Institute for Developmental Research

Okazaki, Japan

Institute for Developmental Research

Okazaki, Japan
SEARCH FILTERS
Time filter
Source Type

McKinsey G.L.,University of California at San Francisco | Lindtner S.,University of California at San Francisco | Trzcinski B.,University of Michigan | Visel A.,Lawrence Berkeley National Laboratory | And 6 more authors.
Neuron | Year: 2013

Mammalian pallial (cortical and hippocampal) and striatal interneurons are both generated in the embryonic subpallium, including the medial ganglionic eminence (MGE). Herein we demonstrate that the Zfhx1b (Sip1, Zeb2) zinc finger homeobox gene is required in the MGE, directly downstream of Dlx1&2, to generate cortical interneurons that express Cxcr7, MafB, and cMaf. In its absence, Nkx2-1 expression is not repressed, and cells that ordinarily would become cortical interneurons appear to transform toward a subtype of GABAergic striatal interneurons. These results show that Zfhx1b is required to generate cortical interneurons, and suggest a mechanism for the epilepsy observed in humans with Zfhx1b mutations (Mowat-Wilson syndrome). © 2013 Elsevier Inc.


Iida S.,Nagoya University | Iida S.,Institute for Developmental Research | Nakao T.,Ottawa Health Research Institute | Ohira H.,Nagoya University
Cognitive, Affective and Behavioral Neuroscience | Year: 2012

It has been reported that engagement in several kinds of cognitive activity can successfully inhibit unpleasant emotions. In this study, we tried to replicate the previous finding that cognitive activity can modulate subsequent psychological and physiological emotional processes and to investigate whether prior cognitive activity can attenuate implicit emotional processes triggered by subliminal emotional stimuli. Sixty students were randomly divided into three groups (cognitive task group, noncognitive task group, control group). The cognitive task group was asked to engage in an n-back task, while the control group was asked to stay calm. The noncognitive task group was asked to do a handgrip-squeezing task. All participants then engaged in a version of a subliminal affective priming task where they were unconsciously exposed to affectively negative pictures. The cognitive task group showed lower negative experiences after the subliminal affective priming task and a substantial reduction in their heart rate responses, as compared with the other groups. These results provide evidence that engagement in cognitive activity can attenuate emotional processes in an automatic and unconscious manner. © Psychonomic Society, Inc. 2012.


Iida S.,Nagoya University | Iida S.,Institute for Developmental Research | Nakao T.,Japan Society for the Promotion of Science | Ohira H.,Nagoya University
Cognitive, Affective and Behavioral Neuroscience | Year: 2011

The successful regulation of emotion relies heavily on executive function. Until very recently, however, the specific effects of executive function activity on other processes havereceived relatively little empirical attention. The link between executive function and emotional responses suggests that the activation of executive function may play an important role in the attenuation of emotional responses. We conducted twoexperiments to test the hypothesis that decrements in emotional responses following cognitive task performance might be caused, at least in part, by the activation of executive function. First, we sought to test whetherthe activation of executive function reducedemotional responsesimplicitly, without any volitional effort. Next, we sought to examine the link between prior activation of executivefunction and the attenuation of subsequent emotional responses, by comparing the effects of an executive-function-demanding task with the effects of a task that is equally effortful but does not engage executive function. We discuss our results in the context of the role of executive function in the attenuation of emotion. © Psychonomic Society, Inc. 2011.


Iio A.,Gifu University | Iio A.,Institute for Developmental Research | Takagi T.,Osaka Medical College | Miki K.,Osaka Medical College | And 3 more authors.
Biochimica et Biophysica Acta - Gene Regulatory Mechanisms | Year: 2013

