In vivo optical imaging of cortical spreading depression in rat

2003 ◽  
Author(s):  
Shangbin Chen ◽  
Pengcheng Li ◽  
Weihua Luo ◽  
Hui Gong ◽  
Haiying Cheng ◽  
...  
2002 ◽  
Vol 88 (5) ◽  
pp. 2726-2735 ◽  
Author(s):  
Alyssa M. Ba ◽  
Michael Guiou ◽  
Nader Pouratian ◽  
Arpitha Muthialu ◽  
David E. Rex ◽  
...  

Cortical spreading depression (CSD) is an important disease model for migraine and cerebral ischemia. In this study, we exploit the high temporal and spatial resolution of optical imaging to characterize perfusion-dependent and -independent changes in response to CSD and to investigate the etiology of reflectance changes during CSD. In this experiment, we characterized the optical response to CSD at wavelengths that emphasize perfusion-related changes (610 and 550 nm), and we compared these results with 850 nm and blood volume data. Blood volume changes during CSD were recorded using an intravascular fluorescent dye, Texas Red dextran. We observed triphasic optical signals at 850 and 550 nm characterized by spreading waves of increased, decreased, then increased reflectance (Fig. 1 ) which expanded at a rate of approximately 3–5 mm/min. The signal at 610 nm had a similar initial phase, but the phase 2 response was slightly more complex, with a parenchymal decrease in reflectance but a vascular increase in reflectance. Reflectance values decreased in phase three. Blood volume signals were delayed relative to the optical intrinsic signals and corresponded temporally to phases 2 and 3. This is the first study to characterize optical imaging of intrinsic signal responses to CSD, in vivo, at multiple wavelengths. The data presented here suggest that changes in light scattering precede perfusion responses, the blood volume increase (phase 2) is accompanied by a reduction in deoxyhemoglobin, and the blood volume decrease (phase 3) is accompanied by an increase in deoxyhemoglobin. Previous studies have suggested the oligemia of spreading depression was a result of decreased metabolic demand. This study suggests that during the oligemic period there is a greater reduction in oxygen delivery than in demand.


2018 ◽  
Vol 109 (4) ◽  
pp. 912-918 ◽  
Author(s):  
Takeshi Imamura ◽  
Takashi Saitou ◽  
Ryosuke Kawakami

2014 ◽  
Vol 124 (8) ◽  
pp. E312-E319 ◽  
Author(s):  
Joel Y. Sun ◽  
Jiayin Shen ◽  
Joel Thibodeaux ◽  
Gang Huang ◽  
Yiguang Wang ◽  
...  

2015 ◽  
Vol 27 (2) ◽  
pp. 404-413 ◽  
Author(s):  
Kazuhide Sato ◽  
Alexander P. Gorka ◽  
Tadanobu Nagaya ◽  
Megan S. Michie ◽  
Roger R. Nani ◽  
...  

1997 ◽  
Vol 17 (5) ◽  
pp. 586-590 ◽  
Author(s):  
Sachiko Osuga ◽  
Antoine M. Hakim ◽  
Hitoshi Osuga ◽  
Matthew J. Hogan

We report autoradiographic measurements of the in vivo uptake of [3H]nimodipine during the nonischemic depolarization of cortical spreading depression (CSD) in rat brain. [3H]Nimodipine uptake in brain was determined regionally in rats undergoing CSD (n = 8) and was significantly increased in cortex (14 ± 7%) and hippocampus (10 ± 6%) on the stimulated side relative to the contralateral hemisphere when compared with the same measurements in a control group (n = 8). A similar measurement using the physiologically inert radiotracer [14C]iodoantipyrine to control for potential effects of CSD on radioligand distribution showed a minimal increase (2.4 ± 0.7%) of radiotracer uptake in cortex after CSD. This increase was significantly less than that observed in the [3H]nimodipine uptake studies. We hypothesize that increased in vivo [3H]nimodipine uptake in CSD identifies regions of depolarization and thus infers activation of the L-type voltage sensitive calcium channels.


2001 ◽  
Vol 172 (2) ◽  
pp. 342-353 ◽  
Author(s):  
Daniel P. Bradley ◽  
Martin I. Smith ◽  
Chaiyapoj Netsiri ◽  
Justin M. Smith ◽  
Kurt H.J. Bockhorst ◽  
...  

2009 ◽  
Vol 14 (1) ◽  
pp. 014023 ◽  
Author(s):  
Nobuyuki Kosaka ◽  
Mikako Ogawa ◽  
Michelle R. Longmire ◽  
Peter L. Choyke ◽  
Hisataka Kobayashi

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