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( A ) Image of the cerebral vasculature under 530 nm <t>illumination</t> through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Locomotion-triggered spatial pattern average of ΔHbT aligned to locomotion onset (n = 54 events in 1 mouse). Note visible changes within ∼100 miliseconds. ( C ) Average of locomotion onset and offset triggered response of ΔHbT (n = 7 mice) in veins at different locations. ( D ) As in ( C ) but for ΔHbO-HbR (n = 7 mice). ( E ) Average total hemoglobin change (ΔHbT) during the initial phase of locomotion (0-1 second after locomotion onset, left) and sustained locomotion (2-5 seconds after locomotion onset, right) in veins at different locations. In response to voluntary locomotion onset, we observed a fast decrease of ΔHbT in superior sagittal sinus (SSS, -11.07 ± 5.33 µM, Wilcoxson rank sum test, p = 0.0003) and bridging veins (BV, -14.80 ± 10.02 µM, Wilcoxson rank sum test, p = 0.0003), while ΔHbT of pial veins in the FL/HL (−3.60 ± 8.92 µM, Wilcoxson rank sum test, p = 0.09) and Wh (0.33 ± 6.01 µM, Wilcoxson rank sum test, p = 0.7164) did not change significantly. In response to constant locomotion, the initially decreased ΔHbT returned to baseline level for both the SSS (−8.82 ± 10.45 µM, Wilcoxson rank sum test, p = 0.09) and the BV (−11.18 ± 24.87 µM, Wilcoxson rank sum test, p = 0.3445), while ΔHbT of pial veins in the FL/HL (17.60 ± 12.21 µM, Wilcoxson rank sum test, p = 0.0169) and Wh (16.87 ± 5.51 µM, Wilcoxson rank sum test, p = 0.0006) increase significantly. ( F ) As in ( E ) but for ΔHbO-HbR. In response to voluntary locomotion onset, no significant change of ΔHbO-HbR was observed in superior sagittal sinus (SSS, 3.48 ± 10.50 µM, Wilcoxson rank sum test, p = 0.7164), bridging veins (BV, 10.28 ± 15.68 µM, Wilcoxson rank sum test, p = 0.7164), and pial veins in the FL/HL (11.84 ± 16.30 µM, Wilcoxson rank sum test, p = 0.9327) and Wh (10.97 ± 12.08 µM, Wilcoxson rank sum test, p = 0.9980). During locomotion, significant increases of ΔHbO-HbR were observed in superior sagittal sinus (SSS, 61.33 ± 24.34 µM, Wilcoxson rank sum test, p = 0.0006), bridging veins (BV, 84.79 ± 29.85 µM, Wilcoxson rank sum test, p = 0.0006), and pial veins in the FL/HL (84.66 ± 33.03 µM, Wilcoxson rank sum test, p = 0.0006) and Wh (57.28 ± 23.55 µM, Wilcoxson rank sum test, p = 0.0006).
Led Light Illumination, supplied by Thorlabs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


