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Biomedical subjects

F Ikuta

Publications and source records attributed to F Ikuta.

At least 163 records · Page 9Linked to original sources
PubMed1984

Three-dimensional architecture of cerebral microvessels with a scanning electron microscope: a cerebrovascular casting method for fetal and adult rats.

Vascular casting for scanning electron microscopic studies on microvascular architecture is in common use for various visceral organs in the field of anatomy. However, only a few studies have been performed on the brain using the previously reported casting method, and no detailed descriptions deal with suitable methodology for producing brain vascular casts. Our casting method, introduced here, for the CNS from the fetal to the adult stage involves the following modifications: (1) Perfusion fixation of the brain is carried out before injecting the plastic resin for casting into the cerebral blood vessels; (2) digestion of nervous tissue is accomplished with a sodium hydroxide and sodium hypochlorite solution; and (3) vascular casts are dried by a freeze-drying method, while the nondigested brain slices opposite the casts can be investigated with light microscopy and transmission electron microscopy. This modified casting method enables one to represent the microvascular system of the rat brain three-dimensionally from embryonal day 17 onward. It is hoped that this method will prove to be a useful tool in morphological vascular research on the nervous system.

Animals↗
PubMed1984

[Topography of the serotonin neurons in the brain stem of human fetus: an immunohistochemical study].

The distribution of serotonin neurons in the central nervous system (CNS) has been intensively examined in mammals, such as rats, cats and monkeys. However, the details of serotonin neuron system have been remained uncertain in human CNS, although two fluorescence histochemical studies were reported in human fetus. In this study, we performed immunohistochemical examination on the distribution of serotonin neurons in the brain stem of human fetuses. The brain stems from five human fetuses (CRL: 120-275 mm, GA: 15-27 wks) were fixed with 4% paraformaldehyde, dehydrated with graded ethanol, and embedded in paraffin. Serial sections, 6 micron in thickness, were cut from seven different levels of the brain stem of each fetus. The initial several sections were used for usual histological observations. The following serial ones were stained by peroxidase-antiperoxidase (PAP) technique using anti-serotonin sera. The anti-serotonin sera used were raised in rabbits by the methods of Ranadive and Sehon (1967), Grota and Brown (1974), and Steinbusch et al (1978). Before the use, the specificity of the antisera was confirmed by the immunohistochemical examination of the CNS of rat embryos and adults. Positively stained serotonin neurons were clearly demonstrated in the brain stems of all cases examined (Figs. 1A-1H). They were small to medium in size, 10 X 20 micron to 20 X 40 micron, and varied in shape, showing round to oval cell somata with unipolar, bipolar and multipolar processes. The distribution of serotonin neurons in the brain stems was almost the same among five human fetuses (Figs. 2A-2K). A large number of serotonin neurons were located in the midline raphe nuclei. In addition, numerous serotonin neurons were observed widely in the other tegmental area. The nuclei containing serotonin neurons were listed in Table 2 according to the terminology by Olszewski and Baxter (1982). The distribution of the serotonin neurons in the raphe nuclei of human fetuses was fundamentally similar to those of many mammals reported previously. However, the lateral extension of serotonin neurons to the other tegmental area beyond the midline raphe nuclei in human fetuses was much greater than in any other mammals. This distribution pattern of serotonin neurons was considered to be peculiar to human fetus. Since the histological architecture of the brain stems of five fetuses examined was very similar to that of human adults, the distribution of serotonin neurons demonstrated here may also represent that of human adults.

Brain Mapping↗
PubMed1984

Alterations in brain gangliosides and other lipids of patients with Creutzfeldt-Jakob disease and subacute sclerosing panencephalitis (SSPE).

Lipid composition was examined with cerebral cortices of three cases of Creutzfeldt-Jakob (C-J) disease and one case of subacute sclerosing panencephalitis (SSPE). Phosphatidylethanolamine decreased in both C-J and SSPE brains. Sphingomyelin increased in CJ. The levels of cholesterol esters which occurred in a trace amount in normal control were elevated in C-J and more severely in SSPE. The total amounts of gangliosides were reduced in C-J and SSPE. Gangliosides GD1b, GT1b and GQ1b in the biosynthetic pathway B [23] specifically decreased in C-J, while GM1 and GD3 increased. An increased content of GD3 may be related to the proliferation of reactive astrocytes. A decrease of 22:6 (n-3) accompanied with an increase of oleic acid in the fatty acid composition of the acidic phospholipid fraction was observed. This might be a cause for alterations in membrane function.

