bluuebunny/crossref_metadata_2025 huggingface dataset:
A HISTOCHEMICAL STUDY OF FIBRE TYPES IN RAT EXTRAOCULAR MUSCLES
Authors: VITA G. F. , MASTAGLIA F. L. , JOHNSON M. A.
Published: May 2008

Vita G.F., Mastaglia F.L. & Johnson M.A. (1980) Neuropathology and Applied Neurobiology 6, 449–463

A histochemical study of fibre types in rat extraocular muscles

The histochemical fibre type composition of the rat superior and medial rectus (SR and MR), superior oblique (SO) and levator palpebrae superioris (LPS) muscles was studied using the myofibrillar ATPase and NADH‐tetrazo‐lium reductase (NADH‐TR) techniques. In the SR, MR and SO a peripheral zone containing small fibres and a central zone containing both small and large fibres could be identified. Four fibre types were present in the central zone of these muscles and were categorised as Type 1, Type 2a, Type 2a', and Type 2b. Four fibre types were also identified in the peripheral zone–Type 1, Type 2a, Type 2a' and Type 2c. In the LPS Type 1, Type 2, Type 2a', Type 2b and Type 2c fibres were evenly intermixed without a zonal arrangement. The Type 1, Type 2a, Type 2b and Type 2c fibres correspond to accepted fibre types in the rat limb muscles. The Type 2a' and Type 2a' fibres were differentiated from the Type 2a fibres on the basis of size and pattern and intensity of staining with the NADH‐TR technique. The Type 2c fibres, which possess both acid‐stable and alkali‐stable myofibrillar ATPase, are considered to represent intermediate fibres in the process of transformation from Type 2 to Type 1, rather than fibres with a dual innervation as has been suggested in the past. The implications of these histochemical findings are considered in relationship to the physiology of individual motor units and to the function of the extraocular muscles.
VARIATION WITH AGE IN THE VOLUMES OF GREY AND WHITE MATTER IN THE CEREBRAL HEMISPHERES OF MAN: MEASUREMENTS WITH AN IMAGE ANALYSER
Authors: MILLER A. K. H. , ALSTON R. L. , CORSELLIS J. A. N.
Published: May 2008

Miller A. K. H., Alston R. L. & Corsellis J. A. N. 1980 Neuropathology and Applied Neurology 6, 119–132

Variation with age in the volumes of grey and white matter in the cerebral hemispheres of man: measurements with an image analyser

The total volumes and relative quantities of grey and white matter have been measured in sixty‐five normal male and sixty‐five normal female cerebral hemispheres. Fixed hemisphere volume was found to fall linearly at 35% per decade for men from 641 ml at the age of 20 to 463 ml at the age of 100. For women the decrease was 1–9% per decade from 531 ml at 20 years to 462 ml at 100 years. After correction for the effects of fixation and for the secular increase in brain size, it was concluded that mean hemisphere volume remained roughly constant between the ages of 20 and 50 years (558 ml for men, 474 ml for women). After the age of 50 the mean volume in both sexes fell at about 2% per decade. The ratio of the volumes of grey to white matter was the same for the two sexes at all ages. Its mean value was 1–3 at the age of 20, falling to 11 at the age of 50, then rising steadily to over 1–5 at 100 years. It is impossible in practice to correct these measurements for the effects of fixation or secular change. Fourteen hemispheres from thirteen elderly female dements were also measured. The total volume was 18% lower than for an age‐matched group of normals, but the ratio of grey to white matter was identical.
LYSOSOMAL HYDROLASES IN LONG TERM CULTURES OF HUMAN GLIOMAS: TOTAL ENZYME ACTIVITIES AND RATE OF EXTRACELLULAR ACCUMULATION
Authors: MCCORMICK D. , MAUNOURY R. , DELPECH B.
Published: May 2008

McCormick D., Manoury R. & Delpech B. 1980 Neuropathology and Applied Neurobiology 6, 133–141

Lysosomal hydrolases in long term cultures of human gliomas: total enzyme activities and rate of extracellular accumulation

A number of investigations have suggested a fundamental role for lysosomal enzymes in growth control of normal cells and in the loss of growth control which occurs in neoplasia and in cell cultures transformed by oncogenic viruses. In this investigation total enzyme activities and rates of extracellular accumulation of enzyme were measured in long term cultures of gliomas and normal human astrocytes. Marked differences were found between the cultures with regard to total enzyme activity. Exocytosis rates of the enzymes also showed differences, with one group of tumours demonstrating low or intermediate rates and another smaller group with high rates. There was no positive correlation between the enzyme profile of the cultures and their tumorigenicity in nude mice.
FURTHER ULTRASTRUCTURAL OBSERVATIONS OF VIRUS MORPHOGENESIS AND MYELIN PATHOLOGY IN JHM VIRUS ENCEPHALOMYELITIS
Authors: FLEURY H. J. A. , SHEPPARD RACHEL D. , BORNSTEIN M. B. , RAINE C. S.
Published: May 2008

Fleury H.J.A., Sheppard R.D., Bornstein M.B. & Raine C.S. 1980 Neuropathology and Applied Neurobiology 6,165–179

Further ultrastructural observations of virus morphogenesis and myelin pathology in JHM virus encephalomyelitis

