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F Ikuta

Publications and source records attributed to F Ikuta.

At least 19 recordsLinked to original sources
PubMed1992

Immunocytochemical localization of synaptic vesicle-specific protein in Lewy body-containing neurons in Parkinson's disease.

We carried out an immunocytochemical examination of the brainstem and sympathetic ganglia of 5 autopsied patients with Parkinson's disease, using monoclonal antibodies against microtubule-associated protein 2 (MAP2) and synaptic vesicle-specific 38 kDa protein (SVP38). Lewy bodies (LBs) in the nerve cell somata were often immunoreactive for MAP2. Immunoreactivity of SVP38 in the somata of nerve cells was rarely demonstrated in the peripheral portion of the LBs. On the other hand, SVP38-immunoreactive (IR) LB-containing nerve cell processes were frequently found in the brainstem and sympathetic ganglia, considerably outnumbering MAP2-IR LB-containing nerve cell processes. These findings suggested that SVP38 is stored in LB-containing nerve cell processes and indicate that the majority of these processes are axons.

Aged↗
PubMed1992

Ultrastructural localization of inositol 1,4,5-trisphosphate 3-kinase in rat cerebellar cortex.

Subcellular localization of inositol 1,4,5-trisphosphate 3-kinase in the rat cerebellar cortex was studied immunohistochemically using a monoclonal antibody. Electron microscopy revealed intense immunoreactivity in the dendritic spines of Purkinje cells forming synapses with the parallel fibers, climbing fibers and recurrent collaterals of Purkinje cell axons. The labelling was associated with the hypolemmal cisternae, surrounding matrix and plasmalemma including the postsynaptic densities. Weaker immunoreactivity was present in the dendritic spines of basket cells and in certain segments of Purkinje cell recurrent collaterals. The postsynaptic regions of the dendritic trunks of Purkinje and basket cells were negative. These results indicate that inositol 1,4,5-trisphosphate 3-kinase is distributed amongst the spines of various synaptic relations with different electrophysiological properties, and that axon terminals of certain cell types are another functional site for the enzyme.

Animals↗
PubMed1992

Remote astrocytic response of prefrontal cortex is caused by the lesions in the nucleus basalis of Meynert, but not in the ventral tegmental area.

The nucleus basalis of Meynert (nbM) was lesioned by injection of ibotenic acid, in 200 g male Wistar rats. The rats were killed 1, 3, 7 or 21 days after surgery, the brains were removed and the prefrontal cortices were subjected to immunohistochemical and Western blot analysis for the expression of glial fibrillary acidic protein (GFAP). In some rats, vehicle was injected into the nbM and in others 6-hydroxydopamine (6-OHDA) was injected into the ventral tegmental area (VTA). Quantitative Western blot analysis revealed significantly greater immunoreactivity for GFAP in the prefrontal cortex of nbM-lesioned rats. Immunohistochemical examination revealed fibrous and hypertrophic GFAP-positive astrocytes even one day after surgery, and this reaction was stronger at 3 days after surgery. After this peak, GFAP-immunoreactivity of the astrocytes decreased from 7 days to 21 days. In contrast, GFAP-positive astrocytes were not observed in the brains of vehicle-injected or VTA-lesioned rats, even 21 days after surgery. The present results indicate that cortical astrocytes respond to cholinergic deafferentation. In addition, our findings provide new insights into the abnormalities of cortical glial cells after cholinergic deafferentation in Alzheimer's disease.

Acetylcholine↗
PubMed1992

Does methylmercury intoxication induce arteriosclerosis in humans? A pathological investigation of 22 autopsy cases in Niigata, Japan.

In order to clarify whether or not arterio- and/or arteriolosclerosis is induced or exacerbated in patients with methylmercury (Me-Hg) intoxication, the pathological features of arteries and arterioles in specific areas in 22 patients and 36 control subjects were examined qualitatively and quantitatively. Vessels investigated were: (1) small arteries and arterioles in the subarachnoid space and cortex of the postcentral gyrus, transverse temporal gyrus, first visual area and cerebellar vermis, as well as the myocardium and renal cortex; (2) the lateral striate artery; (3) the internal carotid, anterior, middle and posterior cerebral, basilar and vertebral arteries, as well as the coronary and renal arteries; and (4) the aorta. The arteriosclerotic changes observed in the patients with Me-Hg intoxication were indistinguishable both qualitatively and quantitatively from those of controls. The results indicate that Me-Hg intoxication does not induce or exacerbate sclerotic changes in arteries and arterioles. Thus, the peculiar neurological symptoms and neuropathological features of Me-Hg intoxication are thought to be induced not by ischemia but by selective primary degeneration of the neurons in specific regions.

