Archives of Histology and Cytology
Online ISSN : 1349-1717
Print ISSN : 0914-9465
ISSN-L : 0914-9465
Volume 66, Issue 3
Displaying 1-9 of 9 articles from this issue
Review article
  • Takuro Murakami, Aiji Ohtsuka
    Article type: Review
    Subject area:
    2003 Volume 66 Issue 3 Pages 195-207
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    Cell bodies and their dendrites of motor neurons, motor-related neurons, and certain other subsets of neurons such as GABAergic interneurons in the mature brain and spinal cord possess intensely negatively charged perineuronal or perisynaptic nets of proteoglycans which are linked to the nerve cell surface glycoproteins. These perineuronal nets of proteoglycans are digested by chondroitinase ABC, hyaluronidase, or collagenase, but not by endo-alpha-N-acetylgalactosaminidase, which is reactive to the nerve cell surface glycoproteins. Aggrecan, versican, neurocan, and brevican are members of a family of chondroitin sulfate proteoglycans that bind to hyaluronan. Neurocan-or brevican-deficient mice showed a regionally heterogeneous composition of proteoglycans in perineuronal nets. Aggrecan glycoforms contribute to the molecular heterogeneity of the perineuronal nets. Proteoglycans such as phosphacan are included in matrix-associated proteoglycans. The extracellular matrix glycoprotein tenascin-R is accumulated in the perineuronal nets. The perineuronal proteoglycans are produced by associated satellite astrocytes just before weaning, while the nerve cell surface glycoproteins are produced by the associated nerve cells at earlier stages after birth. The perineuronal proteoglycans may entrap the tissue fluid and form a perineuronal gel layer which protects the synapses as a “perisynaptic barrier”. Degradation of the perineuronal proteoglycans or perisynaptic barrier by treatment with chondroitinase ABC or hyaluronidase reactivates the neuronal plasticity or promotes the functional recovery of a severed nervous system. Another set of perineuronal nets occurs, which are intensely positively charged and contain guanidino compounds. It is considered that these intensely positively charged nets are intermingled with the intensely negatively charged ones of proteoglycans.
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Original articles
  • Yasuhiro Tsukamoto, Tatsuro Yamamoto, Haruo Okado, Ken-ichi Nibu, Tosh ...
    Article type:
    Subject area:
    2003 Volume 66 Issue 3 Pages 209-220
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    The present study tested whether a gene-transfer based upon the retrograde axonal transport of the lacZ adenovirus is effective in the spinal descending tracts of the adult mouse. A small volume of a replication-defective recombinant adenovirus encoding E. coli β-galactosidase was injected into the upper lumbar cord, and, seven days later, the mice were transcardially perfused by a fixative solution. X-gal staining of coronal or sagittal sections of the spinal cord and the brain revealed that many sites of origin for rubrospinal, vestibulospinal, and reticulospinal tracts were retrogradely labeled, whereas few of the corticospinal tract neurons were retrogradely labeled. Ependymal cells surrounding the central canal of the spinal cord, which were located far from the injection site, showed a high expression of β-galactosidase activity. Motoneurons around the injection site were strongly stained by X-gal staining, and their axons in the ventral root were anterogradely labeled. Afferent fibers in the dorsal root were labeled by the transganglionic transport of β-galactosidase. To examine the efficacy of the uptake and retrograde transport of HRP and adenovirus, we injected a mixed solution of 10% HRP and recombinant adenovirus. The number of HRP-labeled corticospinal neurons overwhelmed the number of X-gal stained ones, while the numbers of HRP-labeled rubrospinal and subcoeruleus-spinal neurons were smaller in comparison with the numbers of β-galactosidase-positive counterparts. The present study revealed that the origins for the spinal descending tracts except for corticospinal neurons could be efficiently genetransferred by the retrograde infection of a recombinant adenovirus. Such a difference in efficacy of retrograde infection among the spinal descending tracts is practically important when an adenovirus-mediated gene transfer is designed to treat certain neurological diseases affecting the spinal descending tracts.
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  • Hiroshi Kitahara, Tadashi Hayami, Kunihiko Tokunaga, Naoto Endo, Haruk ...
    2003 Volume 66 Issue 3 Pages 221-228
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    The localization and expression of chondromodulin-I (ChM-I), an angiogenesis inhibitor, in the rat articular cartilage during maturation from 2 to 10 weeks of age were examnied by immunohistochemistry, Western blot analysis and ribonuclease protection assay, and the results were compared with those in the epiphyseal cartilage. ChM-I was found to be diffusely immunostained in the inter-territorial space of the cartilage matrix from the intermediate to the deep layers at the immature stage. As the articular cartilage matured, the immunoreactivity was localized around the hypertrophic chondrocytes in the deep layer and the immunoreactivity became weak after maturation. In contrast, the ChM-I immunoreactivity was intense in the epiphyseal cartilage at all ages examined. ChM-I was detected by Western blotting as a broad band or occasionally as a cluster of multiple bands (∼25 kDa) in both the articular and the epiphyseal cartilage. The intensity of the bands decreased gradually with age in the articular cartilage, but was unchanged in the epiphyseal cartilage at all ages. Ribonuclease protection assay revealed that ChM-I mRNA also decreased gradually with age in the articular cartilage in parallel with the maturation of the articular cartilage, while no decrease in ChM-I mRNA was found in the epiphyseal cartilage. The expression of ChM-I mRNA in the articular cartilage was less than that in the epiphyseal cartilage at all ages. The decrease in amount of ChM-I in the mature articular cartilage suggests That ChM-I plays a more important role in the maintenance of avascularity in the immature articular cartilage than in the mature one. The avascular condition may be preserved by angiogenic inhibitors or mechanisms other than ChM-I in the mature articular cartilage.
