Item request has been placed! ×
Item request cannot be made. ×
loading  Processing Request

Direct Deviations in Astrocyte Free Ca2+ Concentration Control Multiple Arteriole Tone States

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
  • معلومة اضافية
    • بيانات النشر:
      Multidisciplinary Digital Publishing Institute, 2021.
    • الموضوع:
      2021
    • نبذة مختصرة :
      Astrocytes elicit bidirectional control of microvascular diameter in acutely isolated brain slices through vasoconstriction and vasodilation pathways that can be differentially recruited via the free Ca2+ concentration in endfeet and/or the metabolic status of the tissue. However, the Ca2+-level hypothesis has not been tested using direct manipulation. To overcome this, we used Ca2+-clamp whole-cell patching of peri-arteriole astrocytes to change astrocyte-free Ca2+ to different concentrations and examined the vascular response. We discovered that clamping Ca2+ at the approximate resting value (100 nM) had no impact on arteriole diameter in a pre-constricted arteriole. However, a moderate elevation to 250 nM elicited sustained vasodilation that was blocked by the COX-1 antagonist SC-560 (500 nM). The vasodilation to 250 nM Ca2+ was sensitive to the metabolic state, as it converted to vasoconstriction when oxygen tension was dramatically elevated. In normal oxygen, clamping astrocyte Ca2+ well above the resting level (750 nM) produced sustained vasoconstriction, which converted to vasodilation in the 20-HETE blocker HET0016 (1 μM). This response was fully blocked by the addition of SC-560 (500 nM), showing that 20-HETE-induced vasoconstriction dominated the dilatory action of COX-1. These data demonstrate that direct changes in astrocyte free Ca2+ can control multiple arteriole tone states through different mediators.
    • File Description:
      application/pdf
    • ISSN:
      2571-6980
    • الرقم المعرف:
      10.3390/neuroglia2010006
    • Rights:
      OPEN
    • الرقم المعرف:
      edsair.doi.dedup.....e484203dd11db7c9b1d50b34ac4b8397