Data from: Age-dependent cerebral vasodilation induced by volatile anesthetics is mediated by NG2+ vascular mural cells
Data files
Sep 24, 2026 version files 260.98 KB
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README.md
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SourceData_Fig_1.xlsx
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SourceData_Fig_2.xlsx
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SourceData_Fig_3.xlsx
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SourceData_Fig_4.xlsx
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SourceData_Fig_5.xlsx
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SourceData_Fig_6.xlsx
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SourceData_Fig_7.xlsx
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SourceData_Fig_8.xlsx
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Abstract
Anesthesia can influence cerebral blood flow by altering vessel diameter. Using in vivo two-photon imaging, we examined the effects of volatile anesthetics, sevoflurane and isoflurane, on vessel diameter in young and adult mice. Our results show that these anesthetics induce robust dilation of cortical arterioles and arteriole-proximate capillaries in adult mice, with milder effects in juveniles and no dilation in infants. This anesthesia-induced vasodilation correlates with decreased cytosolic Ca2+ levels in NG2+ vascular mural cells. Optogenetic manipulation of these cells bidirectionally regulates vessel diameter, and their ablation abolishes the vasodilatory response to anesthetics. In immature brains, NG2+ mural cells are fewer in number and express lower levels of Kir6.1, a subunit of ATP-sensitive potassium channels. This likely contributes to the age-dependent differences in vasodilation, as Kir6.1 activation promotes, while its inhibition reduces, anesthesia-induced vasodilation. These findings highlight the essential role of NG2+ mural cells in mediating anesthesia-induced cerebral vasodilation.
Dataset DOI: 10.5061/dryad.9s4mw6mzw
Description of the data and file structure
This dataset contains the underlying numeric source data for main figures presented in the associated article (DOI: 10.1038/s42003-024-07200-7).
Files and variables
File: SourceData_Fig_1.xlsx
Description: Source data for Figure 1, panel g.
Variables
- Fig_1g: Quantification of sevoflurane (SEVO)-induced vasodilation over time (min) in cortical arterioles (n = 73 vessels from 3 mice) and venules (n = 56 vessels from 3 mice). Data are presented as mean percentage change relative to baseline with 95 % confidence intervals (CI).
File: SourceData_Fig_2.xlsx
Description: Source data for Figure 2, panels b, c, d, e, f, g, i, and j.
Variables
- Fig_2b: Relative changes in arteriole diameter (% of baseline) over time in P14, P18, and P60 mice (n = 88, 80, and 76 arterioles from 5 mice per group). Data presented as mean ± SEM.
- Fig_2c: Magnitude of SEVO-induced arteriole dilation (%) at 15 min across development (postnatal days). Data points represent group means (n = 41–55 arterioles from 2–3 mice per age group) used for sigmoidal model fitting.
- Fig_2d: Relative changes in arteriole diameter (% of baseline) over time during air control exposure in P14, P18, and P60 mice (n = 88, 80, and 76 arterioles from 5 mice per group). Data presented as mean ± SEM.
- Fig_2e: Relative changes in venule diameter (% of baseline) over time after SEVO exposure in P14, P18, and P60 mice (n = 61, 56, and 68 venules from 5 mice per group). Data presented as mean ± SEM.
- Fig_2f: Frequency distribution (%) of initial baseline vessel diameters (µm) for sampled arterioles in P14, P18, and P60 mice (n = 88, 80, and 76 arterioles from 5 mice per group).
- Fig_2g: Paired values of initial arteriole diameter (µm) and corresponding SEVO-induced dilation (%) at 15 min for individual vessels in P14, P18, and P60 mice (n = 88, 80, and 76 arterioles from 5 mice per group) used for linear regression analyses.
- Fig_2i_2j: Paired initial vessel diameters (µm, range 2–10 µm) and SEVO-induced dilation (%) at 15 min for individual capillaries (n = 199, 246, and 298 vessels from 4–5 mice per group) across P14, P18, and P60 age groups, used for correlation and distribution comparisons.
File: SourceData_Fig_3.xlsx
Description: Source data for Figure 3, panels b, c, d, and f.
Variables
- Fig_3b: Relative changes in arteriole diameter (% of baseline) over time upon exposure to isoflurane (ISO) in P14, P19, and P90 mice (n = 41, 47, and 43 arterioles from 3 mice per group). Data presented as mean ± SEM.
- Fig_3c: Relative changes in venule diameter (% of baseline) over time upon exposure to ISO in P14, P19, and P90 mice (n = 51, 44, and 46 venules from 3 mice per group). Data presented as mean ± SEM.
- Fig_3d: Paired initial vessel diameters (µm) and ISO-induced dilation (%) at 15 min for individual arterioles in P14, P19, and P90 mice (n = 41, 47, and 43 arterioles from 3 mice per group) used for linear regression analyses.
- Fig_3f: ISO-induced vasodilation (%) at 15 min in capillaries, categorized by initial vessel diameter (<5 µm and 5–10 µm), in P14, P19, and P60 mice (n = 80–119 vessels from 3 mice per group).
File: SourceData_Fig_4.xlsx
Description: Source data for Figure 4, panels b, c, e, f, and i.
Variables
- Fig_4b: Line density (µm –1) of α-SMA+ smooth muscle bands along pial arterioles in P14, P18, and P60 mice (n = 32, 22, and 26 arterioles from 3 mice per group).
- Fig_4c: Normalized α-SMA fluorescence intensity (% of P60 mean) in pial arterioles (n = 32, 22, and 20 arterioles) and penetrating arterioles (n = 24, 17, and 20 arterioles) across P14, P18, and P60 mice.