( A ) Image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Locomotion-triggered spatial pattern average of ΔHbT aligned to locomotion onset (n = 54 events in 1 mouse). Note visible changes within ∼100 miliseconds. ( C ) Average of locomotion onset and offset triggered response of ΔHbT (n = 7 mice) in veins at different locations. ( D ) As in ( C ) but for ΔHbO-HbR (n = 7 mice). ( E ) Average total hemoglobin change (ΔHbT) during the initial phase of locomotion (0-1 second after locomotion onset, left) and sustained locomotion (2-5 seconds after locomotion onset, right) in veins at different locations. In response to voluntary locomotion onset, we observed a fast decrease of ΔHbT in superior sagittal sinus (SSS, -11.07 ± 5.33 µM, Wilcoxson rank sum test, p = 0.0003) and bridging veins (BV, -14.80 ± 10.02 µM, Wilcoxson rank sum test, p = 0.0003), while ΔHbT of pial veins in the FL/HL (−3.60 ± 8.92 µM, Wilcoxson rank sum test, p = 0.09) and Wh (0.33 ± 6.01 µM, Wilcoxson rank sum test, p = 0.7164) did not change significantly. In response to constant locomotion, the initially decreased ΔHbT returned to baseline level for both the SSS (−8.82 ± 10.45 µM, Wilcoxson rank sum test, p = 0.09) and the BV (−11.18 ± 24.87 µM, Wilcoxson rank sum test, p = 0.3445), while ΔHbT of pial veins in the FL/HL (17.60 ± 12.21 µM, Wilcoxson rank sum test, p = 0.0169) and Wh (16.87 ± 5.51 µM, Wilcoxson rank sum test, p = 0.0006) increase significantly. ( F ) As in ( E ) but for ΔHbO-HbR. In response to voluntary locomotion onset, no significant change of ΔHbO-HbR was observed in superior sagittal sinus (SSS, 3.48 ± 10.50 µM, Wilcoxson rank sum test, p = 0.7164), bridging veins (BV, 10.28 ± 15.68 µM, Wilcoxson rank sum test, p = 0.7164), and pial veins in the FL/HL (11.84 ± 16.30 µM, Wilcoxson rank sum test, p = 0.9327) and Wh (10.97 ± 12.08 µM, Wilcoxson rank sum test, p = 0.9980). During locomotion, significant increases of ΔHbO-HbR were observed in superior sagittal sinus (SSS, 61.33 ± 24.34 µM, Wilcoxson rank sum test, p = 0.0006), bridging veins (BV, 84.79 ± 29.85 µM, Wilcoxson rank sum test, p = 0.0006), and pial veins in the FL/HL (84.66 ± 33.03 µM, Wilcoxson rank sum test, p = 0.0006) and Wh (57.28 ± 23.55 µM, Wilcoxson rank sum test, p = 0.0006).

Journal: bioRxiv

Article Title: Ultrafast venous and sagittal sinus constrictions in the brain driven by abdominal pressure

doi: 10.64898/2026.05.02.722426

Figure Lengend Snippet: ( A ) Image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Locomotion-triggered spatial pattern average of ΔHbT aligned to locomotion onset (n = 54 events in 1 mouse). Note visible changes within ∼100 miliseconds. ( C ) Average of locomotion onset and offset triggered response of ΔHbT (n = 7 mice) in veins at different locations. ( D ) As in ( C ) but for ΔHbO-HbR (n = 7 mice). ( E ) Average total hemoglobin change (ΔHbT) during the initial phase of locomotion (0-1 second after locomotion onset, left) and sustained locomotion (2-5 seconds after locomotion onset, right) in veins at different locations. In response to voluntary locomotion onset, we observed a fast decrease of ΔHbT in superior sagittal sinus (SSS, -11.07 ± 5.33 µM, Wilcoxson rank sum test, p = 0.0003) and bridging veins (BV, -14.80 ± 10.02 µM, Wilcoxson rank sum test, p = 0.0003), while ΔHbT of pial veins in the FL/HL (−3.60 ± 8.92 µM, Wilcoxson rank sum test, p = 0.09) and Wh (0.33 ± 6.01 µM, Wilcoxson rank sum test, p = 0.7164) did not change significantly. In response to constant locomotion, the initially decreased ΔHbT returned to baseline level for both the SSS (−8.82 ± 10.45 µM, Wilcoxson rank sum test, p = 0.09) and the BV (−11.18 ± 24.87 µM, Wilcoxson rank sum test, p = 0.3445), while ΔHbT of pial veins in the FL/HL (17.60 ± 12.21 µM, Wilcoxson rank sum test, p = 0.0169) and Wh (16.87 ± 5.51 µM, Wilcoxson rank sum test, p = 0.0006) increase significantly. ( F ) As in ( E ) but for ΔHbO-HbR. In response to voluntary locomotion onset, no significant change of ΔHbO-HbR was observed in superior sagittal sinus (SSS, 3.48 ± 10.50 µM, Wilcoxson rank sum test, p = 0.7164), bridging veins (BV, 10.28 ± 15.68 µM, Wilcoxson rank sum test, p = 0.7164), and pial veins in the FL/HL (11.84 ± 16.30 µM, Wilcoxson rank sum test, p = 0.9327) and Wh (10.97 ± 12.08 µM, Wilcoxson rank sum test, p = 0.9980). During locomotion, significant increases of ΔHbO-HbR were observed in superior sagittal sinus (SSS, 61.33 ± 24.34 µM, Wilcoxson rank sum test, p = 0.0006), bridging veins (BV, 84.79 ± 29.85 µM, Wilcoxson rank sum test, p = 0.0006), and pial veins in the FL/HL (84.66 ± 33.03 µM, Wilcoxson rank sum test, p = 0.0006) and Wh (57.28 ± 23.55 µM, Wilcoxson rank sum test, p = 0.0006).

