Noninvasive Brain Physiology Monitoring for Extreme Environments: A Critical Review.

Our ability to monitor the brain physiology is advancing; however, most of the technology is bulky, expensive, and designed for traditional clinical settings. With long-duration space exploration, there is a need for developing medical technologies that are reliable, low energy, portable, and semiautonomous. Our aim was to review the state of the art for noninvasive technologies capable of monitoring brain physiology in diverse settings. A literature review of PubMed and the Texas Medical Center library sites was performed using prespecified search criteria to identify portable technologies for monitoring physiological aspects of the brain physiology. Most brain-monitoring technologies require a moderate to high degree of operator skill. Some are low energy, but many require a constant external power supply. Most of the technologies lack the accuracy seen in gold standard measures, due to the need for calibration, but may be useful for screening or monitoring relative changes in a parameter. Most of the technologies use ultrasound or electromagnetic radiation as energy sources. There is an important need for further development of portable technologies that can be operated in a variety of extreme environments to monitor brain health.

Dynamic control of excitatory synapse development by a Rac1 GEF/GAP regulatory complex.

The small GTPase Rac1 orchestrates actin-dependent remodeling essential for numerous cellular processes including synapse development. While precise spatiotemporal regulation of Rac1 is necessary for its function, little is known about the mechanisms that enable Rac1 activators (GEFs) and inhibitors (GAPs) to act in concert to regulate Rac1 signaling. Here, we identify a regulatory complex composed of a Rac-GEF (Tiam1) and a Rac-GAP (Bcr) that cooperate to control excitatory synapse development. Disruption of Bcr function within this complex increases Rac1 activity and dendritic spine remodeling, resulting in excessive synaptic growth that is rescued by Tiam1 inhibition. Notably, EphB receptors utilize the Tiam1-Bcr complex to control synaptogenesis. Following EphB activation, Tiam1 induces Rac1-dependent spine formation, whereas Bcr prevents Rac1-mediated receptor internalization, promoting spine growth over retraction. The finding that a Rac-specific GEF/GAP complex is required to maintain optimal levels of Rac1 signaling provides an important insight into the regulation of small GTPases.