Hemodynamic and metabolic responses to neuronal inhibition

Neuroimage. 2004 Jun;22(2):771-8. doi: 10.1016/j.neuroimage.2004.01.036.


Functional magnetic resonance imaging (fMRI) was used to investigate the changes in blood oxygenation level dependent (BOLD) signal, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen consumption (CMR(O(2))) accompanying neuronal inhibition. Eight healthy volunteers performed a periodic right-hand pinch grip every second using 5% of their maximum voluntary contraction (MVC), a paradigm previously shown to produce robust ipsilateral neuronal inhibition. To simultaneously quantify CBF and BOLD signals, an interleaved multislice pulsed arterial spin labeling (PASL) and T(2)*-weighted gradient echo sequence was employed. The CMR(O(2)) was calculated using the deoxyhemoglobin dilution model, calibrated by data measured during graded hypercapnia. In all subjects, BOLD, CBF and CMR(O(2)) signals increased in the contralateral and decreased in the ipsilateral primary motor (M1) cortex. The relative changes in CMR(O(2)) and CBF were linearly related, with a slope of approximately 0.4. The coupling ratio thus established for both positive and negative CMR(O(2)) and CBF changes is in close agreement with the ones observed by earlier studies investigating M1 perfusion and oxygen consumption increases. These findings characterize the hemodynamic and metabolic downregulation accompanying neuronal inhibition and thereby establish the sustained negative BOLD response as a marker of neuronal deactivation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Brain / anatomy & histology
  • Brain / blood supply
  • Brain / physiology*
  • Brain Mapping / methods
  • Carbon Dioxide / pharmacology
  • Cerebrovascular Circulation / drug effects
  • Cerebrovascular Circulation / physiology*
  • Functional Laterality
  • Hand Strength
  • Humans
  • Kinetics
  • Magnetic Resonance Imaging / methods
  • Motor Cortex / physiology*
  • Muscle Contraction
  • Muscle, Skeletal / innervation
  • Muscle, Skeletal / physiology
  • Neurons / drug effects
  • Neurons / physiology*


  • Carbon Dioxide