Article Snippet: Reflectance images were acquired during periods of green LED light illumination at 530 nm (M530L3, Thorlabs, Newton, NJ) or red LED light illumination at 630 nm (M625L4, Thorlabs, Newton, NJ), whereas a 500-nm long-pass filter (FELH0500, Thorlabs, Newton, NJ) mounted in front of the camera enabled imaging of GCaMP fluorescence during periods of illumination with blue LED light with a wavelength around 470 nm (M470L3, Thorlabs, Newton, NJ).

Techniques:

( A ) Schematic showing the pial vasculature in the mouse brain. Left, dorsal view in vivo under 530 nm illumination with veins traced in blue and arteries in magenta; Top right, images showing the dural venous sinuses after transcardial perfusion with FITC and gelatin and fixation; Bottom right, schematic showing the coronal view of the mouse brain. ( B ) Left, schematic of the experimental setup for widefield IOS imaging of awake head fixed mice. Right, image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( C ) Example data showing hemodynamic changes of veins at different locations (shown in B ) during voluntary locomotion. FL/HL, forelimb/hindlimb representation of the somatosensory cortex; Wh, vibrissae cortex. ΔHbT, total hemoglobin; ΔHbO-HbR, differences of oxy- and deoxy-hemoglobin. The shaded area denotes the period of locomotion. ( D ) Averaged locomotion onset- and offset-triggered responses of ΔD/D 0 (n = 7 mice) in veins at different locations. ( E ) Average venous diameter change (ΔD/D 0 ) during the initial phase of locomotion (0-1 second after locomotion onset, left) and sustained locomotion (2-5 seconds after locomotion onset, right) in veins at different locations. There was a rapid constriction in superior sagittal sinus (SSS, -1.18 ± 0.42%, Wilcoxson rank sum test, p = 0.0003) and bridging veins (BV, -0.76 ± 0.84%, Wilcoxson rank sum test, p = 0.0084) in response to locomotion onset, while pial veins in the FL/HL (−0.63 ± 1.22%, Wilcoxson rank sum test, p = 0.09) and Wh (0.13 ± 0.51%, Wilcoxson rank sum test, p = 0.9327) did not change significantly. In response to constant locomotion, the initially constricted BV return to baseline level (−0.34 ± 2.01%, Wilcoxson rank sum test, p = 0.3450), while the SSS stayed constricted (−2.13 ± 0.92%, Wilcoxson rank sum test, p = 0.0003) and returned to baseline level within seconds after the cessation of voluntary locomotion. ( F ) Significant negative relationship (slope = -0.0172, 95% confidence interval [-0.0225, -0.0119], goodness of fit R 2 = 0.6296, p = 4.7358e-7) between the venous diameter change and baseline vessel diameter, showing the large collecting vessels constrict in response to locomotion.

Journal: bioRxiv

Article Title: Ultrafast venous and sagittal sinus constrictions in the brain driven by abdominal pressure