Groups of 3, 17, and 28‐day‐old Swiss mice were inoculated intracerebrally with JHM virus, the neurotropic strain of mouse hepatitis virus (MHV), and studied serially by virologic and morphologic techniques. Beginning 2–5 days post‐inoculation, all groups of infected mice developed CNS lesions which were destructive in the 3‐day‐old group and demyelinative in the 17 and 28‐day‐old animals. Infectious virus could be isolated from the brain, spinal cord, and liver. Electron microscopy demonstrated the virus to be pantropic in the CNS with virions occurring within ependymal cells, astrocytes, neurons, oligodendrocytes, endothelial cells, and cell of haematogenous origin. Giant cell formation was a constant feature. In regions of demyelination, oligodendrocytes exhibited a propensity to proliferative aberrant membrane. Myelin degradation was accompanied by membrane vesiculation and by the stripping action of macrophages. The lesions were not due to CNS elements in the inoculum since in animals inoculated with normal CNS suspensions from appropriate age groups failed to show lesions. The morphogenesis of JHM virions was followed ultrastructurally as was the formation of syncytia in the different cell types. In addition to delineating virus morphogenesis and myelin pathology, the results underscore the pantropic nature of JHM virus in the CNS, the systemic nature of the infection, and that oligodendrocytes were the principal targets.
CYCLOLEUCINE ENCEPHALOPATHY
Authors: GRECO CLAUDIA M. , POWELL H. C. , GARRETT R. S. , LAMPERT P. W.
Published: May 2008

Greco C. M., Powell H. C, Garrett R. S. & Lampert P. W. (1980) Neuropathology and Applied Neurobiology 6,349–360

Cycloleucine encephalopathy

Cycloleucine, a non‐metabolizable amino acid analogue produces status spongiosus in cerebral white matter of rats and mice as well as a distinctive lesion of astrocytes. Its mechanisms of action include competition with natural amino acids from transport across the blood‐brain barrier leading to inhibition of entry of circulating amino acids into brain, interference with ribosomal RNA maturation, and blockage of transmethylation reactions, including the conversion of homocystine to methionine. Cycloleucine also affects the kidney, producing aminoaciduria. Electron microscopy of cerebral white matter reveals spongiform changes of myelin sheaths caused by separation of myelin lamellae along intraperiod lines and accumulation of whorls of filaments in astrocytes. The myelinopathy is dose related and its toxicity is cumulative due to its long half‐life in animals. The findings are discussed with reference to other spongiform myelinopathies, including status spongiosus observed in homocystinuria and other aminoacidurias.
PERIPHERAL NEUROPATHY IN MOUSE HEREDITARY DIABETES MELLITUS. II. ULTRASTRUCTURAL CORRELATES OF DEGENERATIVE AND REGENERATIVE CHANGES
Authors: CARSON K. A. , BOSSEN E. H. , HANKER J. S.
Published: May 2008

Carson K.A., Bossen E.H. & Hanker J.S. (1980) Neuropathology and Applied Neurobiology 6,361–374

Peripheral neuropathy in mouse hereditary diabetes mellitus. II. Ultrastructural correlates of degenerative and regenerative changes

The fine structural changes in some peripheral nerves and sensory ganglia from mice (C57BL/K & J, db/db) with an hereditary diabetic syndrome, similar to human maturity‐onset diabetes mellitus, were studied during development of the mild peripheral neuropathy. The abnormalities observed included axonal degeneration, disruption of myelin, accumulation of electron‐dense material in axons, satellite cells and Schwann cells, increased frequency of it granules of Reich in Schwann cells, enlarged mitochondria, and proliferated and thickened Schwann cell basal laminae. Distal hind limb nerves were most affected. Sensory ganglion neurons were normal except for occasional chro‐matolytic cells, so that nerve cell loss was not present in this peripheral neuropathy. Morphological indications of Schwann cell hyperplasia, hypertrophy, and axonal sprouting supported the contention that a continuous cycle of axonal degeneration and regeneration was occurring. The ultrastructural changes and accumulation of electron‐opaque, lipid material suggested that a defect in lipid metabolism, secondary to the diabetic condition, could be an important factor in the peripheral neuropathy in the diabetic mouse.
STUDY OF AXONAL DYSTROPHY. II. DYSTROPHY AND ATROPHY OF THE PRESYNAPTIC BOUTONS: A DUAL PATHOLOGY
Authors: FUJISAWA K. , SHIRAKI H.
Published: May 2008

Fujisawa K. & Shiraki H. (1980) Neuropathology and Applied Neurobiology 6, 387–398

Study of axonal dystrophy. II. Dystrophy and atrophy of the presynaptic boutons: a dual pathology

In succession to the previous quantitative work, a qualitative study has been carried out on the nature of a dual pathology affecting presynaptic boutons in the posterior tract nuclei of ageing rats. Based on the morphology of dystrophic boutons in early stage, it is concluded that the initial and therefore essential characteristic of dystrophic process is an abnormal increase of normal axonal components within the presynaptic boutons, and that various abnormal substructures of spheroids hitherto reported in the literature are probably the result of their secondary metamorphosis. The dystrophic process within the posterior tract nuclei is a selective one, involving presynaptic boutons and preterminal axons only of the posterior tract fibres. Comparison of the frequency of early dystrophic boutons and of fully grown‐up spheroids indicates that a small percentage of boutons deriving from posterior tract fibres become dystrophic and of these dystrophic boutons only a small percentage again continue to develop unto large spheroids, throughout lifespan of the animals. On the other hand, in search of a morphological counterpart for the age‐related decrease of volume ratio of presynaptic boutons to the neuropil, some dubious atrophic changes were also found in presynaptic boutons, which could have been easily missed from observation if studied qualitatively alone. Accordingly, no less numerous boutons other than dystrophic ones are supposed to atrophy ‘independently’ and to disappear ‘silently’ during the same period. The dystrophic and the atrophic changes involve different boutons (of different or the same terminal axons) within the same gray matter. This dual pathology of boutons needs further elucidation of its neurocytopathological as well as neurobiological background in the future.
NEURONAL UPTAKE OF IRON: SOMATOPETAL AXONAL TRANSPORT AND FATE OF CATIONIZED AND NATIVE FERRITIN, AND IRON‐DEXTRAN AFTER INTRAMUSCULAR INJECTIONS
Authors: OLSSON T. , KRISTENSSON K.
Published: May 2008

