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en: Neural Mechanisms of Vestibular Compensation and Development of Drugs for Facilitating the Processes of Vestibular Compensation

ja: 前庭代償の神経メカニズムの解明と前庭代償促進薬の開発 (武田憲昭教授退任記念総説集)

ja: 耳鼻咽喉科臨床 補冊


en: HIZ(high intensity zone)に対するthermal annuloplasty

en: Monthly Book Orthopaedics

ja: Monthly Book Orthopaedics


en: How does the Human Brain differentiate? -Normal and Abnormal Development-

en: Forma

ja: Forma


en: Effects of ethanol on the development of circadian time keeping sysytem

ja: 脳発達期アルコール曝露による概日リズムの障害

en: Japanese Journal of Alcohol Studies & Drug Dependence

ja: 日本アルコール・薬物医学会雑誌


en: Rolling mouse Nagoya におけるCaイオンチャンネルの異常と運動失調

en: Clinical Neuroscience

ja: Clinical Neuroscience


en: Normal and abnormal neuronal migration in the developing cerebral cortex

en: Neuronal migration is the critical cellular process which initiates histogenesis of cerebral cortex. Migration involves a series of complex cell interactions and transformation. After completing their final mitosis, neurons migrate from the ventricular zone into the cortical plate, and then establish neuronal lamina and settle onto the outermost layer, forming an "inside-out" gradient of maturation. This process is guided by radial glial fibers, requires proper receptors, ligands, other unknown extracellular factors, and local signaling to stop neuronal migration. This process is also highly sensitive to various physical, chemical and biological agents as well as to genetic mutations. Any disturbance of the normal process may result in neuronal migration disorder. Such neuronal migration disorder is believed as major cause of both gross brain malformation and more special cerebral structural and functional abnormalities in experimental animals and in humans. An increasing number of instructive studies on experimental models and several genetic model systems of neuronal migration disorder have established the foundation of cortex formation and provided deeper insights into the genetic and molecular mechanisms underlying normal and abnormal neuronal migration.

en: The Journal of Medical Investigation : JMI


en: Ca2+チャンネル病マウスにおける小脳の異常と運動失調

ja: Ca2+チャンネル病マウスにおける小脳の異常と運動失調

en: Shikoku Acta Medica

ja: 四国医学雑誌


en: Expression of tyrosine hydroxylase in cerebellar Purkinje cells of ataxic mutant mice:its relation to the onset and/or development of ataxia

en: This report describes recent studies on tyrosine hydroxylase (TH) expression in Purkinje cells of the cerebellum of ataxic mutant mice. An increased expression of TH in some Purkinje cells has been observed in two allelic groups of mutant mice, tottering and dilute. TH-positive Purkinje cells appeared preceding the onset of ataxia. Northern blot analysis revealed 2.1 kb of TH mRNA in the mutant cerebella, and the size was identical to that of TH transcripts in other brain regions. However, TH in Purkinje cells did not seem to participate in catecholamine biosynthesis. In vitro studies showed that cultured non-catecholaminergic neurons expressed the TH transcripts following Ca2+ influx. Therefore, abnormal TH expression in the mutant Purkinje cells may indicate neuronal dysfunction caused by misregulation of intracellular Ca2+ concentrations.

ja: The Journal of Medical Investigation : JMI


en: Ataxic mutant mice with defects in Ca2+ channel a1A subunit gene: morphological and functional abnormalities in cerebellar cortical neurons.

en: Congenital Anomalies

ja: Congenital Anomalies


en: Application of stereology to the central nervous system: estimation of numerical densities of neurons and synapses or neuron number