- Fig_4e: Density of NG2+ DAPI+ cells (cells/mm -2) in cortical sections across developmental ages (P13, P16, P19, and P60; n = 12 slices from 4 mice per group).
- Fig_4f: Density of total DAPI+ nuclei (cells/mm -2) in cortical sections across developmental ages (P13, P16, P19, and P60; n = 12 slices from 4 mice per group).
- Fig_4i: Capillary density measured as total vessel length per unit parenchymal volume (µm/103 µm3) across cortical depths (µm) in P13, P16, P19, and P60 mice (n = 3 mice per group).
File: SourceData_Fig_5.xlsx
Description: Source data for Figure 5, panels b, d, e, g, and k.
Variables
- Fig_5b: Normalized intracellular Ca2+ levels (% of baseline) in NG2+ pericytes at baseline, 15 min and 60 min during SEVO exposure, and 60 min post-emergence (n = 225 cells from 4 adult mice).
- Fig_5d: Changes in arteriole diameter (% of baseline) following 10 min of 595 nm light stimulation in eNpHR3.0-expressing adult mice (n = 23 arterioles from 3 mice).
- Fig_5e: Time-course of relative arteriole diameter changes (%) in ChR2-SSFO-expressing adult mice subjected to alternating optogenetic stimulation (470 nm / 595 nm) and SEVO exposure (n = 25 arterioles from 3 mice).
- Fig_5g: Relative frequency distribution (%) of EYFP+ NG2+ cell body positions across cortical distances from the midline (mm; n = 3 mice).
- Fig_5k: Comparative EYFP fluorescence intensity (arbitrary units) in smooth muscle cells versus cells with pericyte morphology (n = 3 mice).
File: SourceData_Fig_6.xlsx
Description: Source data for Figure 6, panels c, d, f, h, and i.
Variables
- Fig_6c: Spatial distribution of viral transduction measured by EGFP fluorescence intensity (arbitrary units) as a function of distance from the midline (mm) in control and ablated cortical hemispheres (n = 3 mice per group).
- Fig_6d: Cleaved caspase-3 immunofluorescence intensity (arbitrary units) in control (EGFP+) versus ablated (DTR-EGFP+) cortical regions (n = 9 slices from 3 mice).
- Fig_6f: Density of NG2+ DAPI+ pericytes (cells/mm –2) in control and ablated cortical hemispheres (n = 12 slices from 3 mice per group).
- Fig_6h: Relative changes in arteriole diameter (% of baseline) over time (min) during SEVO exposure in control (n = 64 vessel segments from 4 mice) and NG2-ablated (n = 58 vessel segments from 4 mice) cortex.
- Fig_6i: Frequency distribution (%) of initial baseline vessel diameters (µm) for sampled arterioles in control and ablated cortex (n = 64 and 58 segments from 4 mice per group).
File: SourceData_Fig_7.xlsx
Description: Source data for Figure 7, panels c, d, f, g, i, and j.
Variables
- Fig_7c: Spatial profile of Kir6.1 fluorescence intensity (arbitrary units) across the cell membrane (µm) of NG2+ pericytes in P13 (n = 7), P16 (n = 7), P19 (n = 7), and P60 (n = 6) mice.
- Fig_7d: Peak Kir6.1 membrane fluorescence intensity (arbitrary units) in cortical NG2+ cells across developmental ages (P13, P16, P19, and P60; n = 6–7 mice per group).
- Fig_7f: Relative change in arteriole diameter (% of baseline) 15 min after intracortical pinacidil injection in awake P13 (n = 88 arterioles from 4 mice) and P60 (n = 83 arterioles from 4 mice) mice.
- Fig_7g: Intracellular Ca2+ levels (% relative to baseline) in NG2+ cells before and 15 min after pinacidil injection in awake P13 (n = 211 cells) and P60 (n = 218 cells) mice (n = 3 mice per group).
- Fig_7i: Relative change in arteriole diameter (% of baseline) during SEVO exposure, before and after intracortical glibenclamide injection in P13 (n = 61 arterioles) and P60 (n = 67 arterioles) mice (n = 3 mice per group).
- Fig_7j: Intracellular Ca2+ levels (% relative to baseline) in NG2+ cells during SEVO exposure, before and after intracortical glibenclamide injection in P13 (n = 189 cells) and P60 (n = 204 cells) mice (n = 3 mice per group).
File: SourceData_Fig_8.xlsx
Description: Source data for Figure 8, panels c and f.
Variables
- Fig_8c: Average spontaneous intracellular Ca2+ activity (∆F/F0; %) of individual cortical pyramidal neurons in awake P13 (n = 141 cells) and P60 (n = 204 cells) mice before and 15 min after intracortical pinacidil injection (n = 3–4 mice per group).
- Fig_8f: Average spontaneous intracellular Ca2+ activity (∆F/F0; %) of individual cortical pyramidal neurons across experimental conditions (awake baseline, SEVO exposure, and SEVO + intracortical glibenclamide injection) in P13 (n = 328 cells) and P60 (n = 359 cells) mice (n = 5 mice per group).
Code/software
The data is provided in Microsoft Excel format (.xlsx). It can be opened using free and open-source software such as LibreOffice Calc, Apache OpenOffice, or Google Sheets, as well as Microsoft Excel. No custom code or scripts are required to view or access this dataset. All data, metadata, and column descriptions are self-contained within the file worksheets.
Access information
The data was generated directly from our experiments and was not derived from external secondary sources.
Detailed descriptions of data collection and analysis methods are provided in the associated article.
