Abstract
Nearly all the blood supplying the cortex exits via the bridging veins (BVs) that drain into the superior sagittal sinus (SSS), making these vessels key chokepoints for cerebral blood flow. Using optical imaging in head-fixed mice, we found that the SSS and BVs exhibit ultrafast contractions (<0.1 s) at the onset of locomotion, following whisker stimulation, and upon awakening from sleep. Contractions of the BV and SSS were strongly correlated with abdominal muscle EMG activity and were tightly correlated with respiration at rest. The rapid decrease in blood volume caused by venous constrictions resulted in spurious increases in fluorescence in mice expressing fluorescent reporter proteins, creating artifacts that mimic functional signals. Venous contractions with the same amplitude and dynamics could be generated in anesthetized mice by abdominal pressure application, showing that these contractions were generated by mechanical coupling with the abdomen. Externally imposed abdominal pressures also drove a rapid but transient increase in blood flow. Unlike the pial and parenchymal microvasculature whose diameters are controlled by local signals, the diameters of SSS/BV are dynamically controlled during behavior by abdominal muscle regulation of intracranial pressure, establishing a pathway for regulation of cerebral hemodynamics via mechanical coupling between the central nervous system and the viscera.
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Abstract
Nearly all the blood supplying the cortex exits via the bridging veins (BVs) that drain into the superior sagittal sinus (SSS), making these vessels key chokepoints for cerebral blood flow. Using optical imaging in head-fixed mice, we found that the SSS and BVs exhibit ultrafast contractions (<0.1 s) at the onset of locomotion, following whisker stimulation, and upon awakening from sleep. Contractions of the BV and SSS were strongly correlated with abdominal muscle EMG activity and were tightly correlated with respiration at rest. The rapid decrease in blood volume caused by venous constrictions resulted in spurious increases in fluorescence in mice expressing fluorescent reporter proteins, creating artifacts that mimic functional signals. Venous contractions with the same amplitude and dynamics could be generated in anesthetized mice by abdominal pressure application, showing that these contractions were generated by mechanical coupling with the abdomen. Externally imposed abdominal pressures also drove a rapid but transient increase in blood flow. Unlike the pial and parenchymal microvasculature whose diameters are controlled by local signals, the diameters of SSS/BV are dynamically controlled during behavior by abdominal muscle regulation of intracranial pressure, establishing a pathway for regulation of cerebral hemodynamics via mechanical coupling between the central nervous system and the viscera.
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