Adult↗
PubMed1992

Clarke's column in sporadic amyotrophic lateral sclerosis.

Histological, ultrastructural and morphometrical observations on Clarke's column were carried out in 18 patients with sporadic amyotrophic lateral sclerosis (ALS) and 15 age-matched control subjects. Of the 18 ALS patients 6 had been on a respirator before death. Bunina bodies were found in the neuronal cytoplasm in 7 of the 12 non-respirator-supported ALS patients and in 3 of the 6 respirator-supported patients. The number of spheroids was significantly higher in the non-respirator-supported patients (P < 0.01) than in the control subjects; however, the number in the respirator-supported patients was about equal to that in the controls. The number of neurons in Clarke's column in the non-respirator-supported ALS patients was not reduced, but in the respirator-supported patients they tended to disappear with time after respiratory support. These findings suggest that Clarke's column neurons are also involved primarily in the disease process in sporadic ALS. However, they may begin to disappear only after the patients require respiratory support.

Adult↗
PubMed1992

Primary leptomeningeal glioma: ultrastructural and laminin immunohistochemical studies.

We studied a case of primary leptomeningeal glioma (PLG) on the left parietal lobe of a 74-year-old woman and compared the tissue with heterotopic glial tissue from another case. The PLG tumor consisted of spindle-shaped cells with marked nuclear atypism, which tended to be arranged in a fascicular pattern, and the majority of its cells were positive for glial fibrillary acidic protein. Ultrastructural examination demonstrated that most of the tumor cells contained intermediate filaments and often junctional complexes were present on their plasma membranes. Frequently, basal lamina-like structures surrounding the tumor cell surfaces were observed. Laminin immunohistochemistry clearly demonstrated a fine network of linear positive staining around the cytoplasm and processes of the tumor cells. The ultrastructure of the heterotopic glial tissue consisted of many astrocytes partially surrounded by basal lamina. These findings strongly suggest that PLG is a distinct tumor, which arises from the heterotopic astrocytes within the subarachnoid space.

Aged↗
PubMed1992

Temporal lobe tumor demonstrating ganglioglioma and pleomorphic xanthoastrocytoma components. Case report.

The case is reported of a 16-year-old boy with a left temporal lobe tumor composed of a ganglioglioma and a pleomorphic xanthoastrocytoma. Histologically, the tumor had two different components. One component involved the cortex of the left posterior temporal lobe and showed an aggregation of neuronal cells with an astroglial stroma. Ultrastructurally, numerous dense-cored vesicles, diagnosed as ganglioglioma, were found in the neuronal cells. The other component involved the adjacent cortex and white matter of the left anterior temporal lobe and the surrounding subarachnoid space. This was composed of pleomorphic cells with many multinucleated giant cells and occasional foamy cells. Most of the tumor cells were positive for glial fibrillary acidic protein. These features correspond well to earlier descriptions of pleomorphic xanthoastrocytoma. At 24 months following total tumor extirpation, the patient is alive and has had no evidence of tumor recurrence.

Adolescent↗
PubMed1992

Syringomyelia. A neuropathological study of 18 autopsy cases.

Eighteen autopsy cases of syringomyelia were studied neuropathologically. In six cases associated with Chiari II malformation, the central canal was patent from the fourth ventricle to the syrinx, and the syrinx was simply a dilated central canal. In four cases associated with Chiari I malformation, the syrinx was irregularly shaped and communicated with the subarachnoid space at the entry zone of the posterior nerve roots. In six cases associated with spinal cord or posterior fossa tumors, the syrinx was located adjacent to the tumor tissues, and occupied the medullary gray matter or the spinal intermediate zone and the ventral part of the posterior horn. With regard to the pathogenesis of syringomyelia, we concluded that in cases associated with Chiari II malformation, vermian protrusion and direct continuity between the fourth ventricle and the syrinx were essential. In cases associated with Chiari I malformation, in addition to tonsillar protrusion, communication between the syrinx and the subarachnoid space was thought to play an important role, and in cases associated with tumors, the circulatory disturbance due to the presence of the tumors caused the syrinx.