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  • Eisuke Sakuma, Damon C. Herbert, Tsuyoshi Soji
    2003 Volume 66 Issue 3 Pages 229-238
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    We investigated the relationship between gap junction formation and the sex steroids testosterone, progesterone and 17β-estradiol in the anterior pituitary glands of castrated male rats and ovariectomized female rats. Male and female 30-day-old Wistar-Imamichi strain rats were castrated or ovariectomized, and 30 days later they were subcutaneously injected with the above sex steroids. They were divided into six groups according to the injected materials: sesame oil (control), testosterone, progesterone, 17β-estradiol, testosterone with 17β-eestradiol, and progesterone 17β-estradiol, with 17β-estradiol. Five rats from each group were sacrificed 1, 2, 3, 4 and 5 days after the injections, and the anterior pituitary glands were prepared for observation by transmission electron microscopy. We quantified the number of follicles and gap junctions and calculated the rate of occurrence of gap junctions as the ratio of the number of gap junctions existing between folliculo-stellate cells per intersected follicle profile in electron photomicrographs. The administration of testosterone to castrated male rats increased the rate of gap junctions between folliculo-stellate cells; however, progesterone and 17β-estradiol did not affect the formation of gap junctions. The administration of progesterone to ovariectomized female rats increased the rate of gap junctions between folliculo-stellate cells; this progesterone effect was prevented by the simultaneous administration of 17β-estradiol, which by itself did not affect the rate of gap junctions between folliculo-stellate cells. These observations indicate that the formation of gap junctions within the anterior pituitary gland is regulated differently by sex steroids in castrated male and ovariectomized female rats.
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  • Yuko Ohtani, Bai-jun Wang, Raksawan Poonkhum, Osamu Ohtani
    2003 Volume 66 Issue 3 Pages 239-252
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    It has long been a mystery how fluid and migrating cells in the hepatic sinusoids reach lymphatic vessels in the portal tract. Here we describe previously-unknown channels that connect the space of Disse with the portal tract in the rat liver. Transmission electron microscopy was performed on livers injected with either horseradish peroxidase (HRP) or lipopolysaccharide, and scanning electron microscopy was carried out on livers macerated with KOH. Transmission electron microscopy revealed the presence of channels with collagen fibers traversing the limiting plate. A tracer study showed that HRP was in the channels as well as along inlet venules. Dendritic cells in the hepatic sinusoids or between hepatocytes of the limiting plate were also observed extending their pseudopodia through the channels in the limiting plate to the interstitial space of the portal tract. Scanning electron microscopy further showed that many channels (1-3μm in diameter) penetrated through the limiting plate independently of blood vessels and connected the space of Disse with the interstitial space of the portal tract. In addition, the portal tract possessed prelymphatic vessels that were lined with fibroblast-like cells and frequently contained dendritic cells. The initial segment of the portal lymphatic vessels opened to the interstitial tissue space. These results indicate that fluid and dendritic cells in the hepatic sinusoids probably pass through both the space of Disse and the channels traversing the limiting plate, enter the interstitial space of the portal tracts, and finally move from the prelymphatic vessels to the portal lymphatic vessels.
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  • Noriatsu Shigemura, Hirohito Miura, Yuko Kusakabe, Akihiro Hino, Yuzo ...
    2003 Volume 66 Issue 3 Pages 253-260
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    Leptin is a hormone that regulates food intake, energy expenditure and body weight. Our previous studies have demonstrated that the taste organ is a new peripheral target for leptin in mice. Leptin selectively inhibits the responses of taste nerves and receptor cells to sweet substances without affecting responses to sour, salty, and bitter substances. Still, there is no convincing evidence for the existence of leptin receptors (Ob-Rs) in taste receptor cells, especially the functional isoform Ob-Rb. We investigated the expression of 5 different Ob-R isoforms (a-e) and 6 STAT (signal transducers and activators of transcription) members in mouse taste cells. STATs are considered to be involved in the leptin signaling via Ob-Rb. Semiquantitative RT-PCR analysis showed that Ob-Rb was expressed in the taste buds of the fungiform and circumvallate papillae, but not so clearly in the surrounding epithelial tissue. The expression pattern among the three different tissues was similar to that of the taste cell specific G-protein, α-gustducin. The other Ob-R isoforms were widely detected in either the taste papillae or the epithelial tissue. Among 6 STAT members, STAT3 showed the highest relative abundance of mRNA in the taste buds. Consistently, in situ hybridization analysis showed that while Ob-Rb and STAT3 signals were detected in some taste bud cells, the signals were not clearly observed in the epithelial tissue cells. In conclusion, the present study provides evidence of the existence of the leptin receptor, Ob-Rb, and STAT3 in the mouse taste bud cells. This finding further confirms the involvement of leptin in the control of taste sensitivities to sweet substances in mice.