In various human malignancies, widespread dysregulation of microRNA (miRNA) expression is reported to occur and affects various cell growth programs. Recent studies suggest that the expression levels of miRNAs that act as tumor suppressors are frequently reduced in cancers because of chromosome deletions, epigenetical changes, aberrant transcription, and disturbances in miRNA processing. MiR-143 and -145 are well-recognized miRNAs that are highly expressed in several tissues, but down-regulated in most types of cancers. However, the mechanism of this down-regulation has not been investigated in detail. Here, we show that DEAD-box RNA helicase 6, DDX6 (p54/RCK), post-transcriptionally down-regulated miR-143/145 expression by prompting the degradation of its host gene product, NCR143/. 145 RNA. In human gastric cancer cell line MKN45, DDX6 protein was abundantly expressed and accumulated in processing bodies (P-bodies). DDX6 preferentially increased the instability of non-coding RNA, NCR143/145, which encompasses the miR-143/145 cluster, and down-regulated the expression of mature miR-143/145. In human monocytic cell line THP-1, lipopolysaccharide treatment promoted the assembly of P-bodies and down-regulated the expression of NCR143/145 and its miR-143/145 rapidly. In these cells, cycloheximide treatment led to a loss of P-bodies and to an increase in NCR143/145 RNA stability, thus resulting in up-regulation of miR-143/145 expression. These data demonstrate that DDX6 contributed to the control of NCR143/145 RNA stability in P-bodies and post-transcriptionally regulated miR-143/145 expression in cancer cells. © 2013 Elsevier B.V.


Karasawa T.,Institute for Developmental Research | Lombroso P.J.,Yale University
Neuroscience Research | Year: 2014

Striatal-enriched protein tyrosine phosphatase (STEP) is a brain-specific tyrosine phosphatase that plays a major role in the development of synaptic plasticity. Recent findings have implicated STEP in several psychiatric and neurological disorders, including Alzheimer's disease, schizophrenia, fragile X syndrome, Huntington's disease, stroke/ischemia, and stress-related psychiatric disorders. In these disorders, STEP protein expression levels and activity are dysregulated, contributing to the cognitive deficits that are present. In this review, we focus on the most recent findings on STEP, discuss how STEP expression and activity are maintained during normal cognitive function, and how disruptions in STEP activity contribute to a number of illnesses. © 2014 Elsevier Ireland Ltd and the Japan Neuroscience Society.


Watanabe M.,Institute for Developmental Research
Development Growth and Differentiation | Year: 2010

The pathway from the retina to the brain in mammals provides a well-defined model system for investigation of not only surviving axotomy but also axonal regeneration of injured neurons. Here I introduce our recent works on axonal regeneration in the optic nerve (OpN) of adult cats. Fibers of retinal ganglion cells (RGCs) extend beyond the crush site of OpN with injections of a macrophage stimulator (oxidized galectin-1) or a Rho kinase (ROCK) inhibitor (Y-39983 or Y-27632) while axonal extension is blocked with injection of saline. Elongation of crushed optic fibers, however, is slowed after 2 weeks. Transplantation of peripheral nerve makes RGCs regenerate their transected axons into a graft but regenerated fibers extend only a few mm in the brain. Effectiveness of combination of the drugs and treatments has to be verified in future. © 2010 Japanese Society of Developmental Biologists.


Shimada A.,Institute for Developmental Research | Hasegawa-Ishii S.,Institute for Developmental Research
Aging and Disease | Year: 2011

The Senescence-Accelerated Mouse (SAM) represents a group of inbred mouse strains developed as a model for the study of human aging and age-related diseases. Senescence-prone (SAMP) strains exhibit an early onset of age-related decline in the peripheral immunity such as thymic involution, loss of CD4+ T cells, impaired helper T cell function, decreased antibody-forming capacity, dysfunction of antigen-presenting cells, decreased natural killer activity, increased auto-antibodies, and susceptibility to virus infection. Senescence-prone SAMP10 mice undergo age-related changes in the brain such as brain atrophy, shrinkage and loss of cortical neurons, retraction of cortical neuronal dendrites, loss of dendritic spines, loss of synapses, impaired learning and memory, depressive behavior, accumulation of neuronal DNA damage, neuronal ubiquitinated inclusions, reduced hippocampal cholinergic receptors, decreased neurotrophic factors, decreased hippocampal zinc and zinc transporters, increased sphyngomyelinase, and elevated oxidative-nitrative stress. Recent data indicating increased pro-inflammatory cytokines in the brain of SAMP10 mice are directing investigators toward an integration of immune and neural abnormalities to enhance understanding of the principles of brain aging. We highlight how mouse brain cells adopt cytokine-mediated responses and how SAMP10 mice are defective in these responses. SAMP10 model would be useful to study how age-related disturbances in peripheral immunity have an impact on dysregulation of brain tissue homeostasis, resulting in age-related neurodegeneration.