Aged↗
PubMed1992

[Development of the fetal brain and lesion repair].

The process of lesion repair in the dramatically developing fetal brain shows a distinctive feature from that in the developed normal brain. The reason for the difference probably can be clarified by the anatomic features of the fetal brain. First, a wide extracellular space, which is necessary for the cell motility when a brain develops, preexists in the fetal brain. Secondly, it is also important that there are no cell-to-cell junctions in a fetal brain and each cell can freely locomote. Therefore, necrotized neuroblasts can be easily removed as they are "in the normal condition" by macrophages. As the astrocytes, which play an extremely important role in the developed adult brain for the repair of lesion, are still before gliogeneses or under differentiation in the fetal brain, there is little or no astrocytosis as compared with the developed brain. Therefore, the lesion repair process results in the production of a malformed brain.

Animals↗
PubMed1992

[Dentatorubropallidoluysian atrophy (DRPLA): comparative pathological study on clinical groups classified into juvenile, early adult and late adult types].

We performed a clinicopathological study on 12 autopsied cases of dentatorubropallidoluysian atrophy. They were divided into 3 groups according to the age at onset: juvenile type (6 cases), early adult type (4 cases) and late adult type (2 cases). In juvenile type showing progressive myoclonus epilepsy (PME) syndrome, degeneration of the globus pallidus was more marked than that of the dentate nucleus. Mild to moderate atrophy was seen in the brain stem and spinal cord. In early adult type showing milder symptom of myoclonus and epilepsy, the globus pallidus and dentate nucleus were equally degenerated to various extents in most cases. Atrophy of the brain stem and spinal cord was mild to moderate in degree. In late adult type without PME syndrome, degeneration of the dentate nucleus was more marked than that of the globus pallidus. The brain stem and spinal cord were severely atrophic. On the other hand, the cases showing severe dentate lesion had a tendency to show severe atrophy of the brain stem and spinal cord. We consider that development of myoclonus, epilepsy and choreoathetoid movement in DRPLA patients has close relation to the extent of not only degeneration of the globus pallidus and dentate nucleus, but also atrophy of the brain stem and spinal cord.

Adolescent↗
PubMed1992

[Hereditary dentatorubropallidoluysian atrophy--clinical variants in a family and degeneration of cerebral white matter in a proband].

We describe a family with hereditary dentatorubropallidoluysian atrophy (DRPLA). 4 patients through 3 successive generations showed a wide clinical variety. The female proband with onset in the elderly developed choreiform involuntary movement, dementia, hyperreflexia and, at the progressive stage, mild ataxia. However she had never displayed epilepsy and myoclonus. The 2 sons showed dementia, choreoathetoid movement and ataxia. The grandson developed typical signs and symptoms of progressive myoclonus epilepsy. The brain CT in the proband showed severe cerebellar and brain stem atrophy, moderate cerebral cortical atrophy and diffuse low density lesions in the deep cerebral white matter. Her neuropathological examination revealed the atrophy and gliosis of cerebral and cerebellar white matter concomitant with both dentatorubral and pallidoluysian system degeneration. The present study indicates that hereditary DRPLA can include multiple clinical variants even in the same family and the degeneration of cerebral and cerebellar white matter besides dentatorubral and pallidoluysian system.

Adolescent↗
PubMed1991

Large neurons in the neostriatum in Alzheimer's disease and progressive supranuclear palsy: a topographic, histologic and ultrastructural investigation.

Large neurons in the neostriatum of patients with Alzheimer's disease (AD) and progressive supranuclear palsy (PSP) were investigated topographically, histologically and ultrastructurally. The number of large neurons whose nuclear area is greater than 101 microns2 was uniformly decreased in the neostriatum in PSP, but the decrease of these neurons in AD appeared to be more marked in the nucleus accumbens. Most of the remaining large neurons in both diseases contained neurofibrillary tangles (NFTs). In addition, some of the small neurons in PSP were positive for tau-immunostaining. Curly fibers were frequently observed in AD, but were absent in PSP. Ultrastructurally, NFTs in AD were composed mainly of paired helical filaments, whereas those in PSP contained straight tubules.

Aged↗
PubMed1991

Galactosialidosis: neuropathological findings in a case of the late-infantile type.