Mice were injected into the muscles of the vibrissae with native ferritin (NF), cationized ferritin (CF) and iron‐dextran. CF adsorbed on to the surface of the axon terminal at the neuromuscular junction, while NF did not. Both CF and NF were incorporated into vesicles and vacuoles at the synapse, but CF uptake was detected after injections at much lower concentrations than NF. In contrast to NF, CF was also found histochemically in cell bodies of facial neurones after a single i.m. injection, showing that the electrical charge of a molecule is one factor of importance for its potential to be incorporated in axons and transported somatopetally. Repeated i.m. injection of iron‐dextran into suckling mice resulted in a marked iron load of Schwann cells and nerve cell bodies. This produced no signs of toxicity and the nerve fibre developed normally. Iron had disappeared from the nerve cell bodies after 25 days, while in Schwann cells it still persisted after 223 days.
QUANTITATION AND IN VITRO ANALYSIS OF THE INFLAMMATORY CELLS IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN THE GUINEA‐PIG
Authors: ALLSOPP GRETA , PARKER DARIEN , HINRICHS D.J. , TURK J. L.
Published: May 2008

Inflammatory cells from the meninges of guinea‐pigs with acute EAE have been isolated and quantitated. A mean of 7–5 × 106 cells were recovered from the brains of animals showing clinical signs of disease in contrast to only 1–5 × 106 cells in the controls. The immunological specificity of the meningeal inflammatory cells was determined using the lymphocyte transformation test and compared with another inflammatory cell population, the peritoneal exudate cells (PECs), in the same animal. The meningeal exudate cells responded only to the mitogen Concanavalin A (Con A) and not to the antigens myelin basic protein and tuberculin (PPD). In contrast, the PECs proliferated in the presence of both antigens and the mitogen.
VARIATIONS IN THE PERINEURONAL GLIAL CHANGES AFTER DIFFERENT TYPES OF NERVE LESION: LIGHT AND ELECTRON MICROSCOPIC INVESTIGATIONS ON THE FACIAL NUCLEUS OF THE RAT
Authors: SÖREIDE A. J.
Published: May 2008

The perineuronal glial changes were studied by light and electron microscopy after avulsion or a crush lesion of the facial nerve in rats. The changes consisted of proliferation of microglia, ensheathment of neurons by thin astrocytic processes, and separation of the synaptic boutons from the neuronal surface. Quantitative estimates of the glial proliferation were made with the light microscope. In spite of marked differences in the acute nerve cell reaction, 4 days after the two types of lesion the glial and synaptic changes did not differ significantly. Ultimately, all changes were reversible after crush lesions, while neuronophagia occurred after nerve avulsion. It is concluded that the acute synaptic and glial reactions were not influenced by the type of nerve lesion or the severity of the nerve cell reaction, but the latter stages differed depending upon whether the neurons recovered or disintegrated.
AN ELECTRON MICROSCOPIC STUDY OF SATELLITE CELLS AND REGENERATION IN DYSTROPHIC MOUSE MUSCLE
Authors: SUMMERS P. J. , PARSONS R.
Published: May 2008

Triceps and gastrocnemius muscles from dystrophic (129 Rej dy/dy) and normal mice were examined by electron microscopy at different stages in development for evidence of regeneration. Mitotic satellite cells were present only in dystrophic muscle. Myoblasts containing myofilaments, and multinucleate myotubes were observed within foci of regeneration. Approximately 50% of the myotubes showed features indicative of degeneration or abnormal development. These features included the presence of membrane whorls, and myofibrillar and sarcolemma breakdown. Quantitative studies suggest that the number of satellite cells is increased in dystrophic muscle. It is concluded that there are sufficient satellite cells in dystrophic mouse muscle to allow regeneration, and they are able to proliferate and form well differentiated myotubes. However, subsequent development of the myotubes can be ineffective, or ‘abortive’, reducing the regenerative capacity to the muscle.
ULTRASTRUCTUAL CHANGES IN AXONS CAUSED BY ACRYLAMIDE ABOVE A NERVE LIGATURE
Authors: CAVANAGH J. B. , GYSBERS M. F.
Published: May 2008

The ultrastructural features of the ascending degeneration produced by acrylamide in peripheral nerves above the point of nerve ligature have been described. Before the onset of signs of axonal degeneration abundant accumulations of smooth endoplasmic reticulum and vesicles occur particularly proximal to nodes of Ranvier, but also in internodal regions. Some mitochondrial accumulations occur distal to nodes of Ranvier. The changes closely resemble those found in axons up to 4 mm above a nerve crush in normal animals and appear to be essentially non‐specific in nature. Their significance in relation to the subsequent axonal degeneration can only be guessed at.
TOPOGRAPHY OF NEUROFIBRILLARY TANGLES AND GRANULOVACUOLES IN HIPPOCAMPI OF PATIENTS WITH DOWN'S SYNDROME: QUANTITATIVE COMPARISON WITH NORMAL AGEING AND ALZHEIMER'S DISEASE
Authors: BALL M. J. , NUTTALL K.
Published: May 2008

Ball M. J. & Nuttall, K. (1981) Neuropathology and Applied Neurobiology 7, 13–20

Topography of neurofibrillary tangles and granulovacuoles in hippocampi of patients with Down's syndrome: quantitative comparison with normal ageing and Alzheimer's disease

An XY pen recorder linked potentiometrically to a sampling stage microscope permitted the plotting of topographic ‘scattergrams’ to determine the precise cytoarchitectonic localization of neurofibrillary tangles and granulovacuo‐lar degeneration in hippocampal neurones of Down's syndrome adult brains. The area (and hence volume) of six cortical ‘zones’ surveyed was measured with a digitizer and programmable calculator. In decreasing magnitude of affliction, the rank order for neurofibrillary tangles was: entorhinal > subiculum > H1 > endplate > H2 > presubiculum. That for granulovacuolar change was: subiculum > H1 > H2 > endplate > entorhinal > presubiculum. These striking regional predispositions suggest that a common neurotransmitter deficit may underlie the local selectivity of such lesions in Down's syndrome brains; and the predilections' marked similarities to ranking orders, already noted both in normal aged subjects and especially in senile dements of the Alzheimer type, enhance the importance of the Down's syndrome neuraxis as a key to the puzzle of Alzheimer's dementia.
THE SUPRAHABENULAR RECESS IN THE RAT: A QUANTITATIVE STUDY OF CILIATED CELLS, SUPRAEPENDYMAL CELLS AND SOME SPECIFIC FEATURES OF SUPRAEPENDYMAL FIBRES
Authors: TULSI R. S. , DREOSTI I. E.
Published: May 2008

