Keio University · Neuroscience
Professor Kenji F. Tanaka's research lab focuses on molecular and cellular neuroscience, with a strong emphasis on glial cell biology, neurotransmitter receptor expression, and the role of glial cells in neurological diseases. The lab investigates the molecular mechanisms underlying astrocyte pathology in diseases such as Alexander disease, the functional roles of serotonin and adrenergic receptors in neural circuits, and the dynamic responses of microglia during neuroinflammation and demyelination. Using advanced genetic and molecular techniques—including transgenic models, in situ hybridization, and optogenetics—the lab explores how glial cells contribute to brain homeostasis and disease progression.
Figures are computed from collected data and may differ slightly.
Optogenetics has been enthusiastically pursued in recent neuroscience research, and the causal relationship between neural activity and behavior is becoming ever more accessible. Here, we established knockin-mediated enhanced gene expression by improved tetracycline-controlled gene induction (KENGE-tet) and succeeded in generating transgenic mice expressing a highly light-sensitive channelrhodopsin-2 mutant at levels sufficient to drive the activities of multiple cell types. This method requires
Using in situ hybridization, we describe, for the first time, the profiles of expression of serotonin receptors (Htr/5-HTR) along the dorsal-ventral axis of mouse hippocampus. cRNA probes for most Htrs, excluding Htr6, were used. All hippocampal subregions and the entorhinal cortex cells providing input into the hippocampus were examined. The study shows that some, but not all, Htrs are expressed in the cells of the hippocampal circuitry. At both the subfield and the cell type levels, a somewhat
Abstract We examined the expression and function of β‐adrenergic receptor (β‐AR) subtypes in both isolated primary rat microglia and a rat microglial cell line. RT‐PCR analyses revealed that microglia expressed β 1 ‐ and β 2 ‐ARs but not β 3 ‐ARs, whereas rat primary peritoneal macrophages expressed only β 2 ‐ARs. Stimulation of β‐ARs on microglia by norepinephrine (NE) resulted in an increase in the level of intracellular cAMP and the subsequent expression of interleukin‐1β mRNA. These effects
Alexander disease is caused by a coding mutation in the glial fibrillary acidic protein (GFAP) gene. The pathological hallmark is the formation of cytoplasmic inclusions within astrocytes known as Rosenthal fibers (RFs), which primarily consist of GFAP and several heat shock proteins. The presence of mutant GFAP would appear to be involved in RF formation; however, overproduction of wild type human GFAP in mouse brain also results in RF formation. Here, we investigated the in vivo conditions lea
Demyelination coincides with numerous changes of gene expression in the central nervous system (CNS). Cystatin F, which is a papain-like lysosomal cysteine proteinase inhibitor that is normally expressed by immune cells and not in the brain, is massively induced in the CNS during acute demyelination. We found that microglia, which are monocyte/macrophage-lineage cells in the CNS, express cystatin F only during demyelination. By using several demyelinating animal models and the spinal cord tissue
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