Shinoda T.,Institute for Developmental Research | Ito H.,Institute for Developmental Research | Sudo K.,Institute for Developmental Research | Iwamoto I.,Institute for Developmental Research | And 2 more authors.
Molecular Biology of the Cell | Year: 2010

Septins are a family of conserved guanosine triphosphate/guanosine diphosphate-binding proteins implicated in a variety of cellular functions such as cell cycle control and cytokinesis. Although several members of septin family, including Septin 14 (Sept14), are abundantly expressed in nervous tissues, little is known about their physiological functions, especially in neuronal development. Here, we report that Sept14 is strongly expressed in the cortical plate of developing cerebral cortex. Knockdown experiments by using the method of in utero electroporation showed that reduction of Sept14 caused inhibition of cortical neuronal migration. Whereas cDNA encoding RNA interference-resistant Sept14 rescued the migration defect, the C-terminal deletion mutant of Sept14 did not. Biochemical analyses revealed that C-terminal coiled-coil region of Sept14 interacts with Septin 4 (Sept4). Knockdown experiments showed that Sept4 is also involved in cortical neuronal migration in vivo. In addition, knockdown of Sept14 or Sept4 inhibited leading process formation in migrating cortical neurons. These results suggest that Sept14 is involved in neuronal migration in cerebral cortex via interaction with Sept4. © 2010 by The American Society for Cell Biology.


Ito H.,Institute for Developmental Research | Morishita R.,Institute for Developmental Research | Shinoda T.,Institute for Developmental Research | Iwamoto I.,Institute for Developmental Research | And 3 more authors.
Molecular Psychiatry | Year: 2010

Genetic variations in dysbindin-1 (dystrobrevin-binding protein-1) are one of the most commonly reported variations associated with schizophrenia. As schizophrenia could be regarded as a neurodevelopmental disorder resulting from abnormalities of synaptic connectivity, we attempted to clarify the function of dysbindin-1 in neuronal development. We examined the developmental change of dysbindin-1 in rat brain by western blotting and found that a 50 kDa isoform is highly expressed during the embryonic stage, whereas a 40 kDa one is detected at postnatal day 11 and increased thereafter. Immunofluorescent analyses revealed that dysbindin-1 is enriched at the spine-like structure of primary cultured rat hippocampal neurons. We identified WAVE2, but not N-WASP, as a binding partner for dysbindin-1. We also found that Abi-1, a binding molecule for WAVE2 involved in spine morphogenesis, interacts with dysbindin-1. Although dysbindin-1, WAVE2 and Abi-1 form a ternary complex, dysbindin-1 promoted the binding of WAVE2 to Abi-1. RNA interference-mediated knockdown of dysbindin-1 led to the generation of abnormally elongated immature dendritic protrusions. The present results indicate possible functions of dysbindin-1 at the postsynapse in the regulation of dendritic spine morphogenesis through the interaction with WAVE2 and Abi-1. © 2010 Macmillan Publishers Limited. All rights reserved.


Kouchi Z.,Institute for Developmental Research
Biochemical and Biophysical Research Communications | Year: 2015

Monoacylglycerol lipase (MAGL) is important for neuroinflammation. However, the regulatory mechanisms underlying its expression and function remain unknown. Lipopolysaccharide (LPS) treatment post-translationally upregulated MAGL expression, whereas it downregulated MAGL transcription through a Stat6-mediated mechanism in microglia. Neither MAGL knockdown nor JZL-184, a selective MAGL inhibitor, suppressed LPS-induced upregulation of inflammatory cytokines in microglia. Moreover, exogenous expression of MAGL in BV-2 microglial cell line, which lacks endogenous MAGL, did not promote the induction of inflammatory cytokines by LPS treatment. Interestingly, MAGL knockdown reduced Fcγ receptor-mediated phagocytosis in primary microglia, and introduction of MAGL into the BV-2 cells increased Fcγ receptor-mediated phagocytosis. Collectively, these results suggest that MAGL regulates phagocytosis, but not LPS-mediated cytokine induction in microglia. © 2015 Elsevier Inc. All rights reserved.

Loading Institute for Developmental Research collaborators
Loading Institute for Developmental Research collaborators