ScholarWorksIndianapolis
  • Communities & Collections
  • Browse ScholarWorks
  • English
  • Català
  • Čeština
  • Deutsch
  • Español
  • Français
  • Gàidhlig
  • Italiano
  • Latviešu
  • Magyar
  • Nederlands
  • Polski
  • Português
  • Português do Brasil
  • Suomi
  • Svenska
  • Türkçe
  • Tiếng Việt
  • Қазақ
  • বাংলা
  • हिंदी
  • Ελληνικά
  • Yкраї́нська
  • Log In
    or
    New user? Click here to register.Have you forgotten your password?
  1. Home
  2. Browse by Subject

Browsing by Subject "neurovascular coupling"

Now showing 1 - 2 of 2
Results Per Page
Sort Options
  • Loading...
    Thumbnail Image
    Item
    Change in arteriole diameter of retina with visual simulation
    (Office of the Vice Chancellor for Research, 2016-04-08) Tellapragada, Neelima; Burns, Steven; De Castro Arribas, Alberto; Sawides, Lucie; Othman, Hind
    Neural activity and blood flow in the brain are tightly coupled. This coupling allows the brain to respond to periods of increased neural activity with increased blood flow. This coupling is known as neurovascular coupling. Many vascular based imaging techniques such as Functional MRI scans provide maps of signals of brain activity but they are limited by the resolution of fMRI to a few mm. The fMRI signal is indirect because the scanner is not tracking the neural activity directly but are measuring the changes in the blood oxygen levels. Since the retina and optic tract are part of the central nerves system and they can be measured optically it should be possible to make precise measurements of the retinal vasculature of the human retina and its response to changing stimulation levels. In this study we used an adaptive optics scanning laser ophthalmoscope (AOSLO) with multiply scattered light to measure the change in arteriolar diameter when the retina was stimulated with flickering light. We hypothesized that we could use this technique to measure both arterial dilation and time course. We used information from the reflectance of the vessel to Change in arteriole diameter of retina with visual simulation measure total vessel diameter. Images were acquired at approximately 30 Hz and averaged over 3.3 second periods. Retinal arteries were measured in five observers before, during, and after presentation of a large flickering stimulus. There was a 6-10% dilation of the blood vessels during the flicker. The Vascular dilation occurred within seconds of flickering onset and constricted again following the end of flicker stimulation. This work shows that with modern retinal imaging methods it is possible to make precise measures of vascular constriction and its time course in response to changing tissue demand.
  • Loading...
    Thumbnail Image
    Item
    Integrated Feedforward and Feedback Mechanisms in Neurovascular Coupling
    (Wolters Kluwer, 2024-12) Meng, Lingzhong; Rasmussen, Mads; Meng, Deyi M.; White, Fletcher A.; Wu, Long-Jun; Anesthesia, School of Medicine
    Neurovascular coupling (NVC) is the mechanism that drives the neurovascular response to neural activation, and NVC dysfunction has been implicated in various neurologic diseases. NVC is driven by (1) nonmetabolic feedforward mechanisms that are mediated by various signaling pathways and (2) metabolic feedback mechanisms that involve metabolic factors. However, the interplay between these feedback and feedforward mechanisms remains unresolved. We propose that feedforward mechanisms normally drive a swift, neural activation–induced regional cerebral blood flow (rCBF) overshoot, which floods the tissue beds, leading to local hypocapnia and hyperoxia. The feedback mechanisms are triggered by the resultant hypocapnia (not hyperoxia), which causes cerebral vasoconstriction in the neurovascular unit that counterbalances the rCBF overshoot and returns rCBF to a level that matches the metabolic activity. If feedforward mechanisms function improperly (eg, in a disease state), the rCBF overshoot, tissue-bed flooding, and local hypocapnia fail to occur or occur on a smaller scale. Consequently, the neural activation–related increase in metabolic activity results in local hypercapnia and hypoxia, both of which drive cerebral vasodilation and increase rCBF. Thus, feedback mechanisms ensure the brain milieu’s stability when feedforward mechanisms are impaired. Our proposal integrates the feedforward and feedback mechanisms underlying NVC and suggests that these 2 mechanisms work like a fail-safe system, to a certain degree. We also discussed the difference between NVC and cerebral metabolic rate-CBF coupling and the clinical implications of our proposed framework.
About IU Indianapolis ScholarWorks
  • Accessibility
  • Privacy Notice
  • Copyright © 2025 The Trustees of Indiana University