Microglial control of neuronal activity and injury: recent lessons and future perspectives
Institute of Experimental Medicine, Hungarian Academy of Sciences (Hungary)
Inflammation is an important contributor to brain injury, but the mechanisms involved are improperly defined. Microglia, the main inflammatory cells in the brain become activated in various brain diseases, but their functional role in neuronal injury remains controversial. Using selective microglia manipulation approaches, in vivo two-photon- and SPECT imaging and advanced microscopy, early inflammatory changes including microglia-neuron interactions, neuronal calcium responses, blood brain barrier (BBB) injury, oxidative stress and perfusion changes have been assessed in models of neuroinflammation and brain injury. We show that microglia react rapidly to early changes in neuronal calcium responses, BBB injury and oxidative stress. Dysregulation of neuronal calcium responses is observed after acute brain injury in the absence of functional microglia, leading to increased neuronal death. Microglia exert similarly protective actions in controlling the spread of neurotrophic viral infection in the brain. We also show that systemic inflammation changes microglial responses, leads to lincreased BBB injury and impaired brain perfusion, resulting in to worse neurological outcome after acute brain injury. These results suggest that understanding central and systemic inflammatory mechanisms is essential for the development of novel diagnostic and therapeutic tools in brain diseases.
This seminar will be held in the new headquarters of Achucarro:
Sede Building, Ground Floor
Scientific Park of the UPV/EHU
Barrio Sarriena, s/n