PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Neurofibrils”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

Argentophil neuronal perikarya and neurofibrils induced by postmortem trauma and hypertonic perfusates.

Argentophil neuronal perikarya and perikaryal neurofibrils similar to those illustrated in Ramón y Cajal's classical studies have in the present investigation been found to be manifestations of the chromophil neuron. Conclusive evidence of such association was obtained by silver impregnation with the Bodian technique of sections previously stained with cresyl violet. Regardless of the fixative used, silver-impregnated neurofibrils were evident when (1) normal tissues were fixed by immersion or unsuccessfully fixed by perfusion, (2) normal tissues were exposed and touched after death but before perfusion with the fixative, or (3) flow of perfusates was compromised by the effect of an experimental procedure, as well as when (4) a hypertonic saline solution was used in the first perfusate. These cytologic peculiarities were still discernible after 24 h of postmortem autolysis following a delay in removal of the brain or in immersion of the exposed brain in the fixative. After immersion fixation, argentophilia and chromophilia occurred ubiquitously in the brain of the newborn guinea pig; however, argentophil neurofibrils were noted in the absence of chromophil neurons in the brain stem of the newborn rat, rabbit and cat. After fixation by perfusion, perikaryal neurofibrils were not impregnated in either newborn or old animals or in animals with facial nerve transection. Affinity for Congo red or birefringency, exhibited by neurons with marked neurofilbrillary changes in human senile brain atrophy, were absent in the present material. On the basis of the current light-microscopic observations, it is concluded that argentophilia of neuronal perikarya and perikaryal neurofibrils is another manifestation of the chromophil neuron induced by postmortem trauma and of the ocellate neuron elicited by perfusion with hypertonic saline.

Age Factors↗
PubMed1987

Transformation of degenerating neurofibrils into amyloid substance in Alzheimer's disease: histochemical and immunohistochemical studies.

Degenerating neurofibrils (DNF), which are composed of paired helical filaments (PHF) and amyloid fibrils (AF), are the 2 characteristic pathological fibrillar deposits in Alzheimer cortex. These fibrils were simultaneously studied by 2 techniques: The immunolabelling with a specific antiserum raised against PHF and elective thioflavine S staining of AF. In neuronal perikaryons, neurofibrillary tangles (NFT) consist of 3 populations: firstly, strongly immunolabelled tangles were weakly thioflavine-stained. Secondly, less dense tangles were weakly immunolabelled but strongly thioflavine-stained. Thirdly, ghost tangles which correspond to extracellular NFT were exclusively thioflavine-stained. Thus, it is likely that NFT are degraded to form extracellular AF. Around neuritic plaques and some vessels with amyloid angiopathy, immunolabelled neurites, thioflavine-stained neurites and transition figures were also observed. On the other hand, the central core of plaques and pathological vessel walls were strongly thioflavine-stained but were never immunoreactive. In conclusion, these observations favour catabolism of PHF bundles found in NFT and in degenerating neurites into an amyloid substance. This amyloid substance seems different from other amyloid deposits found in the central core of neuritic plaques and vessel walls.

Aged↗
PubMed1975

Chemical pathology of neurofibrils. Neurofibrillary tangles of Alzheimer's presenile-senile dementia.

A subcellular fraction enriched in twisted tubules was obtained by differential centrifugation of a homogenate of neurons isolated from areas of the brain with many neurofibrillary tangles from patients with Alzheimer's presenile-senile dementia. A unique protein (molecular weight 50,000 daltons) which does not co-migrate with either of the two tubulin monomers of the major neurofilament protein, both purified from human brain, was found in this subcellular fraction on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Similarly processed tissue from areas of the brain poor in neurofibrillary tangles contained low levels of this new protein. The new protein band could not be seen in control patients.

Alzheimer Disease↗
PubMed1987

[Modification of Bielschowsky's method for detecting senile plaques and intracellular neurofibrils].

The distinction of the modification of Bielschowsky's method lies in additional colouring of silver-golden sections with strong solutions of stable cresyl-violet and acetic acid, as well as in recommendations to use precise-profile cortical sections. The given modification helps to obtain preparations with definite orientation and guaranteed identification of different nerve tissue elements. The preparations obtained can be employed for quantitative analysis and for a detailed study of thin specific structures and cytologic properties of pathologically changed nerve and glial cells.

