moderate upregulation of extracellular glutamate that protected neurons from cerebral ischemic injury. These findings provide a novel cellular mechanism of EA and a potential therapeutic target for ischemic stroke.

Figure 1. Ischemic penumbral astroglial CB1R mediates the neuroprotective effects of EA pretreatment.
In this study, the authors investigated the mechanism underlying the neuroprotective effect of EA pretreatment. The findings suggest that EA pretreatment induced an increase of ambient eCBs and subesequent activation of ischemic penumbral astroglial CB1R led to the moderate upregulation of extracellular glutamate, which protected neurons from cerebral ischemic injury. These findings provide clear evidence for the cell-specific and brain region-specific mechanism underlying EA-induced neuroprotection.
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