1997/06 - 2001/07 Nagoya City UniversityGraduate School of Pharmaceutical Sciences
Education
1994/04 - 1997/03 Nagoya City University Graduate School of Pharmaceutical Sciences
1992/04 - 1994/03 Nagoya City University Graduate School of Pharmaceutical Sciences
Association Memberships
日本感染症学会 International Association of Therapeutic Drug Monitoring and Clinical Toxicology 日本乳癌学会 日本化学療法学会 日本神経科学学会 Society for Neuroscience 愛知県病院薬剤師会 日本神経化学会 日本神経精神薬理学会 日本医療薬学会 日本病院薬剤師会 日本基礎老化学会 日本分子生物学会 日本癌学会 日本薬理学会 日本薬学会 日本薬学教育学会
The reduction of methylation on the upstream reagion of shati/nat8l transcription start site is induced by repeated administration of methamphetamine [Not invited]
shati/nat8l and NAA increases with the development in mice
Sumi K; Uno K; Iwamoto R; Nabeshima T; Furukawa-Hibi Y; Miyamoto Y; Nitta A
The 6th Molecular Cellular Cognition Society (MCCS)-Asia Symposium‐Joint International Symposium with Innovative Area (Microendophenotype of psychiatric disorders) and RIKEN BSI-FIRST Program as Neuro2013 Satellite symposium 2013/06
Novel molecules related to psychiatric diseases Hot Topics 覚せい剤精神病マウス側坐核から単離された精神病関連分子について(Novel molecules related to psychiatric diseases: Hot Topics Three new molecules related to psychiatric diseases) [Not invited]
新田 淳美; 日比 陽子; 宇野 恭介; 鍋島 俊隆; 宮本 嘉明
神経化学 2011/09 日本神経化学会
Diversity of brain function created by living environment 神経精神発達に対する幼若期ストレスの影響(Diversity of brain function created by living environment Impact of stressful events during juvenile periods on neuropsychological development)
永井 拓; 尹 錫在; 日比 陽子; 山田 清文
神経化学 2011/09 日本神経化学会
Emotional behaviors are regulated by the overexpression of shati in the dorsal striatum or nucleus accumbens of mice.
A dipeptide, Leu-Ile, prevents the impairment of memory induced by amyloid beta in mice via restraining the hyperphosphorylation of ERK in the hippocampus
Nitta A; Alkam R; Furukawa-Hibi Y; Niwa M; Mizoguchi H; Yamada K; Nabeshima T
39th Annual Meeting of Society for Neuroscience (Neuroscience 2009) 2009/10
A neuroprotective dipeptide, Leu-Ile, prevents the impairment of memory induced by amyloid beta in mice via restraining the hyperphosphorylation of ERK in the hippocampus.
Alkam T; Nitta A; Furukawa-Hibi Y; Niwa M; Yamada K; Nabeshima T
39th Annual Meeting of Society for Neuroscience (Neuroscience 2009) 2009/10
Shati-over-expressed mice shows similar symptoms to the autism.
Liu W; Nitta A; Hibi Y; Nabeshima T; Yamada K
6th Nagoya Nanjing Shenyang pharmacology science symposium 2009/09
Dipeptide Leu-Ile inhibits immobility induced by repeated forced swimming via induction of BDNF. [Not invited]
2nd Annual International Drug Abuse Research Society & international Society for Neurochemistry Satellite Meeting in Association with Korian Society for Drug Abuse Research 2009/08
Y. Miyamoto; N. Iegaki; K. Sumi; Y. Ishikawa; T. Furuta; Y. Furukawa-Hibi; S-I Muramatsu; T. Nabeshima; K. Uno; A. Nitta INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY 17- 57 -57 2014/06
A. Nitta; Y. Ishikawa; N. Iegaki; S-I. Miuramatsu; T. Nabeshima; Y. Furukawa-Hibi; K. Uno; Y. Miyamoto INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY 15- 74 -74 2012/06
Diversity of brain function created by living environment 神経精神発達に対する幼若期ストレスの影響(Diversity of brain function created by living environment Impact of stressful events during juvenile periods on neuropsychological development)
Novel molecules related to psychiatric diseases Hot Topics 覚せい剤精神病マウス側坐核から単離された精神病関連分子について(Novel molecules related to psychiatric diseases: Hot Topics Three new molecules related to psychiatric diseases)
Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research
Date (from‐to) : 2020/04 -2024/03
Author : HIBI YOKO
NPAS4 is a transcription factor thought to be the key to the relationship between stress, GABAergic nervous system disorders, and the onset of psychiatric symptoms. In this study, we have approached this issue from both the basic analysis and the analysis of delirium onset using clinical data. In the basic analysis, we have focused on the analysis of compounds that induce Npas4 expression using cells and animals, as well as the brain-kidney crosstalk. In the field of clinical research, we focused on the possibility that NPAS4 may affect the relationship between benzodiazepine drugs and the onset of delirium, and investigated medical records regarding risk factors for delirium and drugs used. We investigated the effects of the combined use of opioids and benzodiazepine drugs in patients, but no clear trends were found.
Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research
Date (from‐to) : 2017/04 -2022/03
Author : HIBI YOKO
Since dysfunction of suppressive GABAergic nerves due to decreased expression of NPAS4 may cause nerve excitement / suppression imbalance, we investigated the association with seizures. Npas4-knockout mice were shown to have a lower threshold for convulsions. It was suggested that as the mechanism, Npas4 transcripts Homer1a and gives feedback to suppress nerve excitement. Regarding the search for compounds that induce Npas4 promoter activity, we found several compounds that increase Npas4 promoter activity in humans and mice from commercially available active compound libraries.
Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research
Date (from‐to) : 2014/04 -2018/03
Author : HIBI YOKO
Neuronal PAS domain 4 (NPAS4) has recently been shown to regulate the development of GABAergic inhibitory synapses. We previously reported that Npas4 mRNA expression levels were reduced in the hippocampus of mice exposed to social isolation or restraint stress. In the present study, we suggested that restraint stress increase the DNA methylation level of Npas4 promoter region. We analyzed the effect of decrease of Npas4 expression on the function of GABA neurons. Npas4-knockout mice were impaired in pre-pulse inhibition. GABA receptors were decreased in the cerebellum of Npas4-knockout mice. The expression level of Npas4 mRNA was significantly increased after the pentylenetetrazol (PTZ) treatment. Npas4 increased Homer1a promoter activity. Npas4 function as a molecular switch to initiate homeostatic scaling and the targetinc of Npas4-Homer1a signaling may provide new approaches for the treatment of epilepsy.
Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research
Date (from‐to) : 2011/04 -2013
Author : HIBI YOKO; YAMADA Kiyofumi; NAGAI Taku
Neuronal PAS domain 4 (NPAS4) has recently been shown to regulate the development of GABAergic inhibitory synapses. We previously reported that Npas4 mRNA expression levels were reduced in the hippocampus of mice exposed to social isolation or restraint stress. In the present study, to investigate the transcriptional regulation of Npas4 by stress, we focused on the effect of glucocorticoids upon Npas4 transcription. Corticosterone treatment reduced Npas4 expression in the frontal cortex and hippocampus. Putative negative glucocorticoid response elements (GREs) were found -2000 to -1000 upstream of the Npas4 transcription initiation site. Npas4 promoter activity was increased by mutation of the negative GRE sequences. Restraint stress increased the binding of GR to Npas4 promoter region in the hippocampus. These results suggest that transcription of Npas4 is down-regulated by stress via the binding of agonist-bound GR to its promoter.
The role of interferon-induced transmembrane protein 3 (IFITM3) in the CNS is largely unknown, despite the fact that its expression is increased in the brains of patients with neurologic and neuropsychiatric diseases. In the present study we show the role of IFITM3 in long-lasting neuronal impairments in mice following polyI:C-induced immune challenge during the early stages of development. Our findings suggest that the induction of IFITM3 expression in astrocytes by the activation of the innate immune system during the early stages of development has non-cell autonomous effects that affect subsequent neurodevelopment, leading to neuropathological impairments and brain dysfunction, by impairing endocytosis in astrocytes.