PubMed Health⌕ Search

Biomedical subjects

Hidenori Tabata

Publications and source records attributed to Hidenori Tabata.

10 recordsLinked to original sources
PubMed2006

Expression profiles of Insulin-like growth factor binding protein-like 1 in the developing mouse forebrain.

Insulin-like growth factor binding protein-like 1 (IGFBPL-1) has a domain structure that resembles one in the insulin-like growth factor binding proteins (IGFBPs), which is a domain known to be bound by insulin-like growth factors (IGFs) with high affinity and to thereby affect cell growth and metabolism. However, the distribution and functions of IGFBPL-1 in the brain are not known. Thus, to clarify IGFBPL-1 expression profiles during development, we have investigated the expression patterns of IGFBPL-1 mRNA in developing mouse brains using in situ hybridization, focusing especially on the forebrain. On embryonic day (E)12, IGFBPL-1mRNA expressions were localized in the preplate of the neopallium, dorsal thalamus, the differentiating field of the epithalamus, and the hippocampus. On E14, strong expression was recognized in the subventricular zone (SVZ) and intermediate zone (IMZ) in the neopallium, hippocampus, the differentiating field of the epithalamus, and the dorsal thalamus. E14 expressions were generally the strongest among all the stages examined and signals decreased thereafter. At E16 and E18, IGFBPL-1mRNA was strongly detected in the hippocampus and the SVZ of the neopallium. In postnatal stages, mRNA was found only in the granule cell layer of the dentate gyrus (DG). Notably, at P20, expression was restricted to the deep fraction of the granule cell layer, the location of late-born DG neurons.

Animals↗
PubMed2005

The caudal migratory stream: a novel migratory stream of interneurons derived from the caudal ganglionic eminence in the developing mouse forebrain.

The migratory paths of interneurons derived from the ganglionic eminence (GE), and particularly its caudal portion (CGE), remain essentially unknown. To clarify the three-dimensional migration profile of interneurons derived from each part of the GE, we developed a technique involving focal electroporation into a small, defined portion of the telencephalic hemisphere. While the medial GE cells migrated laterally and spread widely throughout the cortex, the majority of the CGE cells migrated caudally toward the caudal-most end of the telencephalon. Time-lapse imaging and an in vivo immunohistochemical study confirmed the existence of a migratory stream depicted by a population of CGE cells directed caudally that eventually reached the hippocampus. Transplantation experiments suggested that the caudal direction of migration of the CGE cells was intrinsically determined as early as embryonic day 13.5. The caudal migratory stream is a novel migratory path for a population of CGE-derived interneurons passing from the subpallium to the hippocampus.

Animals↗
PubMed2005

Neuronal migration in cortical development.

Cortical formation in the developing brain is a highly complicated process involving neuronal production (through symmetric or asymmetric cell division) interaction of radial glia with neuronal migration, and multiple modes of neuronal migration. It has been convincingly demonstrated by numerous studies that radial glial cells are neural stem cells. However, the processes by which neurons arise from radial glia and migrate to their final destinations in vivo are not yet fully understood. Recent studies using time-lapse imaging of neuronal migration are giving investigators an increasingly more detailed understanding of the mitotic behavior of radial glia and the migrating behavior of their daughter cells. In this review, we describe recent progress in elucidating neuronal migration in brain formation and how neuronal migration is disturbed by mutations in genes that control this process.

Brain Diseases↗
PubMed2004

The Wnt/beta-catenin pathway directs neuronal differentiation of cortical neural precursor cells.

Neural precursor cells (NPCs) have the ability to self-renew and to give rise to neuronal and glial lineages. The fate decision of NPCs between proliferation and differentiation determines the number of differentiated cells and the size of each region of the brain. However, the signals that regulate the timing of neuronal differentiation remain unclear. Here, we show that Wnt signaling inhibits the self-renewal capacity of mouse cortical NPCs, and instructively promotes their neuronal differentiation. Overexpression of Wnt7a or of a stabilized form of beta-catenin in mouse cortical NPC cultures induced neuronal differentiation even in the presence of Fgf2, a self-renewal-promoting factor in this system. Moreover, blockade of Wnt signaling led to inhibition of neuronal differentiation of cortical NPCs in vitro and in the developing mouse neocortex. Furthermore, the beta-catenin/TCF complex appears to directly regulate the promoter of neurogenin 1, a gene implicated in cortical neuronal differentiation. Importantly, stabilized beta-catenin did not induce neuronal differentiation of cortical NPCs at earlier developmental stages, consistent with previous reports indicating self-renewal-promoting functions of Wnts in early NPCs. These findings may reveal broader and stage-specific physiological roles of Wnt signaling during neural development.

Animals↗
PubMed2004

Birth-date dependent alignment of GABAergic neurons occurs in a different pattern from that of non-GABAergic neurons in the developing mouse visual cortex.