Tulsi R.S. & Dreosti I.E. (1981) Neuropathology and Applied Neurobiology 7, 21–36

The suprahabenular recess in the rat: a quantitative study of ciliated cells, supraependymal cells and some specific features ofsupraependy‐mal fibres

Using light microscopy, scanning and transmission electron microscopy, an extensive quantitative analysis of ciliated ependymal cells, supraependymal cells and supraependymal fibres in the suprahabenular recess of twenty‐two adult Wistar rats was carried out. In addition, six animals were used to determine the origin of supraependymal fibres and their relationship to ependyma. The findings were as follows: ciliated cells–mean 3–32 ± 0–26 per 1000 μm2 (range 0–10); supraependymal cells–5–91 ± 1–37 per recess (range 2–16). Average number of cilia per cell in different animals ranged from 31 to 33. Sex did not influence the density of ciliated ependyma or supraependymal cells. Evidence was obtained that some supraependymal fibres are closely associated with aberrant commissural fibres. The supraependymal fibres enter the suprahabenular recess and form gap junctions, and other types of junctions, with subjacent ependyma.
THE DEVELOPMENT OF BRAIN TUMOURS PRODUCED IN RATS BY THE INTRACEREBRAL INJECTION OF NEOPLASTIC GLIAL CELLS: A FINE STRUCTURAL STUDY*
Authors: DAVAKI PANAYOTA , LANTOS P. L.
Published: May 2008

Davaki P. & Lantos P.L. (1981) Neuropathology and Applied Neurobiology 7,49–61

The development of brain tumours produced in rats by the intracerebral injection of neoplastic glial cells: a fine structural study

Tumours were produced by the intracerebral injection of a clone of glial cells derived from a glioma induced transplacentally by N‐ethyl‐N‐nitrosourea in a BD‐IX rat. The injection of 5 times 105 cells into the left frontal lobe resulted in a 100% incidence of tumours. To follow the development of the neoplasms, the brains were studied from 1 day to 4 weeks after injection. The tumours maintained their glial characters throughout, but their features changed with time. Ultrastructurally, they were pleomorphic: the proportion of fibrillary astrocytes, undifferentiated and intermediate cell types varied according to tumour size. When smaller (1 and 2 weeks), fibrillary astrocytes predominated, but when larger (3 and 4 weeks), the number of undifferentiated astrocytes considerably increased. A reproducible brain tumour model with a short latency has thus been established and characterized, which may be of use for chemo‐ and radiotherapeutic studies and for examining the mechanisms of cerebral oedema.
A LIGHT AND ELECTRON MICROSCOPIC HISTOCHEMICAL STUDY ON THE MECHANISM OF DFP‐INDUCED ACUTE AND SUBACUTE MYOPATHY
Authors: TÓTH L. , KARCSÚ SAROLTA , POBERAI MÁRIA , SÁVAY GY.
Published: May 2008

Tóth L., Karcsú S., Poberai M. & Sávay Gy. (1981) Neuropathology and Applied Neurobiology 7, 399–410

A light and electron microscopic histochemical study on the mechanism of DFP‐induced acute and subacute myopathy

The histochemical changes occuring in association with the development of acute and subacute myopathy have been studied in the rat diaphragm 30 min‐48 h after a single i.p. injection of 1–82 mg/kg of the irreversible cholinesterase inhibitor organophosphate, diisopropylfluorophosphate (DFP). In addition to a considerable inhibition of the AChE activity of the motor end‐plates, accumulation of ionic Ca2+ and an increase in neutral protease activity in the subjunctional sarcoplasm have been demonstrated. A temporal and causal relationship has been established between the histochemical changes and the development of the ultrastructural signs of myopathy.
COMPARATIVE MORPHOLOGY OF MEASLES VIRUS AND PARAMYXOVIRUS‐LIKE TUBULES IN MULTIPLE SCLEROSIS USING RUTHENIUM RED STAIN
Authors: NARANG H. K.
Published: May 2008

Narang H.K. (1981) Neuropathology and Applied Neurobiology 7, 411–420 Comparative morphology of measles virus and paramyxovirus‐like tubules in multiple sclerosis using ruthenium red stain

Morphology of intracytoplasmic nucleocapsid measles virus from mouse brain and tissue culture was studied with the use of ruthenium red by tilting and high resolution electron microscopy and compared with the paramyxovirus‐like tubules found in multiple sclerosis (MS). Both in vivo and in vitro the measles nucleo‐protein profiles were surrounded by ‘fuzzy’ material which could be resolved in a pentagon shape and this stained specifically with ruthenium red. The tubules found in MS appeared not to have a ‘fuzzy’ coat and also did not stain with ruthenium red. The main difference observed between infected tissue culture cells and mouse brain was that in the latter no alignment of measles nucleoprotein was observed under the cell membrane and no budding particles were seen. The virus could not be passed to mice or tissue culture from the infected mouse brain.
A QUANTITATIVE STUDY OF AGE‐RELATED CHANGES IN THE VASCULAR ARCHITECTURE OF THE RAT CEREBRAL CORTEX
Authors: WILKINSON J. H. , HOPEWELL J. W. , REINHOLD H. S.
Published: May 2008

