Biomedical subjects

Tomiyoshi Setsu

Publications and source records attributed to Tomiyoshi Setsu.

4 recordsLinked to original sources

PubMed2006

The superficial layers of the superior colliculus are cytoarchitectually and myeloarchitectually disorganized in the reelin-deficient mouse, reeler.

The causative gene for the reeler mouse is reelin which encodes Reelin protein, an extracellular molecule. In the present study, we have examined the cytoarchitecture, myeloarchitecture, and afferent/efferent systems of the superior colliculus (SC) of the reeler mouse. In the reeler, the laminar structures of the superficial three layers of the SC were disorganized and intermingled into a single layer, i.e., the superficial fused layer (SuF), as previously reported in the reelin-deficient SRK rat (Sakakibara et al., Develop. Brain Res. 141:1-13). Next, we have investigated the course and terminals of visual corticotectal and retinotectal projections with an injection of biocytin into the visual cortex or an injection of cholera toxin subunit B into the retina, respectively. In the reeler, anterogradely labeled visual corticotectal and retinotectal fibers took an aberrant course within the SuF, resulting in abnormal myeloarchitecture of the superficial SC of the reeler. Retrograde labeling of tectospinal tract neurons could not show any differences between the normal and reeler mice, suggesting that the deep layers of the reeler SC are cytoarchitectually normal. In situ hybridization and immunohistochemical studies have shown that reelin mRNA and Reelin protein were both recognized in the normal SC. These results suggest that Reelin protein plays some roles in histogenesis of the superficial layers of the SC.

Animals↗

PubMed2005

Expression of reelin in the dorsal cochlear nucleus of the mouse.

The cytoarchitecture of dorsal cochlear nucleus (DCN), characterized by a distinct laminar structure similar to the cerebellar cortex of the normal mouse, is known to be disrupted in the Reelin-deficient mouse, reeler. Here, we have reexamined both the cytoarchitecture and myeloarchitecture of this nucleus and described expression pattern of Reelin protein during perinatal periods. Reelin-immunopositive granule cells were firstly recognized in the external granular layer of the DCN at embryological day 16 (E16). Next, we examined the cytoarchitecture of the DCN of the normal and reeler mice with Ca2+/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha) immunostaining. CaMKIIalpha-immunoreactive cartwheel cells were laminarly distributed in the layer II of the normal DCN, but scattered throughout the reeler DCN. Injection of retrograde tracer, Fluoro-Gold (FG) into the inferior colliculus of the reeler mouse resulted in that retrogradely labeled neurons in the DCN were radially scattered instead of being confined to a single layer as seen in the normal mouse. To examine whether CaMKIIalpha-immunopositive cartwheel cells are neurons projecting to the inferior colliculus or not, double labeling with CaMKIIalpha immunohistochemistry and retrograde labeling with an injection of FG into the inferior colliculus were made, which revealed that CaMKIIalpha-immunoreactive cartwheel cells do not send axons to the inferior colliculus. The present findings imply that Reelin may have some roles in the formation of laminar structures of the DCN.

Animals↗

PubMed2005

Congenital semilunar valvulogenesis defect in mice deficient in phospholipase C epsilon.

Phospholipase Cepsilon is a novel class of phosphoinositide-specific phospholipase C, identified as a downstream effector of Ras and Rap small GTPases. We report here the first genetic analysis of its physiological function with mice whose phospholipase Cepsilon is catalytically inactivated by gene targeting. The hearts of mice homozygous for the targeted allele develop congenital malformations of both the aortic and pulmonary valves, which cause a moderate to severe degree of regurgitation with mild stenosis and result in ventricular dilation. The malformation involves marked thickening of the valve leaflets, which seems to be caused by a defect in valve remodeling at the late stages of semilunar valvulogenesis. This phenotype has a remarkable resemblance to that of mice carrying an attenuated epidermal growth factor receptor or deficient in heparin-binding epidermal growth factor-like growth factor. Smad1/5/8, which is implicated in proliferation of the valve cells downstream of bone morphogenetic protein, shows aberrant activation at the margin of the developing semilunar valve tissues in embryos deficient in phospholipase Cepsilon. These results suggest a crucial role of phospholipase Cepsilon downstream of the epidermal growth factor receptor in controlling semilunar valvulogenesis through inhibition of bone morphogenetic protein signaling.

Alleles↗

PubMed2004

[Modified grant method protocol for dissecting and identifying the brachial plexus].

Dissection of the brachial plexus is an important part in the anatomical course, but it is difficult for medical students to identify individual nerves of the brachial plexus due to its complexity and numerous variations. We have recently adopted the Grant method (1991) to guide students in the successful identification of this plexus. However, according to the Grant method the part of the upper limb including the brachial plexus is dissected before the neck part, which makes it impossible to identify the roots, trunks, and cords of the brachial plexus, and to identify the nerve branches extending from the brachial plexus. Here, we propose of anatomical dissection protocol of the brachial plexus a modified Grant method for medical students and instructors. The points of the modified protocols are: (1) to dissect the brachial plexus after the dissection of the neck part, (2) to identify the nerve trunks at the scalenus gap after dissecting the lateral, medial and posterior cords. The modified Grant method can be adapted to any other dissecting protocol of the brachial plexus, and will allow students to cope with many variations of the brachial plexus when they occur.

Anatomy↗