Elicitation interval dependent spatiotemporal evolution of cortical spreading depression waves revealed by optical intrinsic signal imaging

2007 ◽  
Author(s):  
Shangbin Chen ◽  
Hui Gong ◽  
Shaoqun Zeng ◽  
Qingming Luo ◽  
Pengcheng Li
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Spatiotemporal Evolution ◽  
Intrinsic Signal ◽  
Optical Intrinsic Signal

Blood volume and optical intrinsic signal imaging of cortical spreading depression

NeuroImage ◽  
2000 ◽  
Vol 11 (5) ◽  
pp. S770
Author(s):  
A.M. O'Farrell ◽  
D.E. Rex ◽  
A. Muthialu ◽  
G.K. Wong ◽  
N. Pouratian ◽  
...  
Keyword(s):  
Blood Volume ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Intrinsic Signal ◽  
Optical Intrinsic Signal

Distinct Vascular Conduction With Cortical Spreading Depression

2007 ◽  
Vol 97 (6) ◽  
pp. 4143-4151 ◽  
Author(s):  
Kevin C. Brennan ◽  
Luis Beltrán-Parrazal ◽  
Hector E. López-Valdés ◽  
Jeremy Theriot ◽  
Arthur W. Toga ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Field Potential ◽  
Cortical Surface ◽  
Intrinsic Signal ◽  
Optical Intrinsic Signal ◽  
Vasomotor Activity ◽  
High Concentrations ◽  
The Relationship

Cortical spreading depression (CSD) is associated with significant vasodilatation and vasoconstriction, but the relationship between the cortical parenchymal and vascular phenomena remains poorly understood. We used optical intrinsic signal (OIS) imaging and electrophysiology to simultaneously examine the vascular and parenchymal changes that occur with CSD in anesthetized mice and rats. CSD was associated with a propagated multiphasic change in optical reflectance, with correlated negative DC shift in field potential. Dilatation of cortical surface arterioles propagated with a significantly greater intrinsic velocity than the parenchymal CSD wavefront measured by OIS and electrophysiology. Dilatation traveled in a circuitous pattern along individual arterioles, indicating specific vascular conduction as opposed to concentric propagation of a parenchymal signal. Arteriolar dilatation propagated into areas beyond the spread of parenchymal OIS and electrophysiological changes of CSD. Conversely, vasomotor activity could be experimentally dissociated from the parenchymal CSD wave. Frequent repetitive CSD evoked by continuous stimulation was associated with a reduced or absent arteriolar response despite preserved parenchymal OIS and electrophysiological changes. Similarly, dimethylsulfoxide at high concentrations (10%) inhibited arteriolar reactivity despite preserved parenchymal OIS and electrophysiological changes. These results suggest a mechanism, intrinsic to the vasculature, for propagation of vasodilatation associated with CSD. Distinct vascular conduction could be important for the pathogenesis of conditions that involve CSD, including migraine, stroke, and traumatic brain injury.

Multiwavelength Optical Intrinsic Signal Imaging of Cortical Spreading Depression

2002 ◽  
Vol 88 (5) ◽  
pp. 2726-2735 ◽  
Author(s):  
Alyssa M. Ba ◽  
Michael Guiou ◽  
Nader Pouratian ◽  
Arpitha Muthialu ◽  
David E. Rex ◽  
...  
Keyword(s):  
Optical Imaging ◽  
Blood Volume ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Phase 2 ◽  
Volume Data ◽  
Metabolic Demand ◽  
Intrinsic Signal ◽  
Optical Intrinsic Signal

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.

scholarly journals Optogenetic induction of cortical spreading depression in anesthetized and freely behaving mice

2016 ◽  
Vol 37 (5) ◽  
pp. 1641-1655 ◽  
Author(s):  
Thijs Houben ◽  
Inge CM Loonen ◽  
Serapio M Baca ◽  
Maarten Schenke ◽  
Johanna H Meijer ◽  
...  
Keyword(s):  
Laser Doppler Flowmetry ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Laser Doppler ◽  
Doppler Flowmetry ◽  
Intrinsic Signal ◽  
Non Invasive ◽  
Optical Intrinsic Signal ◽  
Dc Potential ◽  
Freely Behaving

Cortical spreading depression, which plays an important role in multiple neurological disorders, has been studied primarily with experimental models that use highly invasive methods. We developed a relatively non-invasive optogenetic model to induce cortical spreading depression by transcranial stimulation of channelrhodopsin-2 ion channels expressed in cortical layer 5 neurons. Light-evoked cortical spreading depression in anesthetized and freely behaving mice was studied with intracortical DC-potentials, multi-unit activity and/or non-invasive laser Doppler flowmetry, and optical intrinsic signal imaging. In anesthetized mice, cortical spreading depression induction thresholds and propagation rates were similar for invasive (DC-potential) and non-invasive (laser Doppler flowmetry) recording paradigms. Cortical spreading depression-related vascular and parenchymal optical intrinsic signal changes were similar to those evoked with KCl. In freely behaving mice, DC-potential and multi-unit activity recordings combined with laser Doppler flowmetry revealed cortical spreading depression characteristics comparable to those under anesthesia, except for a shorter cortical spreading depression duration. Cortical spreading depression resulted in a short increase followed by prolonged reduction of spontaneous active behavior. Motor function, as assessed by wire grip tests, was transiently and unilaterally suppressed following a cortical spreading depression. Optogenetic cortical spreading depression induction has significant advantages over current models in that multiple cortical spreading depression events can be elicited in a non-invasive and cell type-selective fashion.