Wilkinson J.H., Hopewell J.W. & Reinhold H.S. (1981) Neuropathology and Applied Neurobiology 7, 451–462

A quantitative study of age‐related changes in the vascular architecture of the rat cerebral cortex

A quantitative study of age related changes in the vascular architecture of the rat cerebral cortex is described. A special vessel‐filling technique, which allowed the simultaneous fixation of the vasculature, aided the identification of the vessels in histological sections. Vascular parameters, which included the total number of vessel fragments, a blood volume and a vessel wall‐surface area index were obtained using a Quantimet 720 shape‐analysing computer. In animals aged 13–83 weeks, there was an increase in the above vascular parameters which could mainly be attributed to an increase in the number of vessels with a diameter > 8 μm. In very old rats, aged 124 weeks, the vascularity of the cerebral cortex was severely reduced. These changes, which are very similar to those reported in the ageing human cerebral cortex, may be explained by either direct or indirect effects on the cerebral vasculature. Possible mechanisms are discussed in relation to similar changes observed in the cerebral vasculature after several different insults.
THE EFFECT OF PROTECTING GUINEA‐PIGS AGAINST EAE ON THE MENINGEAL INFLAMMATORY CELL‐INFILTRATE
Authors: ALLSOPP GRETA , PARKER DARIEN , TURK J. L.
Published: May 2008

Allsopp G., Parker D. & Turk J.L. (1981) Neuropathology and Applied Neurobiology 7, 477–487

The effect of protecting guinea‐pigs against EAE on the meningeal inflammatory cell infiltrate

Guinea‐pigs were found to be fully protected from the clinical signs of EAE when they were given spinal cord in FIA either 3, 7 or 14 days before immunization with spinal cord in FCA. If the animals were protected by the recruitment of suppressor cells then cyclophosphamide (CY) might break this protection. CY at 300 mg/kg) and 20 mg/kg was given either before the protective inoculum to try to eliminate suppressor cell precursors or before immunization to eliminate the suppressor cells themselves. No clinical signs of EAE developed in any of these groups of guinea‐pigs. It was found, however, that large numbers of meningeal inflammatory cells could be isolated from the brains of guinea‐pigs protected from EAE when the protective inoculum was given only 1 week before immunization. These cell numbers were further significantly increased by giving CY in addition to the protective inoculum. The meningeal inflammatory cells and peritoneal exudate cells (PECs) from guinea‐pigs protected against EAE were compared to those isolated from animals with acute EAE. These cells from guinea‐pigs with acute EAE responded, in the lymphocyte transformation test, to the mitogen. The PECs also responded to the brain antigen, myelin basic protein (MBP) and to tuberculin (PPD). The meningeal inflammatory cells did not respond to either antigen. The PECs from animals protected against EAE responded to mitogen and PPD, but not to MBP, but the meningeal inflammatory cells did not respond to antigen or mitogen. The percentage of T lymphocytes in the meningeal inflammatory infiltrates of protected and unprotected guinea‐pigs was similar, but that of phagocytic cells was significantly depressed in the inflammatory infiltrates of animals protected against EAE.
EFFECTS OF AGE ON CEREBRAL AMYLOID PLAQUES IN MURINE SCRAPIE
Authors: BRUCE MOIRA E. , FRASER H.
Published: May 2008

Bruce M.E. & Fraser H. (1982) Neuropathology and Applied Neurobiology 8, 71–74

Effects of age on cerebral amyloid plaques in murine scrapie

The frequency of cerebral amyloid plaques in murine scrapie was not influenced by the age of the mouse at injection in a study using several combinations of agent strain and mouse strain. In addition amyloid plaques were not seen in a series of extremely old uninfected mice.
A QUANTITATIVE STUDY OF VASCULAR PERMEABILITY TO HORSERADISH PEROXIDASE, AND THE SUBSEQUENT FATE OF THE TRACER, IN RAT BRAINS AFTER PORTOCAVAL ANASTOMOSIS
Authors: SUMNER B. E. H.
Published: May 2008

Sumner B. E. H. (1982) Neuropathology and Applied Neurobiology 8, 117–133

A quantitative study of vascular permeability to horseradish peroxidase, and the subsequent fate of the tracer, in rat brains after portocaval anastomosis

Labelled blood vessel segments, exudation patches, and pericytic granular cells were counted in sections of rat brain which had been fixed and tested with DAB from 3 min to 24 h after intravenous injection of horseradish peroxidase (HRP).

In normal rats, 3 min after injection, only 1% of the total blood vessel segments had walls penetrated by HRP, but in rats 14 days after portocaval anastomosis (PCA) 44% of the total segments had labelled walls, a frequency of 3033 permeable segments/mm3 of brain. In normal rats no exudation patches were found, but after PCA there were seven patches/mm3 of brain. Maximum vascular wall labelling and maximum exudation occurred in the cerebellum and medulla of the operated rats. Hardly any pericytic cells were labelled 3 min after injection.

In operated rats 2 h after injection of HRP, labelled vascular walls were fewer and exudation had disappeared, but 204 pericytic cells/mm3 of brain contained HRP‐labelled granules, i.e. 60% of the total pericytes. Highest numbers were found in the most anterior section of the brain sample. Later after injection these numbers declined.