Aging↗
PubMed1977

Preparation of antisera to neurofilament protein from chicken brain and human sciatic nerve.

Antigens isolated by hydroxyapatite chromatography from human sciatic nerve (SN1 protein) and from 8 M urea extracts of chicken brain were selectively localized by immunofluorescence to neurofibrils in rat and chicken CNS. Absorption of the antisera with SN1 protein, chicken antigen or GFA protein abolished the staining. Antisera raised against antigen isolated with the same procedure from buffer extracts of chicken brain stained both neurofibrils and glial fibrils by immunofluorescence. Neurofibrillary staining was selectively abolished by absorption of the antisera with SN1 protein. Antisera prepared against axonal preparations isolated from bovine white matter only stained astroglia and were thus undistinguishable from anti-GFA sera in this respect. The data suggested that the protein subunits of neurofilament and glial filaments, although difficult to separate in brain extracts by standard biochemical procedures and by subcellular fractionation in bovine white matter, still retain immunological specificity. In addition, the immunological cross reactivity between human and chicken antigens suggested that neurofilaments, as other constituents of the cytoskeleton such as microtubules and actin microfilaments, show a high degree of evolutionary stability.

Animals↗
PubMed1988

Alzheimer's disease: a new evidence for common epitopes between microtubule associated protein Tau and paired helical filaments (PHF): demonstration at the electron microscope level by a double immunogold labelling.

Paired helical filaments (PHF) are neuronal landmarks of Alzheimer's disease. These pathological filaments are antigenically related to proteins present in the normal cytoskeleton, particularly to microtubule associated protein Tau. The evidence for these common epitopes was studied on sections of cortex from Alzheimer brains after Araldite embedding. Two rabbit immune sera were used: one was raised against PHF isolated from Alzheimer cortex; the other against Tau proteins extracted from bovine cortex. The comparison of adjacent semi-thin sections alternatively treated with anti-PHF and anti-Tau immune sera reveals that both stained degenerating neurofibrils in pyramidal perikarya and in neurites surrounding senile plaques. On ultra-thin sections, double immunogold labelling of PHF was obtained. These results are in accordance with the hypothesis that Tau proteins are major antigenic components of PHF.

Alzheimer Disease↗
PubMed1975

Neurofilament and glycogen changes during cold acclimation in the trochlear nucleus of lizards (Sceloporus undulatus).

In lizards (Sceloporus undulatus), long term (13 or 19 weeks) acclimation to an environment of 6 degrees C produces a striking increase in the argyrophilic neurofibrillar network in most large perikarya of the trochlear nucleus. In electron micrographs the cells contain numerous bundles of 10-30 regularly-spaced 90 A neurofilaments. In the cells from warm acclimated animals, a plexus of neurofibrils is seen by light microscopy. The electron micrographs show scattered neurofilaments and fewer, thinner bundles than in the cold. Within the cell bodies of the cold animals, glycogen particles are organized in regional accumulations from which other organelles are excluded except for the bundles of neurofilaments which are distributed throughout the cytoplasm. The aggregations of rough endoplasmic reticulum (RER) are also penetrated by the neurofilament bundles. The increased neurofilamentous network in the cold is not accompanied by obvious changes in the amount or distribution of RER or of microtubules which are present in limited numbers in both conditions. The dendrites of trochlear cells and axon terminals within the nucleus also show a cold induced increase in neurofilaments, as well as in the distinctive accumulations of glycogen particles.

Acclimatization↗
PubMed1979

Neurofibrillary pathology: current status and research perspectives.

The neurofibrils seen in the light microscope are shown, by electron microscopy, to be heterogeneous structures, formed of neurotubules and neurofilaments. A variety of pathological conditions (especially, presenile and senile dementia (are characterized by the presence of neurofibrillary tangles, formed either of paired helical filaments or of single filaments. The morphology, distribution and biochemistry of these various fibrillary structures is reviewed. Particular attention is devoted to the assembly of neurotubules, to the mechanism of action of drugs which prevent assembly, and to possible implications for the experimental induction of neurofibrillary pathology. Of central importance in the arguments is the emphasis on the normal neurofibrillary structures being single forms of pleomorphic proteins. The healthy neuron assembles these proteins into the required form as is necessary for the needs of that neuron. Interference with this process in neuronal cell biology may lead to the deposition of neurofibrillary tangles. On the basis of the morphological and biochemical evidence, several approaches to the experimental study of neurofibrillary pathology are proposed.

