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Blood volume and optical intrinsic signal imaging of cortical spreading depression
NeuroImage
11, Number
5, 2000,
Part 2 of 2 Parts 1 n E al@
PHYSIOLOGY
Blood Volume and Optical Intrinsic Signal Imaging of Cortical Spreading Depression A.M. O’Farrell, D.E. Rex, A. Muthialu, G.K. Wong, N. Pouratian, J.W.Y. Chen, A.F. Came&a, A.W. Toga Department of Neurology, University of California, Los Angeles Cortical spreading depression (CSD) is a wave of depolarization that spreads across the cortex at 2-5 mm/mm and is followed by a 5-10 minute reduction in EEG activity. It is induced in animal models by ischemia, trauma, high potassium solution, or electrical stimulation, and it is believed to be the causative mechanism for migraine in humans. In these experiments, cortical pin-prick was used to induce CSD in 8 adult male Sprague-Dawley rats, and optical intrinsic signals (01s) or blood volume measurements were recorded simultaneously with EEG. The animals were prepared for imaging, under halothane anesthesia by thinning the parietal bone until it was translucent. For OIS, cortex was epi-illuminated with white light; the images were filtered at 850 nm, and collected with a cooled charged coupled device (CCD) camera. For blood volume measurements, we administered an intravascular fluorescent dye, Texas Red dextran (Mw 70,000, Molecular Probes), epi-illuminated the cortex with 590 ~1 light, and filtered the reflected light at 650 nm. All imaging was performed under enflurane anesthesia. EEG was recorded simultaneously, with a 12 megaohm unipolar electrode, advanced to a depth of approximately lmm. OIS recordings during CSD had a characteristic triphasic appearance with a slow rate of spread (4.2+-1.0 mm/mm) consistent with previous studies of CSD. The optical signal spread outward fairly symmetrically in all directions, with a uniform wavefront. The first phase was an initial increase in reflectance which lasted 19.0+-2.9 seconds; the second phase was a decrease in reflectance which lasted 35.6+-8.3 seconds; the third phase was an increase in reflectance which lasted at least 15 min. Blood volume measurements demonstrated a very different pattern of response to CSD. The spatial pattern was much more diffuse, with inhomogeneous borders and rate of spread. The pattern was biphasic, with a transient increase (l-2 minute duration), then decrease in blood volume. In all cases, there was a flattening of the EEG during CSD. These studies indicate that OIS recordings may be tightly coupled to CSD. They also suggest that blood volume changes may not be tightly coupled to neuronal activity during CSD, and that factors other than blood volume contribute to the 01s recordings.
This research
was suported
by NIH
grants
GM08042,
MH19950,
and MIUNS52083.
s770
11, Number
5, 2000,
Part 2 of 2 Parts 1 n E al@
PHYSIOLOGY
Blood Volume and Optical Intrinsic Signal Imaging of Cortical Spreading Depression A.M. O’Farrell, D.E. Rex, A. Muthialu, G.K. Wong, N. Pouratian, J.W.Y. Chen, A.F. Came&a, A.W. Toga Department of Neurology, University of California, Los Angeles Cortical spreading depression (CSD) is a wave of depolarization that spreads across the cortex at 2-5 mm/mm and is followed by a 5-10 minute reduction in EEG activity. It is induced in animal models by ischemia, trauma, high potassium solution, or electrical stimulation, and it is believed to be the causative mechanism for migraine in humans. In these experiments, cortical pin-prick was used to induce CSD in 8 adult male Sprague-Dawley rats, and optical intrinsic signals (01s) or blood volume measurements were recorded simultaneously with EEG. The animals were prepared for imaging, under halothane anesthesia by thinning the parietal bone until it was translucent. For OIS, cortex was epi-illuminated with white light; the images were filtered at 850 nm, and collected with a cooled charged coupled device (CCD) camera. For blood volume measurements, we administered an intravascular fluorescent dye, Texas Red dextran (Mw 70,000, Molecular Probes), epi-illuminated the cortex with 590 ~1 light, and filtered the reflected light at 650 nm. All imaging was performed under enflurane anesthesia. EEG was recorded simultaneously, with a 12 megaohm unipolar electrode, advanced to a depth of approximately lmm. OIS recordings during CSD had a characteristic triphasic appearance with a slow rate of spread (4.2+-1.0 mm/mm) consistent with previous studies of CSD. The optical signal spread outward fairly symmetrically in all directions, with a uniform wavefront. The first phase was an initial increase in reflectance which lasted 19.0+-2.9 seconds; the second phase was a decrease in reflectance which lasted 35.6+-8.3 seconds; the third phase was an increase in reflectance which lasted at least 15 min. Blood volume measurements demonstrated a very different pattern of response to CSD. The spatial pattern was much more diffuse, with inhomogeneous borders and rate of spread. The pattern was biphasic, with a transient increase (l-2 minute duration), then decrease in blood volume. In all cases, there was a flattening of the EEG during CSD. These studies indicate that OIS recordings may be tightly coupled to CSD. They also suggest that blood volume changes may not be tightly coupled to neuronal activity during CSD, and that factors other than blood volume contribute to the 01s recordings.
This research
was suported
by NIH
grants
GM08042,
MH19950,
and MIUNS52083.
s770