scholarly journals Pronounced Hypoperfusion during Spreading Depression in Mouse Cortex

2004 ◽  
Vol 24 (10) ◽  
pp. 1172-1182 ◽  
Author(s):  
Cenk Ayata ◽  
Hwa Kyoung Shin ◽  
Salvatore Salomone ◽  
Yasemin Ozdemir-Gursoy ◽  
David A. Boas ◽  
...  
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Imaging Technique ◽  
Thromboxane A2 ◽  
Laser Speckle ◽  
Cerebral Vessels ◽  
Two Dimensional ◽  
Enhanced Resistance ◽  
Mouse Cortex ◽  
Increased Sensitivity

We studied unique cerebral blood flow (CBF) responses to cortical spreading depression in mice using a novel two-dimensional CBF imaging technique, laser speckle flowmetry. Cortical spreading depression caused a triphasic CBF response in both rat and mouse cortex. In rats, mild initial hypoperfusion (approximately 75% of baseline) was followed by a transient hyperemia reaching approximately 220% of baseline. In mice, the initial hypoperfusion was pronounced (40–50% of baseline), and the anticipated hyperemic phase barely reached baseline. The duration of hypoperfusion significantly correlated with the duration of the DC shift. As a possible explanation for the pronounced hypoperfusion, mouse cerebral vessels showed enhanced resistance to relaxation by acetylcholine (3 μM) after K+-induced preconstriction (20, 40, and 80 mM) but dilated normally in response to acetylcholine after preconstriction with U46619, a synthetic thromboxane A2 analog. By contrast, rat vessels dilated readily to acetylcholine after preconstriction by K+. The transient normalization of CBF after hypoperfusion in the mouse was abolished by L-NA but not 7-NI. In summary, the CBF response to cortical spreading depression in mice contrasts with the rat in that the initial hypoperfusion is pronounced, and the hyperemic phase is markedly diminished. The differences in CBF response between species may be in part caused by an increased sensitivity of mouse cerebral vessels to elevated extracellular K+.

TWO-DIMENSIONAL VISUALIZATION OF THE PROPAGATION SPEED OF CORTICAL SPREADING DEPRESSION IN RAT CORTEX

2010 ◽  
Vol 03 (01) ◽  
pp. 75-80
Author(s):  
TINGTING XU ◽  
PENGCHENG LI ◽  
SHANGBIN CHEN ◽  
WEIHUA LUO
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Time Lag ◽  
Polar Angle ◽  
Propagation Speed ◽  
Least Square ◽  
Data Matrix ◽  
Radial Coordinate ◽  
Two Dimensional ◽  
Polar Coordinate

Cortical spreading depression (CSD), which is a significant pathological phenomenon that correlates with migraines and cerebral ischemia, has been characterized by a wave of depolarization among neuronal cells and propagates across the cortex at a rate of 2–5 mm/min. Although the propagation pattern of CSD was well-investigated using high-resolution optical imaging technique, the variation of propagation speed of CSD across different regions of cortex was not well-concerned, partially because of the lack of ideal approach to visualize two-dimensional distribution of propagation speed of CSD over the whole imaged cortex. Here, we have presented a method to compute automatically the propagation speed of CSD throughout every spots in the imaged cortex. In this method, temporal clustering analysis (TCA) and least square estimation (LSE) were first used to detect origin site where CSD was induced. Taking the origin site of CSD as the origin of coordinates, the data matrix of each image was transformed into the corresponding points based on the polar-coordinate representation. Then, two fixed-distance regions of interest (ROIs) are sliding along with the radial coordinate at each polar angle within the image for calculating the time lag with correlating algorithm. Finally, we could draw a two-dimensional image, in which the value of each pixel represented the velocity of CSD when it spread through the corresponding area of the imaged cortex. The results demonstrated that the method can reveal the heterogeneity of propagation speed of CSD in the imaged cortex with high fidelity and intuition.

Chronic paracetamol treatment increases alterations in cerebral vessels in cortical spreading depression model

2014 ◽  
Vol 94 ◽  
pp. 36-46 ◽  
Author(s):  
Waranurin Yisarakun ◽  
Weera Supornsilpchai ◽  
Chattraporn Chantong ◽  
Anan Srikiatkhachorn ◽  
Supang Maneesri-le Grand
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebral Vessels

scholarly journals Persisting Depletion of Brain Glucose following Cortical Spreading Depression, despite Apparent Hyperaemia: Evidence for Risk of an Adverse Effect of Leão's Spreading Depression

2008 ◽  
Vol 29 (1) ◽  
pp. 166-175 ◽  
Author(s):  
Parastoo Hashemi ◽  
Robin Bhatia ◽  
Hajime Nakamura ◽  
Jens P Dreier ◽  
Rudolf Graf ◽  
...  
Keyword(s):  
Adverse Effect ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Laser Speckle ◽  
Comparable Data ◽  
Brain Glucose ◽  
Rapid Sampling ◽  
Extracellular Glucose ◽  
Focal Ischaemia ◽  
Combined Time Series

