Negative Allosteric Modulator of mGluR1 Improves Long-Term Neurologic Deficits after Experimental Subarachnoid Hemorrhage

2020 ◽  
Vol 11 (18) ◽  
pp. 2869-2880
Author(s):  
Hong-Bin Wang ◽  
Wei-qi Wang ◽  
Qing-Jian Wu ◽  
Ya-jun Hou ◽  
Han-xia Li ◽  
...  
2016 ◽  
Vol 12 ◽  
pp. P1016-P1017
Author(s):  
Miki Nakanishi ◽  
Soichi Kawaharada ◽  
Nobuto Nakanishi ◽  
Keisuke Hazama ◽  
Masato Higashino ◽  
...  

2018 ◽  
Vol 109 ◽  
pp. e88-e98 ◽  
Author(s):  
Nadine Lilla ◽  
Christoph Rinne ◽  
Judith Weiland ◽  
Thomas Linsenmann ◽  
Ralf-Ingo Ernestus ◽  
...  

2008 ◽  
Vol 213 (2) ◽  
pp. 336-344 ◽  
Author(s):  
Ken Takata ◽  
Huaxin Sheng ◽  
Cecil O. Borel ◽  
Daniel T. Laskowitz ◽  
David S. Warner ◽  
...  

2019 ◽  
Vol 40 (6) ◽  
pp. 1193-1202 ◽  
Author(s):  
Matilde Balbi ◽  
Max Jativa Vega ◽  
Athanasios Lourbopoulos ◽  
Nicole A Terpolilli ◽  
Nikolaus Plesnila

CO2-reactivity and neurovascular coupling are sequentially lost within the first 24 h after subarachnoid hemorrhage (SAH). Whether and when these impairments recover is not known. Therefore, we investigated the reactivity of pial and intraparenchymal vessels by in vivo two-photon microscopy one month after experimental SAH. C57BL/6 mice were subjected to either sham surgery or SAH by filament perforation. One month later, cerebral blood flow following CO2-challenge and forepaw stimulation was assessed by laser Doppler fluxmetry. Diameters of pial and intraparenchymal arterioles were quantified by in vivo two-photon microscopy. One month after SAH, pial and parenchymal vessels dilated in response to CO2. Neurovascular coupling was almost completely absent after SAH: vessel diameter did not change upon forepaw stimulation compared to a 20% increase in sham-operated mice. The current results demonstrate that neurovascular function differentially recovers after SAH: while CO2-reactivity normalizes within one month after SAH, neurovascular coupling is still absent. These findings show an acute and persistent loss of neurovascular coupling after SAH that may serve as a link between early brain injury and delayed cerebral ischemia, two distinct pathophysiological phenomena after SAH that were so far believed not to be directly related.


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