Comments and Questions:


Comments: 

To investigate the roles and underlying mechanisms of striatal GABAergic neuron in the pathogenesis of cerebral stroke, the author used a mouse model of transient middle cerebral artery occlusion (tMCAO) to explore the involvement of striatal GABAergic neuron (known as a key regulator in adult neurogenesis) by use of optogenetic approach. Laser stimulation/inhibition was delivered via an implanted optical fiber to activate or inhibit the striatal GABAergic neurons in Gad2-Arch-GFP or Gad2-ChR2-tdTomato mice 1 week after 60-minute tMCAO.Neurological severity score, brain atrophy volume, microvessel density, immunohistochemistry, real-time polymerase chain reaction and Western blotting to identify mechanism of striatal GABAergic neuron. The results revealed that optogenetic inhibition of GABAergic neurons upregulated bFGF expression by endothelial cells and promoted neurobehavioral recovery after ischemic stroke. Last but not least, the author use vivo and vitro experiment to explore the regulation of bFGF expression in endothelial cells.

Questions:

1) Since striatum is anatomically complex structure, including the caudate nucleus, putamen, and globus pallidus that could have different functions, how did authors quntify the extent of changes in GABAergic neuronal activity when the tips of laser probes could be implanted in different sites of the striatum?

2) Why did authors studied Nestin+ in the figure 3? 

3) How did authors make the model of transient middle cerebral artery occlusion?

4) If the models that did not show dramatic neurologic signs were excluded, to what extent does this study reflect the general pathologic changes in the brain following tMCAO? 

5How did authors identify the consistency of all tMCAO model in this experiment ?

6How to translate the conclusion of this paper to the treatment of ischemic patients?




2018年10月17日

2018-10-11 Literature Analysis

Lu Jiang et al., Optogenetic Inhibition of Striatal GABAergic Neuronal Activity Improves Outcomes After Ischemic Brain Injury. Stroke, 2017;48:00-00. DOI: 10.1161/STROKEAHA.117.019017., Presented by Dan Cui. Edited by Xiaoran Wang.

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