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Nitric oxide contributes to functional hyperemia in cerebellar cortex

C Iadecola1, J Li, T J Ebner

  • 1Department of Neurology, University of Minnesota Medical School, Minneapolis 55455.

The American Journal of Physiology
|May 1, 1995
PubMed
Summary

Nitric oxide (NO) plays a key role in functional hyperemia, increasing cerebellar blood flow (BFcrb) during neural activation. This study demonstrates NO

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Area of Science:

  • Neuroscience
  • Cerebrovascular Physiology
  • Biochemistry

Background:

  • Neural activity triggers increased blood flow, a phenomenon known as functional hyperemia.
  • The precise molecular mechanisms coupling neural activation to increased blood flow in the cerebellum are not fully understood.
  • Nitric oxide (NO) is a signaling molecule implicated in various physiological processes, including vascular regulation.

Purpose of the Study:

  • To investigate the role of nitric oxide (NO) in mediating the increase in cerebellar cortex blood flow (BFcrb) evoked by parallel fiber (PF) stimulation.
  • To determine the source of NO involved in functional hyperemia in the cerebellar cortex.

Main Methods:

  • Using an in vivo rat model, parallel fibers in the cerebellar cortex were electrically stimulated.

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  • Cerebellar cortex blood flow (BFcrb) was measured using laser-Doppler flowmetry.
  • The effects of nitric oxide synthase (NOS) inhibitors (L-NNA, D-NNA) and methylene blue on BFcrb were assessed.

    • Main Results:

    • Electrical stimulation of parallel fibers significantly increased cerebellar cortex blood flow (BFcrb) by 52%.
    • NOS inhibition with L-NNA dose-dependently attenuated the BFcrb increase, with 1 mM L-NNA reducing it by 50%.
    • L-NNA (1 mM) inhibited NOS activity by 95% but did not affect evoked field potentials, and the inactive isomer D-NNA had no effect.

    Conclusions:

    • Nitric oxide (NO) produced in the cerebellar molecular layer contributes to the functional hyperemia elicited by parallel fiber activation.
    • NO is involved in the coupling of neural activity to blood flow regulation in the cerebellum.
    • These findings support the hypothesis that NO is a mediator of functional hyperemia in the central nervous system.