EEG and multi-wavelength optical intrinsic signal imaging of cortical spreading depression

NeuroImage ◽  
2001 ◽  
Vol 13 (6) ◽  
pp. 979
Author(s):  
M. Guiou ◽  
A.M. O'Farrell ◽  
S. Sheth ◽  
N. Pouratian ◽  
M. Nemoto ◽  
...  
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Intrinsic Signal ◽  
Optical Intrinsic Signal ◽  
Multi Wavelength

EFFECTS OF NAAG AND MPEP ON RAT CORTICAL SPREADING DEPRESSION

2010 ◽  
Vol 03 (02) ◽  
pp. 123-129
Author(s):  
ZHEN WANG ◽  
WEIHUA LUO ◽  
XIAOLI SUN ◽  
PENGCHENG LI ◽  
SHANGBIN CHEN ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Cortical Spreading Depression ◽  
Metabotropic Glutamate Receptors ◽  
Spreading Depression ◽  
Neurological Diseases ◽  
Propagation Mechanism ◽  
Metabotropic Glutamate ◽  
Intrinsic Signal ◽  
Optical Intrinsic Signal ◽  
Potential Recording

Cortical spreading depression (CSD) is a pathophysiological phenomenon. There are sufficient evidences to prove that CSD plays an important role in some neurological disorders. However, exact mechanisms of its initiation and propagation are still unclear. Previous studies showed that glutamate receptors could be concerned with CSD, but those studies were mostly performed oriented to ionotropic glutamate receptors (iGluRs). There is relatively little report about effects of metabotropic glutamate receptors (mGluRs) on CSD. Here, we applied optical intrinsic signal imaging (OISI) combined with direct current (DC) potential recording to examine influences of some mGluRs antagonist (or agonist) on CSD propagation in rat's brain, to indirectly validate actions of some mGluRs on CSD. We found that N-acetyl-L-aspartyl-L-glutamate (NAAG, an agonist at mGluR3) inhibited the propagation of CSD, and the inhibition was gradually developed with time. However, 6-methyl-2-phenylethynyl-pyridine (MPEP, an antagonist of mGluR5) did not produce any significant alterations with the CSD propagation. Our findings suggest that mGluR3 could play an important role in the CSD propagation, but the activity of mGluR5 was comparatively weak. These findings can help to understand the propagation mechanism of CSD, and consider the therapy of some neurological diseases involved with CSD.

ACCURATELY DETERMINING PROPAGATION VELOCITY OF CORTICAL SPREADING DEPRESSION IN RATS BY OPTICAL INTRINSIC SIGNAL IMAGING

2010 ◽  
Vol 03 (02) ◽  
pp. 103-108 ◽  
Author(s):  
XIAOLI SUN ◽  
PENGCHENG LI ◽  
WEIHUA LUO ◽  
BIYING GONG ◽  
QINGMING LUO
Keyword(s):  
Propagation Velocity ◽  
Optical Method ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Average Rate ◽  
Electrophysiological Recording ◽  
Intrinsic Signal ◽  
Spreading Pattern ◽  
Optical Intrinsic Signal ◽  
Dc Potential

Cortical spreading depression (CSD) is a wave of neuronal and glial depolarization that propagates across the cortex at a rate of 2–5 mm/min accompanied by reversible electroencephalogram (EEG) suppression, a negative shift of direct current (DC) potential, and change of optical intrinsic signals (OIS). Propagation velocity of CSD is an important parameter used to study this phenomenon. It is commonly determined in an electrophysiological way that measures the time required for a CSD wave to pass along two electrodes. Since the electrophysiology technique fails to reveal the spreading pattern of CSD, velocity calculated in this manner might be inaccurate. In this study, we combined the electrophysiological recording and OIS imaging (OISI) for detecting changes in DC potential and OIS during CSD simultaneously. An optical method based on OISI to determine the CSD velocity, which is measured by generating a series of regions of interest (ROI) perpendicular to the advancing wavefront along propagation direction of CSD at different time points and then dividing by the distance between ROIs over time, is presented. Comparison of the accuracy of the two approaches in determining the CSD velocity is made as well. The average rate of 33 CSDs is 3.52 ± 0.87 mm/min by use of the optical method and 4.36 ± 1.65 mm/min by use of the electrophysiological method. Because of the information about spreading pattern of CSD provided optically, the velocity determined by OISI is of smaller deviation and higher accuracy.

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