形態形成セミナー 鳥居和枝先生 

日時:平成25年2月22日(金)17:30〜 
場所:慶應義塾大学信濃町キャンパス総合医科学研究棟 2階 会議室2
鳥居和枝先生

Principal Investigator, Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center
Assistant Professor, Department of Pediatrics, Pharmacology and Physiology
, The George Washington University School of Medicine and Health Sciences
Visiting Assistant Professor, Department of Neurobiology, School of Medicine, Yale University


Interaction of Heat Shock Signaling and Prenatal Environment in Neuropsychiatric Disorders.

The developing human brain, when exposed prenatally to various types of environmental challenges, displays increased susceptibility to late-onset neuropsychiatric dysfunction, though the mechanism remains obscure. We recently found that exposure of the human and mouse embryonic cerebral cortex to the challenges such as alcohol and methylmercury activates HSF1 mediated Heat Shock Signaling. In addition, Hsf1 deficiency causes the emergence of structural abnormalities in the mouse cortex upon in utero exposure to subthreshold levels of these challenges, and increases seizure susceptibility after birth. Furthermore, neural progenitor cells differentiated from human induced pluripotent stem cells of Schizophrenia patients show higher variability in the level of challenge-induced HSF1 activation. Altogether, our findings uncover the role of HSF1 in conferring tolerance to prenatal environmental perturbations in the normal cerebral cortex, thereby securing a lowered manifestation of neuropsychiatric disorders, and suggest that HSF1 malresponse may be a key component of the pathogenesis of these disorders.