It is suggested that most of the protein which leaked into the brain after PCA returned to the blood whence it came, but that some was captured and hydrolysed by the granular pericytes.
ANNOTATION: NERVE CELL PROTEIN METABOLISM AND DEGENERATIVE DISEASE
Authors: MANN D. M. A.
Published: May 2008

Mann D.M.A. (1982) Neuropathology and Applied Neurobiology 8, 161–176

Annotation. Nerve cell protein metabolism and degenerative disease

The mechanisms and organelles through which control of protein synthesis within healthy nerve cells is governed are discussed, and the ways in which expression of these biochemical pathways can be related to cell morphology are described. The volumes of the nucleus and nucleolus, and the amount of RNA within the cell body, are all interrelated and seem to be set at genetically predetermined levels which normally match the neurones basal needs for replacement proteins in respect of the size of its' projection field. However, in situations of (induced) hyperactivity or cell damage, or in others where disease may lower nerve cell activity, the protein requirements change, and it is noted that these morphological features also alter in a direction appropriate to the need for greater or lesser amounts of protein. How these alterations in protein synthesis can provide information as to both the basic pathology, or even the pathogenesis, of degenerative disease of the nervous system is illustrated by reference to Alzheimer's disease and motor neurone disease.
THE EFFECTS OF CASTRATION ON THE SUBEPENDYMAL PLATE OF THE RAT
Authors: HOPKINS B. , HOPEWELL J. W.
Published: May 2008

Hopkins B. & Hopewell J. W. (1982) Neuropathology and Applied Neurobiology 8, 189–195

The effects of castration on the subependymal plate of the rat

Earlier studies have shown that glial tumours, produced by the intracerebral implantation of chemical carcinogens, originate from the subependymal plate. In the present study the effects of castration on cell number and proliferation in the subependymal region has been investigated as such treatment has been shown to reduce the incidence of gliomata produced by an implanted carcinogen.

An age‐related reduction in mitotic activity and nuclear density was found in the subependymal plate. Castration produced a consistent reduction in mitotic activity but the nuclear density was unchanged.

The results suggest that the reduction in tumour incidence produced by castration cannot be explained simply on the basis of reduced proliferation in the population believed to be at risk and that other, as yet, undefined factors must be involved.

In addition, it appeared that there was also no simple relationship between brain growth and cell proliferation in the subependymal plate.
THE DEVELOPMENT OF RETINITIS IN MICE WITH NONFATAL HERPES SIMPLEX ENCEPHALITIS
Authors: ANDERSON JANICE R. , FIELD H. J.
Published: May 2008

Anderson J.R. & Field H.J. 1982 Neuropathology and Applied Neurobiology 8, 277–287

The development of retinitis in mice with non‐fatal herpes simplex encephalitis

A mutant strain of herpes simplex virus, type 1 (HSVl), selected for high resistance to acyclovir (ACV) was inoculated intracerebrally into mice. The mice survived with no obvious neurological signs but developed cataracts within 4–8 weeks of inoculation. Histological examination revealed only a mild encephalitis, but around 7 days after injection a florid, necrotizing, viral retinitis developed. There was almost simultaneous involvement of both eyes. Inflammatory cell infiltration and early myelin degeneration along the course of the optic nerve suggested cell to cell spread of virus to the retinal nerve cell bodies. Although virus could only be recovered from the eye in the early stages of retinitis, destruction of the neural retina was frequently complete and subsequently the optic nerves showed Wallerian type degeneration. Visible cataracts were a late complication, but changes in the lens were initiated during the phase of acute retinitis. This experiment shows that antiviral agents may induce mutant forms which cannot reproduce classical disease, but are capable of permissive infection in unexpected sites. Herpes retinitis is occasionally recognized as a complication of fatal HSV encephalitis in man. Theoretically, more effective treatment of encephalitis with nucleoside analogues, for example with acyclovir, could reveal the development of retinitis in survivors.
THE EARLY EVOLUTION OF NEUROFILAMENTOUS ACCUMULATIONS DUE TO 2,5‐HEXANEDIOL IN THE OPTIC PATHWAYS OF THE RAT
Authors: JONES H. B. , CAVANAGH J. B.
Published: May 2008

Jones H.B. & Cavanagh J.B. 1982 Neuropathology and Applied Neurobiology 8, 289–301

The early evolution of neurofilamentous accumulations due to 2,5‐hexanediol in the optic pathways of the rat

Rats were given 2,5‐hexanediol in their water for more than 5 weeks. The changes in the optic pathways were studied both qualitatively and quantitatively. Increase in 10‐nm filaments within axons was noticeable from 10 days onwards in the superior colliculus and in the brachium of the superior colliculus. From then onwards there was a steady increase in the number of affected axons, and their gross enlargement occurred. The proportion of affected fibres in the brachia was in fact few, but all fibres were of retinotectal origin. Less than half of those in the superior colliculus that were swollen were of retinal origin. Measurement of axon diameter versus myelin sheath thickness showed gross relative thinning of the latter. Axon degeneration did not occur but there was increasing ultrastructral evidence of impairment of transport of organelles both centrifugally and centripetally as the filamentous masses accumulated.
THE PATHOKINETICS OF ACRYLAMIDE INTOXICATION: A REASSESSMENT OF THE PROBLEM
Authors: CAVANAGH J. B.
Published: May 2008

Cavanagh J.B. 1982 Neuropathology and Applied Neurobiology 8, 315–336

The pathokinetics of acrylamide intoxication: a reassessment of the problem

Acrylamide was given intraperitoneal^ to rats (30 mg/kg/day, five times/week) for 3 weeks, and the nervous and muscle tissues were examined by conventional methods over 5 weeks. Three striking cellular changes were observed. 1 Scattered degeneration of many Purkinje cells from 5 days onwards. 2 Widespread swelling and argyrophilia of nerve terminals from 10 days in both PNS and CNS. Motor and sensory endings were equally affected in all muscles examined. Synaptic and preterminal swelling also occurred in spinal cord, brain stem, and in certain cerebellar terminals. Degeneration occasionally followed this change, particularly in sensory nerve fibres, but not necessarily. 3 Chromatolysis in spinal ganglion cells and occasionally in anterior horn cells from 7 days onwards before the onset of axonal degeneration. This unique sequence of events is discussed in the light of the metabolic and other changes described by earlier authors.
ETHIDIUM BROMIDE INDUCED DEMYELINATION IN THE SPINAL CORD OF THE CAT
Authors: BLAKEMORE W. F.
Published: May 2008