The neuropathological findings in a 13-year-old Japanese male showing decrease of sialidase and beta-galactosidase activities are reported. The patient was the product of normal pregnancy to consanguineous parents. He started to sit at 8 months, stand at 20 months and walk at age of 2; mental retardation, visual disturbance, cerebellar ataxia, myoclonus and epilepsy developed by the age of 10, and he died at 13. Neuropathological investigation revealed neuronal loss and storage. Severe loss of neurons was observed in the thalamus, globus pallidus, lateral geniculate body, gracile nucleus, Purkinje and retinal ganglion cells. Marked ballooning was seen in the Betz cells and neurons in the basal forebrain, the motor neurons in the cranial nerve nuclei and spinal cord, and in the trigeminal and spinal ganglia. The storage material varied in staining from region to region and from neuron to neuron. Electron microscopic investigation revealed a variety of intracytoplasmic and intranuclear inclusions: membranous cytoplasmic bodies, parallel, wavy-lamellar or tortuous tubular structures, lipofuscin-like irregular-shaped pleomorphic bodies, and cytoplasmic vacuoles with fine granules and lamellar materials. The severity of the neuronal loss did not seem to correlate with the amount of the storage materials, but with the presence of tortuous tubular inclusion.

Brain↗
PubMed1991

Construction of spinal cord cDNA library and application for subtractive cloning of spinal cord-specific cDNAs.

Neurodegenerative diseases are characterized by neuronal degeneration of specific neurons, e.g., degeneration of motoneurons in amyotrophic lateral sclerosis. As an approach to understand molecular mechanisms of neuronal degeneration of human spinal cord motoneurons in various motor neuron diseases, we have constructed a human spinal cord cDNA library and developed a strategy for isolating spinal cord-specific genes by subtractive cloning. We constructed human spinal cord and brain cDNA libraries from postmortem human spinal cord and brain. To isolate human spinal cord-specific cDNAs, a spinal cord-enriched [32P]cDNA probe was generated by the phenol emulsion reassociation technique. Forty-eight cDNA clones out of 10,000 colonies gave strong signals with the subtracted probe, and individual spinal cord cDNA clones were isolated. Northern blotting analysis confirmed that two spinal cord cDNA clones are, in fact, more abundant in spinal cord compared to brain.

Blotting, Northern↗
PubMed1991

Are bunina bodies of endoplasmic reticulum origin? An ultrastructural study of subthalamic eosinophilic inclusions in a case of atypical motor neuron disease.

We carried out an electron microscopic study of eosinophilic intracytoplasmic inclusions in the subthalamic neurons in a case of atypical motor neuron disease. These inclusions were identical in light microscopic morphology and staining characteristics to Bunina bodies. Ultrastructurally, most of the intracytoplasmic inclusions observed were divisible into two different types (I and II). Type I inclusions had features essentially identical to those of Bunina bodies demonstrated previously in the anterior horn cells in cases of motor neuron disease; they consisted of electron-dense, granular material without a particular limiting membrane and often contained a number of translucent areas with entrapped cell organelle-like structures. Type II inclusions were very similar to structures known as multilaminated bodies; at their margin, they sometimes showed continuity with the cisternae of endoplasmic reticulum. The remainder of the inclusions were considered to be transitional forms between these two types, and some of them showed the respective features of both types I and II. These findings suggest that Bunina bodies are of endoplasmic reticulum origin.

Adult↗
PubMed1991

An autopsy case of atypical motor neuron disease with Bunina bodies in the lower motor and subthalamic neurons.

We report a 37-year-old male without any family history of neurological disease who suffered progressive muscular atrophy and sensory impairment of 4 years' duration. Autopsy revealed neuronal loss in the anterior horns of the spinal cord and in the hypoglossal and facial nuclei of the brain stem. The corticospinal tracts of the spinal cord showed only mild degeneration. In addition, there were obvious degenerative lesions manifested by loss of neurons, myelin and axons in the spinal posterior columns, Clarke's column, spinocerebellar tracts and dorsal root ganglia as well as in the subthalamic nucleus, globus pallidus, substantia nigra and cerebellar dentate nucleus. Furthermore, we frequently encountered Bunina bodies not only in the lower motor neurons but also in the subthalamic neurons. We consider this case to be an atypical example of motor neuron disease with features of multisystem degeneration. The fact that Bunina bodies were observed in both lower motor and subthalamic neurons in this case suggests a common etiology of neuronal degeneration in these two different systems.

Adult↗