doi: 10.64898/2026.05.02.722426

Figure Lengend Snippet: ( A ) Schematic showing the pial vasculature in the mouse brain. Left, dorsal view in vivo under 530 nm illumination with veins traced in blue and arteries in magenta; Top right, images showing the dural venous sinuses after transcardial perfusion with FITC and gelatin and fixation; Bottom right, schematic showing the coronal view of the mouse brain. ( B ) Left, schematic of the experimental setup for widefield IOS imaging of awake head fixed mice. Right, image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( C ) Example data showing hemodynamic changes of veins at different locations (shown in B ) during voluntary locomotion. FL/HL, forelimb/hindlimb representation of the somatosensory cortex; Wh, vibrissae cortex. ΔHbT, total hemoglobin; ΔHbO-HbR, differences of oxy- and deoxy-hemoglobin. The shaded area denotes the period of locomotion. ( D ) Averaged locomotion onset- and offset-triggered responses of ΔD/D 0 (n = 7 mice) in veins at different locations. ( E ) Average venous diameter change (ΔD/D 0 ) during the initial phase of locomotion (0-1 second after locomotion onset, left) and sustained locomotion (2-5 seconds after locomotion onset, right) in veins at different locations. There was a rapid constriction in superior sagittal sinus (SSS, -1.18 ± 0.42%, Wilcoxson rank sum test, p = 0.0003) and bridging veins (BV, -0.76 ± 0.84%, Wilcoxson rank sum test, p = 0.0084) in response to locomotion onset, while pial veins in the FL/HL (−0.63 ± 1.22%, Wilcoxson rank sum test, p = 0.09) and Wh (0.13 ± 0.51%, Wilcoxson rank sum test, p = 0.9327) did not change significantly. In response to constant locomotion, the initially constricted BV return to baseline level (−0.34 ± 2.01%, Wilcoxson rank sum test, p = 0.3450), while the SSS stayed constricted (−2.13 ± 0.92%, Wilcoxson rank sum test, p = 0.0003) and returned to baseline level within seconds after the cessation of voluntary locomotion. ( F ) Significant negative relationship (slope = -0.0172, 95% confidence interval [-0.0225, -0.0119], goodness of fit R 2 = 0.6296, p = 4.7358e-7) between the venous diameter change and baseline vessel diameter, showing the large collecting vessels constrict in response to locomotion.

Article Snippet: Reflectance images were acquired during periods of green LED light illumination at 530 nm (M530L3, Thorlabs, Newton, NJ) or red LED light illumination at 630 nm (M625L4, Thorlabs, Newton, NJ), whereas a 500-nm long-pass filter (FELH0500, Thorlabs, Newton, NJ) mounted in front of the camera enabled imaging of GCaMP fluorescence during periods of illumination with blue LED light with a wavelength around 470 nm (M470L3, Thorlabs, Newton, NJ).

Techniques: In Vivo, Imaging

( A ) Image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Averaged spatial distribution of ΔHbT in response to contralateral whisker stimulation (n = 20 events in 1 mouse). ( C ) Group average of contralateral whisker stimulation triggered response of ΔHbT (n = 4 mice) in veins at different locations. Inlet showing a zoom-in view of ΔHbT responses immediately before (330 ms) and after (660 ms) whisker stimulation. ( D ) As in ( C ) but for ΔHbO-HbR (n = 4 mice). ( E ) Average total hemoglobin change (ΔHbT) during the initial phase of contralateral whisker stimulation (0-0.5 second after contralateral whisker stimulation onset, left) and 0.5-3 seconds after whisker stimulation (right) in veins at different locations. During the initial phase after the whisker stimulation, we observed a fast decrease of ΔHbT in superior sagittal sinus (SSS, - 12.83 ± 10.66 µM, Wilcoxson rank sum test, p = 0.0143) and pial veins in the FL/HL (−4.66 ± 4.37 µM, Wilcoxson rank sum test, p = 0.0143), while the ΔHbT of bridging veins (BV, -5.71 ± 4.22 µM, Wilcoxson rank sum test, p = 0.1571) and pial veins in the Wh (−0.11 ± 0.92 µM, Wilcoxson rank sum test, p = 0.9429) did not change significantly. During later phase after the whisker stimulation, the ΔHbT returned to baseline level in SSS (4.38 ± 4.30 µM, Wilcoxson rank sum test, p = 0.1571), while ΔHbT of BV (9.38 ± 6.99 µM, Wilcoxson rank sum test, p = 0.0143), as well as ΔHbT of pial veins in the FL/HL (12.53 ± 5.78 µM, Wilcoxson rank sum test, p = 0.0143) and Wh (8.32 ± 5.31 µM, Wilcoxson rank sum test, p = 0.0143) increase significantly. ( F ) As in ( E ) but for ΔHbO-HbR. During the initial phase after whisker stimulation, no significant change of ΔHbO-HbR was observed in superior sagittal sinus (SSS, -4.77 ± 4.64 µM, Wilcoxson rank sum test, p = 0.1571), bridging veins (BV, -0.20 ± 4.66 µM, Wilcoxson rank sum test, p = 0.6), and pial veins in the FL/HL (−0.25 ± 6.13 µM, Wilcoxson rank sum test, p = 0.6) and Wh (1.17 ± 2.55 µM, Wilcoxson rank sum test, p = 0.9429). During later phase after whisker stimulation, significant increases of ΔHbO-HbR were observed in superior sagittal sinus (SSS, 45.26 ± 3.62 µM, Wilcoxson rank sum test, p = 0.0286), bridging veins (BV, 55.15 ± 33.25 µM, Wilcoxson rank sum test, p = 0.0286), and pial veins in the FL/HL (58.46 ± 12.10 µM, Wilcoxson rank sum test, p = 0.0286) and Wh (33.64 ± 18.73 µM, Wilcoxson rank sum test, p = 0.0286).