Blakemore W.F.1982 Neuropathology and Applied Neurobiology 8, 365–375

Ethidium bromide induced demyelination in the spinal cord of the cat

Small volumes of ethidium bromide were injected into the dorsal column of the spinal cord of cats. Oligodendrocytes and astrocytes showed morphological evidence of intoxication by ethidium bromide from 2 days after injection. However, apart from around the point of injection and the needle tract, demyelination did not occur until between 8 and 14 days. Both oligodendrocytes and astrocytes were absent from the demyelinated area at 14 days and all but a small number of demyelinated axons were remyelinated by Schwann cells. These cells first appeared in the lesion at 10 days, but axon association and myelination did not occur until 16 days. This model of experimental demyelination indicates once again that Schwann cell invasion of demyelinated areas in the CNS occurs if both oligodendrocytes and astrocytes are destroyed. None of the lesions in the present investigation were in continuity with root entry zones, indicating that this location is not a prerequisite for Schwann cell invasion of the CNS.
BASAL GANGLIA DEGENERATION, MYELIN ALTERATIONS, AND ENZYME INHIBITION INDUCED IN MICE BY THE PLANT TOXIN 3‐NITROPROPANOIC ACID
Authors: GOULD DANIEL H. , GUSTINE DAVID L.
Published: May 2008

Gould D. H.&Gustine D. L.1982Neuropathology and Applied Neurobiology 8, 377–393

Basal ganglia degeneration, myelin alterations, and enzyme inhibition induced in mice by the plant toxin 3‐nitropropanoic acid

The plant toxin, 3‐nitropropanoic acid, produced topographically and morphologically distinctive lesions in mice after daily intraperitoneal injections. In the lateral caudate‐putamen there were bilateral and symmetrical lesions consisting of marked swelling and pyknosis of individual cells and processes in otherwise unaffected tissue. The appearance of transitional forms and the usual post‐synaptic location of the swollen processes indicated that affected cells were neurons. A few mice exhibited a more diffuse spongy change in the lateral caudate‐putamen that caused major architectural changes. In the globus pallidus, entopeduncular nucleus, and anterior substantia nigra pars reticulata there was fine spongy change of the neuropil that spared cell bodies, and was primarily due to swelling of dendrites. A third lesion pattern in myelinated tracts of the midbrain, medulla, and spinal cord consisted of adaxonal, intramyelinic cleft formation. Succinate dehydrogenase activities assayed in frozen brain sections and in isolated mitochondria were markedly reduced in intoxicated mice.
ACTION OF PYRETHROID INSECTICIDES ON THE VERTEBRATE NERVOUS SYSTEM
Authors: VIJVERBERG HENK P. M. , BERCKEN JOEP VAN DEN
Published: May 2008

Vijverberg H.P.M. & van den Bercken J.1982 Neuropathology and Applied Neurobiology8, 421–440

Annotation. Action of pyrethroid insecticides on the vertebrate nervous system

The neurotoxic action of the synthetic pyrethroid insecticides has received much interest in recent years, as the number of available pyrethroids and their practical applications have greatly increased. Although the majority of pyrethroids have a low oral toxicity to mammals, they may cause severe neurotoxic symptoms whenever they reach the nervous system in sufficient amount.

The principal effect of pyrethroids in the vertebrate nervous system is to induce repetitive activity, particularly in the sensory nervous system. This repetitive activity originates from a prolongation of the transient increase in sodium permeability of the nerve membrane associated with excitation. Available evidence indicates that pyrethroids primarily interfere with the sodium channels in the nerve membrane. All active pyrethroids affect sodium channel gating in a similar manner, but marked differences in neurotoxic activity exist between the various pyrethroids, especially between ot‐cyano and non‐cyano compounds.
A CHANGE IN SUSCEPTIBILITY OF RAT CEREBELLAR PURKINJE CELLS TO DAMAGE BY ACETALDEHYDE DURING FETAL, NEONATAL AND ADULT LIFE
Authors: PHILLIPS S. C. , CRAGG B. G.
Published: May 2008

Phillips S.C. & Cragg B.G. 1982 Neuropathology a id Applied Neurobiology 8, 455–463

A change in susceptibility of rat cerebellar Purkinje cells to damage by acetaldehyde during fetal neonatal and adult life

The sensitivity of rat cerebellar Purkinje cells to acetaldehyde during fetal, neonatal or adult life has been assessed by histological techniques. A pregnant female rat was exposed to ethanol vapour during the last 2 weeks of gestation while metabolism of acetaldehyde was blocked by injections of disulfiram (200mg/kg) on days E14, E16, E18 and E20. Purkinje cells were counted in the offspring 5 days after birth. The number of Purkinje cells in lobes I and VIII were 52% and 42% less than age matched controls. Smaller reductions were found in lobes V and X. The weight of the cerebellum was reduced by 42%. Neonatal rats received disulfiram (40mg) on the second day after birth and were exposed to ethanol vapour during daylight hours on the third and fourth days. Purkinje cells were counted at 5 days after birth, and losses similar to those described above were found. The weight of the cerebellum was reduced by 47%. Adult male rats were exposed to ethanol vapour for 2 weeks and given disulfiram (200mg/kg) on every second day. No reduction in cerebellar weight or loss of Purkinje cells was detected. When the dura overlying the cerebellum in adult rats was superfused with acetaldehyde solutions for 1 h, a 1–6 M solution caused degeneration whereas a 0–68 M solution did not. Thus the combination of high blood ethanol and acetaldehyde levels is damaging to perinatal Purkinje cells, whereas adult cells are resistant. We found the same ranking of susceptibility with ethanol alone (Philips & Cragg, 1982a and it was surprising that the cell losses with acetaldehyde were only marginally greater than those with ethanol alone, in view of the greater neurotoxicity of acetaldehyde during acute exposure (Phillips, 1981.
THE EFFECTS OF ACRYLAMIDE ON β‐GLUCURONIDASE AND ACID PHOSPHATASE ACTIVITIES IN RAT SCIATIC NERVE ABOVE AND BELOW A LIGATURE
Authors: CAVANAGH J. B. , NOLAN C. C.
Published: May 2008