Adult↗
PubMed1984

[Initial cellular damage in the developing rat brain caused by cytotoxicity of ethylnitrosourea].

Initial cellular degeneration in developing rat fetal brains were induced during the early cytogenetic period of neuroblasts by cytotoxic action of ethylnitrosourea (ENU). This was transplacentally administered. After a single intravenous administration of 60 mg/kg body weight ENU to 16th day-pregnant rats, each fetus was removed surgically from the uteri every hour for 24 hours and every day for 9 days. These were fixed by the transcardial perfusion method to observe them with light and electron microscopes. From 4 hours after the ENU-treatment, the degenerative alteration of cells, characterized ultrastructurally by cytoplasmic condensation and nuclear pyknosis, developed selectively in the matrix cell layer of the fetal cerebrum where active cell division was carried out to produce neuroblasts. Cellular degeneration was first noticed at the zone of DNA synthesis and then all the matrix cell layer including the mitotic phase. Furthermore, the cell processes of matrix cells, or so-called radical fibers, were also recognized to be in the same degenerative processes. These affected cells increased in number and became arranged in columns along the radial fibers through the process of time, and successively migrated to the migrating zone through the outer part of the matrix cell layer. At 10 hours after treatment, many cells were observed in the migrating zone and a few cells were noticed in the matrix cell layer. The degenerated neuroblasts reached the cortical plate about 3 hours after the development of initial degeneration. In contrast, the neuroblasts in the cerebral cortical plate which had already been formed at the time of ENU administration were not affected by the ENU and persisted for the following developments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Revised pathophysiology on BBB damage: the edema as an ingeniously provided condition for cell motility and lesion repair.

Probably, the most important evidence concerning the breakdown of the BBB is a large inflow of hematogenous fluid into the extravascular spaces. Thus all parenchymal cell elements represent freely floating cells in this fluid medium called the edema fluid. These essential morphological alterations, such as extremely expanded extracellular space and freely floating cells within the fluid, were also observed in the developing normal fetal brain. Many neuroblasts were vigorously migrating in the fetal brain, as were the macrophages and reactive astrocytes in the edema fluid. Obviously, hematogenous cells and reactive astrocytes in the edematous lesion take part in its repair. Many astrocytes, GFAP positive, in the 3 or 4 day-old lesions, revealed mitosis. And in vitro, when we immersed these astrocytes in the protein and glucose rich medium, they demonstrated a remarkably changed morphology and were moved into the M and G1 phases, thus gaining the ability of cell motility. This was also true in the edema fluid. Brain edema is definitely a serious "pathological" condition. But it is also conceivable from a different biological aspect that as a result of BBB "opening", free extracellular space essential for cell motility and a source of their energy is ingeniously provided for these cells, and thus the lesion can be effectively repaired. The biological significance of the edema fluid was emphasized and stereotaxic morphology and cinematography, supporting the above evidence, have also been presented.

Animals↗
PubMed1983

Tactile-like corpuscles in neurofibromas: immunohistochemical demonstration of S-100 protein.

Tactile-like corpuscles in neurofibroma tissues were examined by the indirect immunoperoxidase method using rabbit anti-S-100 sera. In all five cases examined, positive staining was observed in their constituent cells, both in the flattened cytoplasm and nuclei. On examination of the normal peripheral nervous system, positive staining was exclusively confined to Schwann cells in the nerve bundles and Schwann-related cells such as lamellar cells in the Meissner corpuscle, whereas staining was negative in perineurial cells. Electron-microscopic examination showed ultrastructural similarity between constituent cells of the tactile-like corpuscles in neurofibroma and lamellar cells in the Meissner corpuscle. These findings may indicate Schwannian nature of the tactile-like corpuscles.

Adolescent↗
PubMed1983

Morphological study on the hereditary neurogenic amyotrophic dogs: accumulation of lipid compound-like structures in the lower motor neuron.