Journal: bioRxiv

Article Title: Ultrafast venous and sagittal sinus constrictions in the brain driven by abdominal pressure

doi: 10.64898/2026.05.02.722426

Figure Lengend Snippet: ( A ) Image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Averaged spatial distribution of ΔHbT in response to contralateral whisker stimulation (n = 20 events in 1 mouse). ( C ) Group average of contralateral whisker stimulation triggered response of ΔHbT (n = 4 mice) in veins at different locations. Inlet showing a zoom-in view of ΔHbT responses immediately before (330 ms) and after (660 ms) whisker stimulation. ( D ) As in ( C ) but for ΔHbO-HbR (n = 4 mice). ( E ) Average total hemoglobin change (ΔHbT) during the initial phase of contralateral whisker stimulation (0-0.5 second after contralateral whisker stimulation onset, left) and 0.5-3 seconds after whisker stimulation (right) in veins at different locations. During the initial phase after the whisker stimulation, we observed a fast decrease of ΔHbT in superior sagittal sinus (SSS, - 12.83 ± 10.66 µM, Wilcoxson rank sum test, p = 0.0143) and pial veins in the FL/HL (−4.66 ± 4.37 µM, Wilcoxson rank sum test, p = 0.0143), while the ΔHbT of bridging veins (BV, -5.71 ± 4.22 µM, Wilcoxson rank sum test, p = 0.1571) and pial veins in the Wh (−0.11 ± 0.92 µM, Wilcoxson rank sum test, p = 0.9429) did not change significantly. During later phase after the whisker stimulation, the ΔHbT returned to baseline level in SSS (4.38 ± 4.30 µM, Wilcoxson rank sum test, p = 0.1571), while ΔHbT of BV (9.38 ± 6.99 µM, Wilcoxson rank sum test, p = 0.0143), as well as ΔHbT of pial veins in the FL/HL (12.53 ± 5.78 µM, Wilcoxson rank sum test, p = 0.0143) and Wh (8.32 ± 5.31 µM, Wilcoxson rank sum test, p = 0.0143) increase significantly. ( F ) As in ( E ) but for ΔHbO-HbR. During the initial phase after whisker stimulation, no significant change of ΔHbO-HbR was observed in superior sagittal sinus (SSS, -4.77 ± 4.64 µM, Wilcoxson rank sum test, p = 0.1571), bridging veins (BV, -0.20 ± 4.66 µM, Wilcoxson rank sum test, p = 0.6), and pial veins in the FL/HL (−0.25 ± 6.13 µM, Wilcoxson rank sum test, p = 0.6) and Wh (1.17 ± 2.55 µM, Wilcoxson rank sum test, p = 0.9429). During later phase after whisker stimulation, significant increases of ΔHbO-HbR were observed in superior sagittal sinus (SSS, 45.26 ± 3.62 µM, Wilcoxson rank sum test, p = 0.0286), bridging veins (BV, 55.15 ± 33.25 µM, Wilcoxson rank sum test, p = 0.0286), and pial veins in the FL/HL (58.46 ± 12.10 µM, Wilcoxson rank sum test, p = 0.0286) and Wh (33.64 ± 18.73 µM, Wilcoxson rank sum test, p = 0.0286).

