Keio University · 신경과학
켄지 히로시 타나카 교수의 연구실은 신경과학 분야에서 신호전달 수용체, 신경세포 기능, 그리고 신경질환과 관련된 유전자 발현 조절 메커니즘을 중심으로 연구를 진행하고 있습니다. 특히 세로토닌 수용체, 아드레날린 수용체, 그리고 아교세포 기반 질환인 올라거병의 분자 기전에 대한 기초 연구를 통해 뇌의 세포 유형 특이적 기능과 병태생리학적 변화를 규명하고자 합니다. 또한 optogenetics 기반 유전자 조절 기술과 동물 모델을 활용한 기능적 신경생물학 연구도 활발히 수행되고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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