Rapid sampling microdialysis (rsMD) directed towards the cerebral cortex has allowed identification of a combined time-series signature for glucose and lactate that characterizes peri-infarct depolarization in experimental focal ischaemia, but no comparable data exist for ‘classical’ cortical spreading depression (CSD) associated with hyperaemia in the normally perfused brain. Here, we examined the rsMD responses of dialysate glucose and lactate to five hyperaemic spreading depressions induced with intracortical microinjections, typically of 1 mol/L KCl, in open-skull preparations in five cats under chloralose anaesthesia. Depolarization was verified with microelectrodes, and laser speckle flowmetry was used to examine propagation of the events and perfusion responses near the MD probe. Ten minutes after depolarization, dialysate glucose fell and lactate rose by 28% and 58% respectively. There was no recovery of dialysate glucose 30 mins after depolarization. Mean baseline indicative cerebral blood flow was 25.5 ± 4.1 mL/100 g/min and mean maximum hyperaemic increase was by 29.6 ± 6 mL/100 g/min; hyperaemia remained present 30 mins after CSD. As CSD events are repetitive, frequent, and often clustered temporally in human acute brain injury, these results indicate a high risk of depletion of extracellular glucose in association with depolarization events of a pattern previously thought to be largely benign.

scholarly journals Dynamic Imaging of Cerebral Blood Flow Using Laser Speckle

2001 ◽  
Vol 21 (3) ◽  
pp. 195-201 ◽  
Author(s):  
Andrew K. Dunn ◽  
Hayrunnisa Bolay ◽  
Michael A. Moskowitz ◽  
David A. Boas
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Resolution ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Focal Cerebral Ischemia ◽  
Speckle Pattern ◽  
Dynamic Imaging ◽  
Laser Speckle ◽  
High Resolution Images

A method for dynamic, high-resolution cerebral blood flow (CBF) imaging is presented in this article. By illuminating the cortex with laser light and imaging the resulting speckle pattern, relative CBF images with tens of microns spatial and millisecond temporal resolution are obtained. The regional CBF changes measured with the speckle technique are validated through direct comparison with conventional laser-Doppler measurements. Using this method, dynamic images of the relative CBF changes during focal cerebral ischemia and cortical spreading depression were obtained along with electrophysiologic recordings. Upon middle cerebral artery (MCA) occlusion, the speckle technique yielded high-resolution images of the residual CBF gradient encompassing the ischemic core, penumbra, oligemic, and normally perfused tissues over a 6 × 4 mm cortical area. Successive speckle images demonstrated a further decrease in residual CBF indicating an expansion of the ischemic zone with finely delineated borders. Dynamic CBF images during cortical spreading depression revealed a 2 to 3 mm area of increased CBF (160% to 250%) that propagated with a velocity of 2 to 3 mm/min. This technique is easy to implement and can be used to monitor the spatial and temporal evolution of CBF changes with high resolution in studies of cerebral pathophysiology.

scholarly journals Regulation of cerebral metabolism during cortical spreading depression

2016 ◽  
Vol 36 (11) ◽  
pp. 1965-1977 ◽  
Author(s):  
Delphine Feuerstein ◽  
Heiko Backes ◽  
Markus Gramer ◽  
Masatoshi Takagaki ◽  
Paula Gabel ◽  
...  
Keyword(s):  
Energy Demand ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Metabolic Response ◽  
Cerebral Metabolism ◽  
Ion Homeostasis ◽  
Glucose Consumption ◽  
Compartment Model ◽  
Laser Speckle ◽  
Rapid Sampling

We analyzed the metabolic response to cortical spreading depression that drastically increases local energy demand to restore ion homeostasis. During single and multiple cortical spreading depressions in the rat cortex, we simultaneously monitored extracellular levels of glucose and lactate using rapid sampling microdialysis and glucose influx using 18 F-fluorodeoxyglucose positron emission tomography while tracking cortical spreading depression using laser speckle imaging. Combining the acquired data with steady-state requirements we developed a mass-conserving compartment model including neurons and glia that was consistent with the observed data. In summary, our findings are: (1) Early breakdown of glial glycogen provides a major source of energy during increased energy demand and leaves 80% of blood-borne glucose to neurons. (2) Lactate is used solely by neurons and only if extracellular lactate levels are >80% above normal. (3) Although the ratio of oxygen and glucose consumption transiently reaches levels <3, the major part (>90%) of the overall energy supply is from oxidative metabolism. (4) During cortical spreading depression, brain release of lactate exceeds its consumption suggesting that lactate is only a circumstantial energy substrate. Our findings provide a general scenario for the metabolic response to increased cerebral energy demand.

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