Article Snippet: Reflectance images were acquired during periods of green LED light illumination at 530 nm (M530L3, Thorlabs, Newton, NJ) or red LED light illumination at 630 nm (M625L4, Thorlabs, Newton, NJ), whereas a 500-nm long-pass filter (FELH0500, Thorlabs, Newton, NJ) mounted in front of the camera enabled imaging of GCaMP fluorescence during periods of illumination with blue LED light with a wavelength around 470 nm (M470L3, Thorlabs, Newton, NJ).

Techniques: Whisker Assay

( A ) Left, schematic of the experimental setup for widefield IOS imaging of head fixed mice. Right, image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Example data showing hemodynamic changes of veins at different locations (shown in A ) during transitions between arousal states. Top, arousal sate scored from EMG/ECoG/whisker and body motion. White break denotes break in data collection between trials. FL/HL, forelimb/hindlimb representation of the somatosensory cortex; Wh, vibrissae cortex. ΔHbT, total hemoglobin; ΔHbO-HbR, differences of oxy- and deoxy-hemoglobin. The shaded area denotes the periods of different arousal states. ( C ) Changes of abdominal muscle EMG (ΔP EMG /P 0 ), ΔHbT, ΔHbO-HbR, ΔD/D 0 during the transition of awake into NREM (n = 4 mice), NREM into REM (n = 2 mice), NREM into awake (n = 4 mice), REM into awake (n = 2 mice). Note that scales are different across conditions. ( D ) Bar plot showing the mean changes in diameter and hemodynamic signals in response to each arousal state transition.

Journal: bioRxiv

Article Title: Ultrafast venous and sagittal sinus constrictions in the brain driven by abdominal pressure

doi: 10.64898/2026.05.02.722426

Figure Lengend Snippet: ( A ) Left, schematic of the experimental setup for widefield IOS imaging of head fixed mice. Right, image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Example data showing hemodynamic changes of veins at different locations (shown in A ) during transitions between arousal states. Top, arousal sate scored from EMG/ECoG/whisker and body motion. White break denotes break in data collection between trials. FL/HL, forelimb/hindlimb representation of the somatosensory cortex; Wh, vibrissae cortex. ΔHbT, total hemoglobin; ΔHbO-HbR, differences of oxy- and deoxy-hemoglobin. The shaded area denotes the periods of different arousal states. ( C ) Changes of abdominal muscle EMG (ΔP EMG /P 0 ), ΔHbT, ΔHbO-HbR, ΔD/D 0 during the transition of awake into NREM (n = 4 mice), NREM into REM (n = 2 mice), NREM into awake (n = 4 mice), REM into awake (n = 2 mice). Note that scales are different across conditions. ( D ) Bar plot showing the mean changes in diameter and hemodynamic signals in response to each arousal state transition.

Article Snippet: Reflectance images were acquired during periods of green LED light illumination at 530 nm (M530L3, Thorlabs, Newton, NJ) or red LED light illumination at 630 nm (M625L4, Thorlabs, Newton, NJ), whereas a 500-nm long-pass filter (FELH0500, Thorlabs, Newton, NJ) mounted in front of the camera enabled imaging of GCaMP fluorescence during periods of illumination with blue LED light with a wavelength around 470 nm (M470L3, Thorlabs, Newton, NJ).

