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Hiroaki Wake

Researcher at Kobe University

Publications -  70
Citations -  7165

Hiroaki Wake is an academic researcher from Kobe University. The author has contributed to research in topics: Microglia & Medicine. The author has an hindex of 27, co-authored 52 publications receiving 5307 citations. Previous affiliations of Hiroaki Wake include National Institutes of Natural Sciences, Japan & National Institute for Basic Biology, Japan.

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Resting Microglia Directly Monitor the Functional State of Synapses In Vivo and Determine the Fate of Ischemic Terminals

TL;DR: The results demonstrate that at least part of the dynamic motility of resting microglial processes in vivo is directed toward synapses and propose that microglia vigilantly monitor and respond to the functional status of synapses.
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The Role of Microglia in the Healthy Brain

TL;DR: This summary is not meant to be a comprehensive review of microglia physiology, but rather to share new results and stimulate further research into the cellular and molecular mechanisms by whichmicroglia influence postnatal development, adult neuronal plasticity, and circuit function.
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Control of Local Protein Synthesis and Initial Events in Myelination by Action Potentials

TL;DR: This work finds that release of glutamate from synaptic vesicles along axons of mouse dorsal root ganglion neurons in culture promotes myelin induction by stimulating formation of cholesterol-rich signaling domains between oligodendrocytes and axons, and increasing local synthesis of the major protein in the myelin sheath, myelin basic protein, through Fyn kinase-dependent signaling.
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Microglia contact induces synapse formation in developing somatosensory cortex.

TL;DR: In vivo multiphoton imaging of layer 2/3 pyramidal neurons in the developing somatosensory cortex is used to demonstrate that microglial contact with dendrites directly induces filopodia formation, and provide further insights into immune system regulation of neuronal circuit development.
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Dual microglia effects on blood brain barrier permeability induced by systemic inflammation.

TL;DR: It is demonstrated that microglia respond to inflammation by migrating towards and accumulating around cerebral vessels, where they initially maintain BBB integrity via expression of the tight-junction protein Claudin-5 before switching, during sustained inflammation, to phagocytically remove astrocytic end-feet resulting in impaired BBB function.