A morphological study was performed on hereditary neurogenic amyotrophic dogs, the clinical features of which especially resembled spinal progressive muscular atrophy (SPMA), a human motor neuron disease. The skeletal muscles showed obvious neurogenic atrophy with endomysial fibrosis. The peripheral nerves revealed axonal degeneration mainly limited to the motor nerve. In the spinal cord, the number of anterior horn cells seemed normal but, interestingly enough, numerous accumulated granules were detected in these anterior horn cells. Histochemically, these granules were interpreted as a lipid compound. Under the electron microscope, the granules were disclosed as multi-lamellar structures, arranged concentrically or in parallel, resembling membranous cytoplasmic bodies (MCBs) or zebra bodies. This finding strongly suggests that hereditary abnormality of lipid metabolism may underlie SPMA in these dogs. However, unlike other metabolic disorders where accumulations of granules are diffusely distributed, in the dogs we examined accumulations were found only in the anterior horn cells of the spinal cord and in the hypoglossal and spinal accessory nuclei. We are unable to explain this occurrence at the present time. Further investigations should be made on dogs because they serve as an important animal model of human motor neuron disease.

Animals↗
PubMed1983

[Immunohistochemistry on tyrosine hydroxylase in the substantia nigra of human autopsied cases].

Despite the numerous data on the distribution of catecholamine (CA) neurons in a wide variety of species, data on that of human are rare because of technical difficulty in applying fluorescent histochemical methods. On the other hand, immunohistochemistry on tyrosine hydroxylase (TH) which was essential for synthesis of CA, was assumed to be applicable to human autopsied brain. We performed indirect immunoperoxidase study on TH using 10% formalin or buffered formalin fixed, paraffin embedded sections of the substantia nigra from 40 autopsied cases, ranging in age 7 to 70 years. TH was purified from the bovine adrenal medulla using the procedure described by Oka et al. with some modification. Purified TH was injected with Freund's complete adjuvant into rabbits. The specificity of the antiserum was demonstrated by the inhibition study of CA relating enzymes, double immunodiffusion and immunoelectrophoresis against tissue homogenate of bovine adrenal medulla. TH immunoreactive (TH-IR) products were restricted to the neuronal soma, axons and dendrities in almost all of the case except for the "dead brain" cases. TH-IR neurons were of large polygonal or multipolar cells, and closely correspond to melanin-pigmented neurons, located in the compact zone and scattered in the reticular zone in the substantia nigra. On the other hand, melanin free neurons in the reticular and compact zone, were of medium or small bipolar cells and were not stained. It was of interest that the non TH-IR melanin-pigmented neurons firstly appeared in the substantia nigra at third decade and increased their number with age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1980

Hirano bodies in the axon of peripheral nerves in a case with progressive external ophthalmoplegia with multisystemic involvements.

Inclusions, ultrastructurally identical with Hirano bodies which were previously believed to be limited to the central nervous system (CNS), were found both within peripheral myelinated nerve axons and within terminal axons of neuromuscular junctions in the ocular muscles of an autopsied woman who had suffered from progressive external ophthalmoplegia with multisystemic involvements. Electron micrographs showed the inclusions to consist of beaded filaments or lattice-like structures with filamentous elements continuing onto neurofilaments in the axon. The corelation of these new pathological findings in peripheral nerve axons and ophthalmoplegia is discussed.

Adult↗
PubMed1980

Neuropathological comparative studies on experimental allergic neuritis (EAN) induced in rabbits by P2 protein-ganglioside complexes.

The light microscopical examinations were performed on the peripheral nerve (PN) lesions in rabbits induced by bovine peripheral nerve (BPN) myelin and by its components. Morphology of the PN lesions induced by P2 protein-ganglioside complex were equivalent to those induced by PN myelin (original EAN); and some of them were more remarkable in severity than the original EAN. The lesions were composed of myelin destruction, numerous macrophages containing myelin debris, completely demyelinated axons and remyelinating fibers. P2-I, acid treated P2-I and P2-II proteins induced PN lesions. Histologically they were moderate to minimal in severity in that order. However, when each protein was injected as the complex with ganglioside, PN lesions obviously became severer, respectively. These findings indicate the possibility that the P2-ganglioside complex may be involved in the chemical principle of EAN, and also the findings strongly support the theory proposed by Nagai et al. that gangliosides may play an essential role in rabbit EAN to give P2 protein a special conformation necessary for antigenic activity.

Animals↗
PubMed1978

Chronic alcoholism: report of an autopsy case and comparison with pseudoulegyric type of hepatocerebral degeneration.

An autopsy case diagnosed as chronic alcoholism was reported. He clinically showed progressive neurological illness. His CNS lesions were composed of disseminated necrotic foci in the cerebral cortices with many Alzheimer type II astrocytes, pachymeningitis hemorrhagica interna, and lesions similar to pellagra and Wernicke encephalopathy. Some clinical and pathological analogous features between chronic alcoholism and pseudoulegyric type of hepatocerebral degeneration were discussed.

Adult↗