The NKCC1 ion transporter contributes to the pathophysiology of common neurological disorders, but its function in microglia, the main inflammatory cells of the brain, has remained unclear to date. Therefore, we generated a novel transgenic mouse line in which microglial NKCC1 was deleted. We show that microglial NKCC1 shapes both baseline and reactive microglia morphology, process recruitment to the site of injury, and adaptation to changes in cellular volume in a cell-autonomous manner via regulating membrane conductance. In addition, microglial NKCC1 deficiency results in NLRP3 inflammasome priming and increased production of interleukin-1β (IL-1β), rendering microglia prone to exaggerated inflammatory responses. In line with this, central (intracortical) administration of the NKCC1 blocker, bumetanide, potentiated intracortical lipopolysaccharide (LPS)-induced cytokine levels. In contrast, systemic bumetanide application decreased inflammation in the brain. Microglial NKCC1 KO animals exposed to experimental stroke showed significantly increased brain injury, inflammation, cerebral edema, and, worse, neurological outcome. Thus, NKCC1 emerges as an important player in controlling microglial ion homeostasis and inflammatory responses through which microglia modulate brain injury. The contribution of microglia to central NKCC1 actions is likely to be relevant for common neurological disorders.

The NKCC1 ion transporter contributes to the pathophysiology of common neurological disorders, but its function in microglia, the main inflammatory cells of the brain, has not been studied to date. Therefore, we generated a novel transgenic mouse line in which microglial NKCC1 was deleted. We show that microglial NKCC1 shapes both baseline and reactive microglia morphology and inflammatory responses. As opposed to systemic NKCC1 blockade, which decreased intracortical lipopolysaccharide (LPS)-induced cytokine levels, neuroinflammation was potentiated by both intracortically administered bumetanide and in the absence of microglial NKCC1, suggesting a considerable role for microglia to influence central NKCC1 actions. Correspondingly, microglial NKCC1 KO animals exposed to experimental stroke showed significantly increased brain injury, inflammation, cerebral edema and worse neurological outcome. Thus, NKCC1 emerges as an important player to shape microglial responses and brain inflammation after CNS injury, which is likely to be relevant for common neurological disorders.

A control strategy based on matching the source and load changes of the order of milliseconds, called peer-to-peer energy transfer, is introduced. This energy transfer enables a decoupled energy transfer system in common bus networks. To realize the transfer with a pair of two-port circuits, a power gyrator is derived from the phasor-based model of a bidirectional ac/dc converter, based on the concept of a time-variable transformer. Powergyrator timing synchronization is achieved by communication, and a peer-to-peer energy transfer system is developed. Experimental and simulation results are compared, and it is demonstrated that peer-to-peer energy transfer can be used for decoupling common bus voltage networks.

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