ナカムラ ノブヒロ   NAKAMURA NOBUHIRO
  中村 暢宏
   所属   京都産業大学  生命科学部 先端生命科学科
   職種   教授
言語種別 英語
発行・発表の年月 2008
形態種別 研究論文
査読 査読あり
標題 Modulation of cellular proliferation and differentiation through GABA B receptors expressed by undifferentiated neural progenitor cells isolated from fetal mouse brain
執筆形態 その他
掲載誌名 Journal of Cellular Physiology
出版社・発行元 WILEY-LISS
巻・号・頁 216(2),pp.507-519
著者・共著者 Fukui, M.,Nakamichi, N.,Yoneyama, M.,Ozawa, S.,Fujimori, S.,Takahata, Y.,Nakamura, N.,Taniura, H.,Yoneda, Y.
概要 In this study, we have attempted to evaluate the possible role of metabotropic GABA(B) receptors (GABA(B)R) expressed by neural progenitor cells prepared from neocortex of embryonic Std-ddY mice. Immunocytochemical analysis confirmed the validity of isolation procedures of neural progenitors, while round spheres were formed with clustered cells during culture with epidermal growth factor (EGF) for 10 days. A reverse transcription polymerase chain reaction analysis revealed constitutive expression of GABA(A)R, GABA(B)R, and GABA(C)R subtypes in undifferentiated progenitors and neurospheres formed within 10 days. Exposure to GABA led to concentration-dependent increases in the total area and proliferation activity of neurospheres at 10-300 mu M, while the GABABR agonist baclofen at 100 mu M significantly increased the size of neurospheres expressing both GABA(B)R1 and GABA(B)R2 subunits in a manner sensitive to a GABABR antagonist. By contrast, a significant decrease was seen in the total areas of neurospheres prepared from mice deficient of the GABA(B)R1 subunit. In neurospheres of GABA(B)R1-null mice, a significant increase was induced in the number of cells immunoreactive for a glial marker protein, with a concomitant decrease in that of a neuronal marker protein, upon spontaneous differentiation after the removal of EGF. These results suggest that GABA(B)R may be functionally expressed by neural progenitor cells to preferentially promote the commitment toward a neuronal lineage after the activation of cellular proliferation toward self-replication in the developing mouse brain.
DOI 10.1002/jcp.21422
ISSN 0021-9541
Put Code(ORCID) 19809399