Unlike any other organ of the body, the brain is critically dependent on a continuous blood supply. Due to its high energy demands, the brain operates under a tight coupling of neuronal electrical activity to the hemodynamic regulation of energy supply and waste removal. The 'neurovascular coupling' entails a complex, highly redundant array of signaling mechanisms aimed at maintaining homeostasis of the brain parenchyma by regulating CBF on a precise spatial and temporal domain. There is increased evidence that such mechanisms result from an integrated action of neurons, glia and blood vessels, which form a 'neurovascular unit' acting at the cellular level to regulate local CBF. Disruption of these mechanisms causes brain dysfunction and disease.
Our laboratory is interested in understanding the mechanisms of CBF regulation during normal and pathological brain states. The fundamental questions related to cerebral blood flow regulation are: 1. What is the smallest vascular unit that adapts independently to brain activity? 2. How is this elemental vascular unit related to the cortical architecture? 3. What are the major signaling pathways, and the key molecules, that translate a change in brain activity into a vascular response?
To address the above questions, we are working on well-defined rodent and non-human primate models of localized functional brain activation, using modern neuroimaging techniques (fMRI or optical microscopy), in combination with electrophysiology recordings of cortical activity. The cerebrovascular coupling will be tested under the presence of agonists and antagonists of several different known mediators or modulators of CBF. Complimentary information on the cerebrovascular coupling will be studied under pathophysiological brain conditions, such as the ones obtained using experimental animal models of brain stroke. More detailed information about our research can be found in our laboratory's webpage: Cerebral Microcirculation Unit