Aging↗
PubMed1979

Recent advances of high voltage electron microscopy in biology.

Recent advances in the understanding of the structure of biological material made possible by the high voltage electron microscope are reviewed by briefly summarizing some of the more important results obtained in the past few years. The examination of thick sections of selectively stained specimens has continued to be the most widely used approach and has yielded information on the three-dimensional organization of a range of organelles, including the Golgi apparatus, neurofibrils and the transverse tubular system of striated muscle. The alternative method of studying intact cells prepared by critical-point drying is becoming increasingly popular, and has already made a significant contribution in demonstrating the microtrabecular systems within the cytoplasm of cultured cells.

Animals↗
PubMed1975

Prurigo nodularis. Histological and electron microscopical study.

We describe a typical case of prurigo nodularis, of 15 years' duration, in a middle-aged woman. Histological and electron microscopical examination of the skin lesions revealed distinct changes in the nerve tissue. There were groups of thickened nerve fibers that formed nodules with numerous Schwann cells. Some of the nerve bundles extended to the dermoepidermal junction. Electron microscopy showed very obvious lesions in the Schwann cells and axons. In the Schwann cells there was a lucent cytoplasm with few mitochondria, an absence of endoplasmic reticulum and a few irregular, membrane-bound vacuoles. While the mesaxons all appeared normal, the axons varied greatly in diameter; the small ones appeared normal and contained neurofibrils and neurotubules, whereas the large onew were empty. Every Schwann cell encircled a large number of axons. It may be assumed that the axon swelling is a nonspecific reaction to injury.

Adult↗
PubMed1987

Fetal tectal or cortical tissue transplanted into brachial lesion cavities in rats: influence on the regrowth of host retinal axons.

Fetal neural tissue was transplanted into suction lesions of the left brachium and pretectal region in young rats. Tectal tissue was grafted into 6-18-day-old rats and cortical tissue was transplanted into 17-20-day-old animals. The aim was to determine whether grafts could potentiate the regrowth of damaged retinal axons and, as a consequence, stimulate the axons to reenter their host target, the superior colliculus (SC). Fifteen to 581 days after transplantation, host retinal projections were traced by injecting the right eye with horseradish peroxidase (HRP). Parallel series of frozen brain sections were stained for HRP histochemistry, acetylcholinesterase, Nissl, or neurofibrils. At all ages studied, grafts survived and grew within the wound cavity; survival was better in the older animals. Most cortical grafts and a small number of tectal grafts filled the wound cavity and formed complete tissue bridges across the lesion. The majority of tectal grafts were attached to one or the other side of the lesion and were connected to the opposite lesion face by glial and connective tissue membranes that formed over the lesion site. In many animals that received tectal transplants, host retinal axons were traced growing into the grafts. Regenerating axons innervated specific, localized areas within the grafts, and it appeared that the axons retained the ability to recognize their appropriate target cells within the graft neuropil. Comparable ingrowth into cortical grafts was not observed. Optic axons were occasionally seen reentering the superficial layers of the host SC; however, compared to fetal tectal grafts, the density of host SC innervation was sparse. The implications of these data are discussed with regard to the possible use of fetal neural tissue grafts as reconstructive tissue bridges in the mammalian central nervous system.

Animals↗
PubMed1992

Diffusion imaging of the human brain in vivo using high-speed STEAM MRI.