In the developing mouse cerebral cortex, gamma-aminobutyric acid (GABA)ergic neurons and non-GABAergic neurons arise in distinct places and migrate into the cortical plate (CP) via different pathways. Although the "inside-out" alignment of projection neurons in the cortex has been thoroughly analyzed, the pattern of interneuron alignment is not well understood. Herein, we show that in the postnatal day (P) 9.5 mouse visual cortex, GABAergic neurons born on embryonic day (E) 12.5 were distributed around two peak locations, mainly around layer V and also around layer II/III, while non-GABAergic neurons born on E12.5 were distributed around only one peak in layer VI. Both cell populations born on E15.5 exhibited only one common peak distribution in layer II/III. The two peak locations of GABAergic neurons born on E12.5 still existed at P30. When the subtypes of GABAergic neurons were analyzed, calretinin-positive cells born on E12.5 were distributed in the cortex around one peak location near layer II/III, whereas somatostatin-positive E12.5 cells were distributed in the cortex around one peak location near layer V. These results suggest that the alignment of interneurons is regulated differently according to subtypes and from that of projection neurons having the same embryonic day of origin.

Animals↗
PubMed2003

Multipolar migration: the third mode of radial neuronal migration in the developing cerebral cortex.

Two distinct modes of radial neuronal migration, locomotion and somal translocation, have been reported in the developing cerebral cortex. Although these two modes of migration have been well documented, the cortical intermediate zone contains abundant multipolar cells, and they do not resemble the cells migrating by locomotion or somal translocation. Here, we report that these multipolar cells express neuronal markers and extend multiple thin processes in various directions independently of the radial glial fibers. Time-lapse analysis of living slices revealed that the multipolar cells do not have any fixed cell polarity, and that they very dynamically extend and retract multiple processes as their cell bodies slowly move. They do not usually move straight toward the pial surface during their radial migration, but instead frequently change migration direction and rate; sometimes they even remain in almost the same position, especially when they are in the subventricular zone. Occasionally, the multipolar cells jump tangentially during their radial migration. Because the migration modality of these cells clearly differs from locomotion or somal translocation, we refer to their novel type of migration as "multipolar migration." In view of the high proportion of cells exhibiting multipolar migration, this third mode of radial migration must be an important type of migration in the developing cortex.

Animals↗
PubMed2003

Cellular and molecular mechanisms of neuronal migration in neocortical development.

The complicated mammalian brain structure arises from accurate movements of neurons from their birthplace to their final locations. Detailed observation of this migration process by various methods revealed that neuronal migration is highly motile and that there are different modes of migration. Moreover, mouse mutants or human disorders that disrupt normal migration have provided significant insights into molecular pathways that control the neuronal migration. Although our knowledge is still fragmentary, it is becoming clear that various molecules are participating in this process. In this review, we outline about the cellular and molecular mechanisms of neuronal migration in the cerebral cortex.

Animals↗
PubMed2002

Neurons tend to stop migration and differentiate along the cortical internal plexiform zones in the Reelin signal-deficient mice.

The Reelin molecule plays a fundamental role in corticogenesis. After Reelin binds to its receptors, the Reelin signal is transduced through tyrosine phosphorylation of the intracellular adaptor protein disabled 1 (Dab1). The reelin-gene-deficient mouse, reeler, and Dab1-deficient mouse, yotari, show disrupted positioning of neurons. Several molecules have been identified recently as being involved in Reelin signaling, however, the biological function of Reelin during cortical plate development was still unknown. We observed the migrating behavior of neurons during development in Reelin-signal-deficient mice. To visualize the migrating neurons directly, we introduced green fluorescent protein (GFP)-expression vectors into the ventricular zone with an in utero electroporation system and allowed the embryos to develop in utero until they were analyzed. The result showed that the migrating cells in the mutants were morphologically indistinguishable from those of normal mice. At the stage when the GFP-expressing cells reached the marginal zone near the pial surface and began dendrite formation in normal mice, the GFP-positive cells were found at various deeper positions in the mutant cortex. They had the morphology of migrating cells extending leading processes toward the pial surface. By contrast, in the mutants these cells tended to stop migration along the borders of the internal plexiform zone, the irregular structure consisting mainly of dendrites in the mutant cortex. Postnatally, these neurons began to develop dendrites later than the cells in the normal cortex. During this process, some neurons above the internal plexiform zone extended and developed dendrites in the opposite direction into the internal plexiform zone. These results suggest that the abnormal positioning of neurons in the Reelin-signal-deficient mice is caused, at least in part, by abnormal formation of the internal plexiform zone in the mutant cortex.

Animals↗
PubMed2002

Involvement of the signal transduction pathway mediated by epidermal growth factor receptor in the differentiation of chicken glandular stomach.

During the development of the chicken proventriculus (glandular stomach), the initially undifferentiated epithelium differentiates into two distinct cell populations: the glandular epithelium, cells of which secrete embryonic chicken pepsinogen (ECPg), and luminal epithelial cells, which express the chicken spasmolytic polypeptide gene (cSP). Based on knowledge of the adult mouse stomach, the ligands of epidermal growth factor (EGF) receptor (EGFR) were expected to affect differentiation of the proventricular epithelium. When EGF was added to the medium in which proventriculi were cultured in vitro, gland formation was suppressed in a dose-dependent manner and the amount of ECPg mRNA decreased, whereas morphological differentiation of luminal epithelium was stimulated. Simultaneous treatment of the proventriculus with EGF and tyrphostin 47 resulted in the attenuation of the effect of EGF, suggesting that EGF, or other ligands of EGFR, may actually be involved in the normal course of development of the proventricular epithelium.

Animals↗