How is gliovascular coupling affected by mild Traumatic Brain Injury?

The brain is critically dependent on a sustained blood flow. Reduction of cerebral blood flow leads to impaired cognitive function and ultimately to irreparable damage of brain tissue. Sufficient blood supply of active brain regions and the immune-privileged status of the CNS are assured by the neurovascular unit (NVU), a functional entity consisting of neural and vascular cells. Astrocytes, glial cells in the brain, are ideally positioned within the NVU to modulate the regulation of blood flow (NVC) and status of the blood-brain barrier (BBB). Injury presenting with rapture of vessels expose the brain to blood-derived factors, which can induce changes in morphology, gene and protein expression and homeostatic function of astrocytes called astrogliosis.

We are currently testing the hypothesis that mTBI causes impaired cerebral blood flow as a result of astrogliosis. This leads to a chronic state of mild hypoxia resulting in neuronal stress, dysfunction and cognitive impairment. We further hypothesize that these impairments are exacerbated when multiple injuries occur. Testing these hypotheses makes strong use of two-photon in vivo imaging. This technique is helpful in identifying the cellular players involved in vascular remodeling after injury and to assess function of neurovascular coupling before and after mTBI. Other assays include but are not limited to immunohistochemistry and confocal imaging, calcium imaging, behavioral assays and electrophysiology.