Techniques: Imaging, Whisker Assay

( A ) Top, schematic of the experimental setup for widefield IOS imaging of awake head fixed mice during whisker stimulation. Bottom, image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Example single trial responses showing hemodynamic changes of veins at different locations (shown in A ) in response to whisker stimulation. FL/HL, forelimb/hindlimb representation of the somatosensory cortex; Wh, vibrissae cortex. ΔHbT, total hemoglobin; ΔHbO-HbR, differences between oxy- and deoxy-hemoglobin. The shaded area denotes the period of whisker stimulation. ( C ) Group average of a short (100 ms) whisker stimulation triggered response of ΔD/D 0 (n = 4 mice) in veins at different locations. Inset showing a zoom-in view of ΔD/D 0 responses immediately before (330 ms) and after (660 ms) whisker stimulation. ( D ) Average venous diameter change (ΔD/D 0 ) during the initial phase of whisker stimulation (0-0.5 second after locomotion onset, left) and after stimulation (0.5-3 seconds after whisker stimulation onset, right) in veins at different locations. There was a rapid constriction in superior sagittal sinus (SSS, -1.24 ± 0.77%, Wilcoxson rank sum test, p = 0.0143), bridging veins (BV, - 0.25 ± 0.30%, Wilcoxson rank sum test, p = 0.0143) and pial veins in the FL/HL (−0.56 ± 0.56%, Wilcoxson rank sum test, p = 0.0143) in response to a short whisker stimulation, while pial veins in the Wh (−0.005 ± 0.09%, Wilcoxson rank sum test, p = 0.9429) did not change significantly. After the initial constriction, SSS (0.18 ± 0.57%, Wilcoxson rank sum test, p =0.1571) and BV (0.17 ± 0.67%, Wilcoxson rank sum test, p =0.1571) return back to baseline levels, while the pial veins in FL/HL (1.27 ± 1.11%, Wilcoxson rank sum test, p = 0.0143) dilated. The pial veins in the Wh did not change significantly (0.88 ± 1.54%, Wilcoxson rank sum test, p = 0.1571).

Journal: bioRxiv

Article Title: Ultrafast venous and sagittal sinus constrictions in the brain driven by abdominal pressure

doi: 10.64898/2026.05.02.722426

Figure Lengend Snippet: ( A ) Top, schematic of the experimental setup for widefield IOS imaging of awake head fixed mice during whisker stimulation. Bottom, image of the cerebral vasculature under 530 nm illumination through a thin-skull window spanning the parietal cortices of both hemispheres. Colored lines denote locations of vessel diameter measurements shown in subsequent figures. ( B ) Example single trial responses showing hemodynamic changes of veins at different locations (shown in A ) in response to whisker stimulation. FL/HL, forelimb/hindlimb representation of the somatosensory cortex; Wh, vibrissae cortex. ΔHbT, total hemoglobin; ΔHbO-HbR, differences between oxy- and deoxy-hemoglobin. The shaded area denotes the period of whisker stimulation. ( C ) Group average of a short (100 ms) whisker stimulation triggered response of ΔD/D 0 (n = 4 mice) in veins at different locations. Inset showing a zoom-in view of ΔD/D 0 responses immediately before (330 ms) and after (660 ms) whisker stimulation. ( D ) Average venous diameter change (ΔD/D 0 ) during the initial phase of whisker stimulation (0-0.5 second after locomotion onset, left) and after stimulation (0.5-3 seconds after whisker stimulation onset, right) in veins at different locations. There was a rapid constriction in superior sagittal sinus (SSS, -1.24 ± 0.77%, Wilcoxson rank sum test, p = 0.0143), bridging veins (BV, - 0.25 ± 0.30%, Wilcoxson rank sum test, p = 0.0143) and pial veins in the FL/HL (−0.56 ± 0.56%, Wilcoxson rank sum test, p = 0.0143) in response to a short whisker stimulation, while pial veins in the Wh (−0.005 ± 0.09%, Wilcoxson rank sum test, p = 0.9429) did not change significantly. After the initial constriction, SSS (0.18 ± 0.57%, Wilcoxson rank sum test, p =0.1571) and BV (0.17 ± 0.67%, Wilcoxson rank sum test, p =0.1571) return back to baseline levels, while the pial veins in FL/HL (1.27 ± 1.11%, Wilcoxson rank sum test, p = 0.0143) dilated. The pial veins in the Wh did not change significantly (0.88 ± 1.54%, Wilcoxson rank sum test, p = 0.1571).

Article Snippet: Reflectance images were acquired during periods of green LED light illumination at 530 nm (M530L3, Thorlabs, Newton, NJ) or red LED light illumination at 630 nm (M625L4, Thorlabs, Newton, NJ), whereas a 500-nm long-pass filter (FELH0500, Thorlabs, Newton, NJ) mounted in front of the camera enabled imaging of GCaMP fluorescence during periods of illumination with blue LED light with a wavelength around 470 nm (M470L3, Thorlabs, Newton, NJ).

Techniques: Imaging, Whisker Assay