Fig. 1.

Optogenetic neuronal stimulation of the cLCN promotes behavioral recovery after stroke. a Thy1 mice-expressing channelrhodopsin 2 (ChR2) were used in this study. Blue laser stimulation activates ChR2 and causes neuronal excitation. b Schematic depicting the optogenetic laser stimulation site (blue bar) in the cLCN. Efferent projections travel through the superior cerebellar peduncle, decussate in the midbrain tegmentum and terminate in the ipsilesional ventrolateral thalamus (blue). Second-order neurons then project to multiple cortical regions including prefrontal, premotor, motor, and posterior parietal cortex. c Schematic illustrating the cortical and striatal infarction produced by transient middle cerebral artery occlusion. d Experimental paradigm. Mice were pre-trained (H) on the rotating beam test prior to the pre-fiber implant baseline (b) and the pre-stroke baseline data (day 0). Each mouse in the treatment group received one session of stimulations daily, from post-stroke day 5 and continued until day 14. Behavior tests were performed at post-stroke days 4, 7, 10, and 14. Mice were sacrificed at day 15 for qPCR and Western blot analysis. e Optogenetic neuronal stimulation paradigm. Each stimulation session consists of three 1-min stimulations with 3-min rest periods in between. Laser ON periods (blue) and laser OFF periods (black) are indicated. f Repeated neuronal stimulations of cLCN produced post-stroke recovery. cLCN-stimulated mice demonstrated significant improvement in speed (cm/s) on the rotating beam task at 10 and 14 days post-stroke. n = 4 for stroke + no stim, n = 4 for stroke + stim. Two-way ANOVA with Bonferroni’s post hoc test, *P < 0.05, ***P < 0.001. Data are expressed as mean ± SD