This paper describes a new method for diffusion imaging of the human brain in vivo that is based on a combination of diffusion-encoding gradients with high-speed STEAM MR imaging. The single-shot sequence 90 degrees-TE/2-90 degrees-TM-(alpha-TE/2-STE)n generates n = 32-64 differently phase-encoded stimulated echoes STE yielding image acquisition times of 576 ms for a 48 x 128 data matrix. Diffusion encoding is performed during the first TE/2-interval as well as during each readout period. Phantom studies reveal a quantitative agreement of calculated diffusion coefficients with literature values. EKG triggering completely eliminates motion artifacts from diffusion-weighted single-shot STEAM images of human brain in vivo. While signal attenuation of the cerebrospinal fluid (CSF) is predominantly due to flow, that observed for gray and white matter results from diffusion. Evaluated diffusion coefficients yield (1.0 +/- 0.1) x 10(-5) cm2 s-1 for gray matter, (0.5 +/- 0.1) x 10(-5) cm2 s-1 for white matter with the diffusion encoding parallel to the main orientation of the myelin sheath of the neurofibrils, and (0.3 +/- 0.1) x 10(-5) cm2 s-1 for white matter and a perpendicular orientation. All studies were performed at 2.0 T using a conventional 10 mT m-1 gradient system.

Brain↗
PubMed1992

The morphology and connectivity of dissociated and reaggregated fetal tectal tissue transplanted to the midbrain of newborn rats.

Tectal tissue from E15 or E16 Wistar rat embryos was dissociated and reaggregated (DR) prior to transplantation on to the midbrain of newborn host rats. We wished to determine how complete disruption of the donor tissue (i) affected the subsequent morphological development of the grafts in the host brain, and (ii) whether this procedure affected the selectivity with which host retinal axons innervated target regions in the tectal transplants. Forty-three to 135 days after transplantation, host rats received binocular injections of wheatgerm agglutinin-conjugated horseradish peroxidase. After perfusion, frozen sections of the grafts and underlying host brainstem were cut and reacted with tetramethylbenzidine to identify retinal projections, or stained for either acetylcholinesterase (AChE), Nissl or neurofibrils. All host brains contained identifiable DR grafts. Each brain contained at least one large transplant and numerous smaller pieces of graft tissue. The fragmentation of DR grafts was greater than that seen in direct, undissociated tectal transplants; however the morphology of individual DR grafts was markedly similar to direct grafts. Of particular interest was the presence in DR grafts of localized, often oval or circular regions, that possessed high AChE activity and contained mostly small (5 to 10 microns) close-packed neurons. AChE-dense patches were found both superficially and deep within DR grafts and appeared identical to those seen in direct transplants. These regions are thought to be homologous to the superficial, retinorecipient layers of normal superior colliculus (SC) and it is likely that the formation of these localized areas resulted from the selective association of presumptive SGS neurons within the reaggregating neuropil. In almost all cases, host retinal input to DR grafts was confined to the localized AChE-dense patches, suggesting that despite the dissociation procedure, specific retinal innervation of regions containing at least some of the appropriate target cells was maintained in DR tectal grafts.

Acetylcholinesterase↗
PubMed1989

An immunohistochemical study of the primitive and maturing elements of human cerebral medulloepitheliomas.

Four examples of human cerebral medulloepithelioma were studied immunohistochemically with a panel of antibodies and antisera to neuronal and glial proteins. The tumors, in addition to primitive medullary epithelium, contained areas of neuroblastic, ganglionic, astrocytic, ependymoblastic and ependymal differentiation, and in one tumor, areas resembling polar spongioblastoma. Tumor cells throughout the primitive medullary epithelium displayed focal immunoreactivity for vimentin, glial fibrillary acidic (GFA) protein and for the neuron-associated class III beta-tubulin isotype. Neuroblasts showed immunoreactivity for the class III beta-tubulin isotype, microtubule-associated protein 2 and neuron-specific enolase. Immunoreactivity for neurofilament epitopes and synaptophysin was detected in areas of ganglionic differentiation and coincided with the demonstration of neurofibrils in Bielschowsky's silver impregnations. Vimentin was the only marker detected in ependymoblastic and ependymal rosettes or in areas of polar spongioblastoma, as well as in mesenchymal cells. The results indicate that, even in very primitive neoplastic neuroepithelium, immunocytochemical evidence of early commitment of some of the cells to a neuronal or glial lineage can be demonstrated. The neuron-associated class III beta-tubulin isotype appears to be one of the earliest markers indicative of neuronal differentiation in normal and neoplastic primitive neuroepithelium.

Adult↗