J. Michael Gee

TL;DR: This study demonstrates that immune responses to brain antigens occur after stroke, and although these responses are likely to be an epiphenomenon of ischemic brain injury, the response to myelin basic protein appears to have clinical consequences.

TL;DR: Through electrophysiological and behavioral analyses, it was determined that GCaMP5G expression had no major impact on nervous system performance and will be instrumental for a variety of brain mapping experiments.

TL;DR: It is suggested that deleterious autoimmunity to brain antigens can be prevented by prophylactically inducing regulatory T-cell responses to those antIGens.

TL;DR: Data is presented to support the hypothesis that the breach in the blood-brain barrier can also be capitalized on to modulate the immune response to create a neuroprotective environment after stroke and to show that this is possible.

TL;DR: Live two-photon imaging of the mouse cortex ubiquitously expressing the genetically encoded Ca2+ indicator GCaMP5G and fluorescent marker tdTomato in central nervous system microglia shows the usefulness of genetically encodedCa2+ indicators for investigation of microglial physiology, and shows that Ca1+ transients were pre-dominantly mediated via purinergic receptors.