64 117 iPS GFP 1981 1983 NIHFogarty International Fellow, NINCDS QFDE1984 1992 QFDE 1992 Virchows Arch., 427:5195271996 Biomed. Rev., 15: 1192004 J. Electron Microsc., 59: 395408201021 2007 20072346712008 Ii iiiiiQdot IIIII iii
117 65 S Physiological roles of cell death signaling in mouse neural development Masayuki Miura 1,2 1 2 CREST, JST Caspases function as regulatory molecules not only in cell death, but also in non-apoptotic functions. Live-imaging analysis with the mouse embryos expressing SCAT3, a fluorescent indicator protein to monitor caspase-3 activation in living cells, revealed that preventing apoptosis by inhibition of caspases disturbed smooth morphological changes of developing neural plates and also reduced the speed of the cranial neural tube closure. A considerable number of olfactory sensory neurons (OSNs) in the developing olfactory epithelium exhibited caspase-3 activity without the apoptotic changes of nuclei. This prompts us to assess whether caspases exert non-apoptotic functions in OSNs during olfactory development. Apaf-1/caspase-9-mediated signaling causes the cleavage of a membrane-anchored member of the semaphorin family of guidance proteins, Sema7A, in the axons of OSNs during development. Analysis of mutant mice deficient for apaf- 1 or caspase-9 revealed that this Apaf-1/caspase-9-mediated nonapoptotic caspase signaling is important for the development of OSNs by affecting axonal pathfinding, synapse formation and maturation status. S Characterization of Early Pathogenesis in the SODGA Mouse Model of ALS. Carol Milligan, Sherry Vinsant, Carol Mansfield, Masaaki Yoshikawa, Ramon Moreno, David Prevette Ronald Oppenheim Department of Neurobiology and Anatomy, and the ALS Center, Wake Forest School of Medicine, WinstonSalem, NC 27157, US Charcot first described Amyotrophic Lateral Sclerosis in 1869 yet, effective, long-term treatment strategies are not available. A mouse model was developed after the identification of mutations in the SOD1 gene approximately 17 years ago, and most of our knowledge of the etiology and pathogenesis of the disease is from studies using this model. Although numerous preclinical trials have been conducted, results have been disappointing in that they did not positively translate in clinical trials. Characterization of the early pathological events may provide insight into disease onset, help in the discovery of presymptomatic diagnostic disease markers, and identify novel therapeutic targets. Many previous studies have identified pathological events in the mutant SOD1 models involving spinal cord, peripheral axons, neuromuscular junctions or muscle; however, few have systematically examined pathogenesis at multiple sites. In this study, we examine both central and peripheral components of the neuromuscular system in the SOD1G93A mouse model of ALS and relate these alterations to early muscle denervation. Our results provide insight into the earliest pathological events in this model. S Nerve injury induced motor neuron death with reference to neuronglia interaction Hiroshi Kiyama Dept. Functional Anatomy & Neurosci., Nagoya Univ. Grad. Sch. Med. The peripheral nerve injury induces changes not only in the injured neurons but also in surrounding glial cells. An interaction between neurons and glial cells might be critical in proper regeneration and functional recovery. One of the prominent glial behaviors seen after motor nerve injury was the microglial migration, proliferation and adhesion to the surfaces of injured motor neurons in response to nerve injury. Although the consequence of this adhesion between the nerve injured motor neurons and microglia seen during the first two weeks is not clear, nerve injured motor neurons, which lacked the initial tight adhesion with microglia, showed degenerative feature. In addition the knockout of a chemokine receptor CCR5, which specifically expressed by microglia in response to nerve injury, accelerated the motor neuron death. These evidences suggest that the microglial behavior seems important perhaps to provide neurons with a signal for survival and regeneration. In this symposium I would like to address morphological characteristics observed in the nerve injury induced motor neuron death and the interactions among injured motor neuron and surrounding glial cells. S Autophagy in the neural network and its impairment Yasuo Uchiyama Dept of Cell Biol & Neurosci, Juntendo Univ Grad Sch of Med Cathepsin D (CD) is distributed in various mammalian cells. We have shown that CNS neurons in CD-deficient mouse brains present a new form of lysosomal accumulation disease with a phenotype resembling neuronal ceroid lipofuscinosis (NCL). The most striking feature of the CD-/- CNS neurons is storage of autophagosomes, autolysosomes, granular osmiophilic deposits (GRODs), and fingerprint profiles, morphological hallmarks of NCLs. Moreover, GRODs are found within nascent autophagosomes, indicating that the GROD is a potent inducer of autophagy in neuronal cells. Autophagosomes, but not GRODs or lysosomes, frequently accumulate in the axon, indicating that subsets required for autophagosome formation are present in the axon. Until recently, it has been reported that impairment of autophagy due to Atg7 or Atg5 deficiency in the axon terminal of Purkinje cells induces neurodegeneration. These results indicate that not only in autophagy-unable neurons but also in neurons with excess of autophagy impairment of autophagy in the axon and its terminal induces neurodegeneration. However, the molecular mechanism of autophagosome formation in the axon and its terminal largely remains unknown.
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