Oral Session

Oral Session 12 一般口演12

O12-1 Astrocyte progenitors require blood vessels for their proper migration and positioning within the cerebral gray matter アストロサイト前駆細胞は大脳灰白質への適正な移動と配置に血管を必要とする Tabata Hidenori（田畑秀典）^1,2，佐々木恵²，稲熊裕¹，伊東秀記¹，林周宏²，竹林浩秀³，依馬正次⁴，池中一裕⁵，永田浩一¹，仲嶋一範² ¹Dept. of Mol. Neurobiol., Inst. for Dev. Res., Aichi Human Service Cen. ²Dept. Anat., Keio Univ. Sch. of Med., Tokyo, Japan ³Div. of Neurobiol. & Anat., Grad. Sch. of Med. & Den. Sci., Niigata Univ., Niigata, Japan ⁴Dept. Stem Cells & Human Disease Models, Res. Cent. for Animal Life Sci. ⁵Div. of Neurobiol. & Bioinformatics, NIPS, Aichi, Japan During cerebral cortical development, neurons and glia are produced directly or indirectly from neural stem cells in the ventricular zone and migrate to their final destinations. Although the migratory process and its molecular mechanisms of cortical neurons are well studied, those of glial progenitors are largely unknown. During our observations of the cells migrating from the cortical ventricular zone, we have noticed that some cells moved in a very unique manner that had not been previously described: these cells moved very rapidly and almost randomly within the intermediate zone and the cortical plate and frequently divided. We named this migration “erratic migration”. The lineage analyses of them both in vitro and in vivo revealed that they were astrocyte progenitors destined for cortical gray matter. Interestingly, these cells frequently migrated along blood vessels, which are running radially in the cortical plate during the embryonic and perinatal stages, and reached superficial layers of the cortical plate. We identified key molecules involved in this process and could observe the migration and positioning failure by inhibiting these genes.		O12-2 The role of CD38 for development of neuron and glial cells 神経及びグリア発達におけるCD38の役割 Hattori Tsuyoshi（服部剛志）¹，Roboon Jureepon¹，Nguyen Dinh¹，東田陽博²，堀修¹ ¹Dept. of Neuroanat, Med. Kanazawa Univ. ²Res Cent for Child Mental Develop, Kanazawa Univ. Glial cells such as astrocytes and oligodendrocytes have emerged as important players in brain function under both physiological and pathological conditions. CD38 is a multifunctional molecule with ADP-ribosyl cyclase activity. While critical roles of CD38 in the adult brain such as oxytocin release and social behavior have been reported, those in the developing brain remain largely unknown. Recently we demonstrated that CD38 is dominantly expressed in astrocytes in developing brain. Furthermore, deletion of CD38 leads to impaired development of astrocytes cell-autonomously and oligodendrocytes non-cell autonomously. In this study, we investigated role of astrocytic CD38 for neuronal development by using systemic and astrocyte-specific conditional CD38 KO mice. Deletion of CD38 in astrocytes changed expression levels of synaptic markers and its morphology. These results suggest that astrocytic CD38 is involved in neuronal development.

O12-3 Neurons induce astrocyte tiling and self-avoidance in vitro 神経細胞によるアストロサイトタイリングの誘導 Hayashi Mariko（林真理子）^1,3，関野祐子²，佐藤薫³ ¹Med., Int.Univ.Health.Welfare ²Pharm., Univ of Tokyo. ³Nat.Inst.Health.Sci. An astrocyte makes thousands of finely branched processes to approach neurons. Branched processes of each astrocyte form an exclusive territory with limited penetration of processes of neighboring astrocytes. This is a phenomenon called tiling. There are two possible mechanisms for astrocyte tiling. One is that spongiform branching of astrocytes interferes entry of other astrocyte processes. The other is that astrocyte processes actively avoid processes of other astrocytes to form exclusive territories. Here we report that 5-6 orders of branching of astrocytes with over a hundred of process tips was successfully induced in our two-dimensional neuron-astrocyte mixed dissociated cultures prepared from neonatal rat cerebrum. Furthermore, astrocytes in this culture formed exclusive territories. The branching pattern of astrocyte processes indicated that astrocyte processes also avoided sister processes originating from the same astrocyte, in addition to processes of neighboring astrocytes. In contrast, neuronal dendrites and astrocyte processes do not avoid each other. After neuronal cell death, astrocytes lose the branched structure, showing importance of direct interaction with live neurons to maintain the branching and tiling of astrocytes. Our results indicate that neurons induce astrocyte-specific self-avoidance that leads to astrocyte tiling.