Cavanagh J.B. & Nolan C.C. 1982 Neuropathology and Applied Neurobiology 8, 465–476

The effects of acrylamide on β‐glucuronidase and acid phosphatase activities in rat sciatic nerve above and below a ligature

The enzymes β‐glucuronidase and acid phosphatase have been assayed by histochemical and by fluorimetric methods above and below a tightly tied ligature on the rat sciatic nerve over the subsequent 10 days. These findings have been compared with similarly treated animals also given four daily doses of acrylamide (50 mg/kg). The following have been found:

1 during this time, acrylamide at this dose causes slight increases in β‐glucuronidase in untied sciatic nerves, detectable both histochemically and fluorimetrically;

2 below the ligature both enzyme activities were greatly increased and this was slightly reduced in the acrylamide‐dosed animals;

3 there was a mild rise in β‐glucuronidase activity in the 10 cm above the ligature in undosed animals demonstrable both histochemically and fluorimetrically;

4 that in the acrylamide‐dosed animals there was a marked rise in β‐glucuronidase activity both 10 cm and 20 cm above the ligature which was intensified at 7 days and at 10 days after dosing. This was demonstrated both histochemically and fluorimetrically.

These results are discussed in the light of the known sheath cell and axonal responses to acrylamide intoxication.
A METHOD FOR DETERMINING TENTORIAL HERNIATION IN CLOSED‐HEAD INJURY FROM A QUANTITATIVE ESTIMATION OF CEREBRAL TRAUMA
Authors: GIBSON P. H.
Published: May 2008

Gibson P.H. 1982 Neuropathology and Applied Neurobiology 8, 489–493

A method for determining tentorial herniation in closed‐head injury from a quantitative estimation of cerebral trauma

Cerebral damage in 42 cases involving closed‐head injury was studied post mortem. The cases were divided into those that showed tentorial herniation and those that did not on the basis of the clinical histories and examination of the intact brains at autopsy. Damage seen histologically in coronal sections through the cerebral hemispheres and brain‐stem was recorded on diagrams. The area of damage was quantified by placing over the diagrams a cm2 grid. The numbers of squares with damage in, length of survival following the accident and the age of the cases were found by a ranking method to be statistically significantly different in herniated and non‐herniated cases. These three parameters were used in an empirically derived expression to give an index that was statistically significantly different for herniated and non‐herniated cases. The purpose of the index was to obtain an objective method of assessing the degree of tentorial herniation in brain‐stem damage resulting from herniation.
THE NEUROPATHY RESULTING FROM MUSCLE‐NERVE TRANSLOCATION
Authors: DUNCAN I. D.
Published: May 2008

The biceps femoris muscle was cut close to its distal tendon in seventeen rats, inserted under the partially freed sciatic nerve and the muscle then resutured leaving the nerve in a translocated position. The rats were killed at intervals from 4 to 22 weeks later and the sciatic nerve above, around, and below the muscle reflection site examined by light and electron microscopy and teased fibre preparations. In all cases, the sciatic nerve was affected to varying degrees at its reflected site ranging from focal sub‐perineurial demyelination and remyelination to widespread myelin sheath abnormalities. Teased fibre studies confirmed that the myelin sheath was predominantly affected with little evidence of active axonal degeneration. There was no proximal and minimal distal sciatic nerve damage. The most likely cause of these changes was thought to be focal compression but the possible role of other factors is also discussed.
CELL PROLIFERATION AND DNA‐SYNTHESIS IN THE EXTERNAL GRANULAR LAYER OF THE POSTNATAL RAT CEREBELLUM: A QUANTITATIVE STUDY
Authors: KOPPEL H. , LEWIS P. D.
Published: May 2008

The external granular layer (EGL) of the rat cerebellum can be subdivided into two morphologically distinct zones, the outer of which consists of proliferating cells, while the inner has generally been considered to contain post‐mitotic cells exclusively. Two criteria, the detection of mitotic figures and the observation of nuclei labelled shortly after an injection of [3H]‐thymidine, were used to locate proliferating cells. Their distribution across the layer was quantified for several ages of animal. Though most frequent superficially, cell proliferation was found to occur at all levels of the EGL. Possible explanations for the existence of a gradient of proliferative activity across the EGL are discussed.
CHRONIC RELAPSING EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS: CEREBROSPINAL FLUID CYTOLOGY AND A COMPARISON WITH MENINGEAL AND SPINAL CORD PATHOLOGY
Authors: SUCKLING A. J. , WILSON N. R. , KIRBY J. A. , RUMSBY M. G.
Published: May 2008

Cerebrospinal fluid (CSF) was taken from strain 13 guinea pigs in various stages of chronic relapsing experimental allergic encephalomyelitis, the spinal cords removed for histological examination and meningeal stretch preparations made. CSF cells were counted and characterized by morphological studies, anti‐IgG and alpha‐naphthyl acetate esterase (ANAE) staining. Approximately 65% of normal CSF lymphocytes were ANAE positive and 10% stained with anti‐IgG. No polymorphonuclear leucocytes were seen. Five out of eight relapsing animals had raised cell counts (up to 152/μl) as did three animals in remission. There was no change in the proportion of various types of CSF cells where increased numbers were recorded. Infiltrating cells in spinal cord sections and meningeal preparations were similarly characterized and the results compared with CSF cell findings. Animals in relapse which had, in addition, macroscopically visible cord plaques showed the most severe infiltrative changes in spinal cord tissue and in the meninges. There were differences between the proportion of various types of CSF cells and meningeal infiltrate cells on ANAE staining reaction. In general there were far more lymphocyte‐type cells in the CSF but more monocyte‐type cells in meningeal infiltrates.