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  • Osamu Ohtani, Yuko Ohtani, Colin J. Carati, Bren J. Gannon
    2003 Volume 66 Issue 3 Pages 261-272
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    The aim of the present study was to examine the organization of lymph fluid and cellular pathways and distribution of the membrane water channel Aquaporin-1 (AQP-1) in rat lymph nodes. Lymph fluid and cellular pathways within lymph nodes were examined by fluorescent protein tracer/confocal microscopy and by scanning electron microscopy (SEM), While the distribution of AQP-1 was studied immunohistochemically. Tracer studies showed the subcapsular sinuses continued directly at the hilum or via the intermediate sinuses to the medullary sinuses, and lymphatic labyrinths originating with blind-ends in the deep cortex drained into medullary sinuses. Afferent lymph tracers were also observed in node cortex interstitium. By SEM, lymphatic labyrinths appeared densely filled with lymphocytes and had few intraluminal sinus reticular cells, while medullary sinuses possessed well-developed networks of sinus reticular cells. The presence of many lymphocytes wedged in the walls of the lymphatic labyrinth suggested that lymphocytes migrate between the node parenchyma and lymphatic labyrinths. AQP-1 was distributed on the membrane of lymphatic endothelium and reticular cells as well as on both luminal and abluminal cell membranes of high endothelial venules (HEVs). Our SEM findings support the concept that lymphocytes migrate from the node parenchyma into lymphatic labyrinths in the deep cortex. The nodal distribution of AQP-1 plus the presence of a polarized distribution of ion pumps and/or ion channels in the HEV endothelium hypothesized in our discussion could explain the mechanism of the reported lymph-to-plasma fluid flux in lymph nodes and also facilitate the entry of afferent lymph antigens into the node cortex interstitium.
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  • Seiichi Kawamata, Junya Ozawa, Masakazu Hashimoto, Tomoyuki Kurose, Ha ...
    2003 Volume 66 Issue 3 Pages 273-279
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    Mammalian skin can extensively slide over most parts of the body. To study the mechanism of this mobility of the skin, the structure of the subcutaneous connective tissue was examined by light microscopy. The subcutaneous connective tissue was observed to be composed of multiple layers of thin collagen sheets containing elastic fibers. These piled-up collagen sheets were loosely interconnected with each other, while the outer and inner sheets were respectively anchored to the dermis and epimysium by elastic fibers. Collagen fibers in each sheet were variable in diameter and oriented in different directions to form a thin, loose meshwork under conditions without mechanical stretching. When a weak shear force was loaded between the skin and the underlying abdominal muscles, each collagen sheet slid considerably, resulting in a stretching of the elastic fibers which anchor these sheets. When a further shear force was loaded, collagen fibers in each sheet seemed to align in a more parallel manner to the direction of the tension. With the reduction or removal of the force, the arrangement of collagen fibers in each sheet was reversed and the collagen sheets returned to their original shapes and positions, probably with the stabilizing effect of elastic fibers. Blood vessels and nerves in the subcutaneous connective tissue ran in tortuous routes in planes parallel to the unloaded skin, which seemed very adaptable for the movement of collagen sheets. These findings indicate that the subcutaneous connective tissue is extensively mobile due to the presence of multilayered collagen sheets which are maintained by elastic fibers.
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  • Kaoruko Nagai, Tsuyoshi Noguchi, Tsuyoshi Hashimoto, Yuzo Uchida, Tats ...
    Article type:
    Subject area:
    2003 Volume 66 Issue 3 Pages 281-288
    Published: 2003
    Released on J-STAGE: June 25, 2004
    JOURNAL FREE ACCESS
    The structural organization of the lamina muscularis mucosae of the human esophagus was studied by light microscopy and scanning electron microscopy (SEM). The organization of the lamina muscularis mucosae varied considerably among the cervical, the thoracic, and the abdominal part of the esophagus. In the cervical part, the lamina muscularis mucosae was not well developed and only islets of the smooth muscle bundles were scattered within the connective tissue. In the thoracic part,the lamina muscularis mucosae consisted of several layers of smooth muscle bundles, individual muscle cells of which ran in a longitudinal direction. In the abdominal esophagus near the cardia, the muscular bundles in the lamina muscularis mucosae ran in various directions forming a reticular configuration. The differences in density and arrangement of the lamina muscularis mucosae are discussed in relation to the swallowing of food and submucosal invasion of esophageal cancer.
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