bluuebunny/crossref_metadata_2025 huggingface dataset:
QUANTITATIVE STUDIES OF MUSCLES TRANSPLANTED BETWEEN NORMAL AND DYSTROPHIC MICE
Authors: NEERUNJUN J. S. , DUBOWITZ V.
Published: May 2008

Quantitative studies of muscles transplanted between normal and dystrophic mice

Auto‐ and heterotransplants of minced tibialis anterior muscle in normal and dystrophic mice, with and without polydimethyl silicone‐capped (PDS) nerve, were examined at 150 days and the following morphological features quantitated: weights of transplants, total number of fibres, frequency and diameter of Type 1 and 2 fibres, number of fibres with internal nuclei, frequency of fibres undergoing splitting, degeneration and regeneration, and the amount of connective tissue. Similar studies were made on intact 150 day old normal and dystrophic muscles. In the intact animals there was no significant difference between male and female muscles, but dystrophic muscles were smaller and contained more connective tissue and fibres showing internal nuclei, splitting, degeneration and regeneration. The diameter of fibres was larger in male muscle of normal and female muscle of dystrophic mice. All 150 day old transplants in normal mice with PDS‐capped nerve and dystrophic mice consisted entirely of connective tissue. Only transplants in normal mice with intact nerve were viable. Both normal and dystropic transplants were smaller than unoperated normal muscle but their fibres differentiated normally and showed less variation in size than those of intact dystrophic muscle. They also contained some fibres with internal nuclei and fibres undergoing splitting. The data indicate that under the influence of the normal nerve dystrophic transplants fare just as well and are quantitatively similar to normal transplants. It is suggested that the motor nervous system plays an important role in the pathogenesis of murine dystrophy.
THE RELATIONSHIP BETWEEN VENTRICULAR FLUID PRESSURE AND THE NEUROPATHOLOGY OF RAISED INTRACRANIAL PRESSURE
Authors: ADAMS J. HUME , GRAHAM D. I.
Published: May 2008

The relationship between ventricular fluid pressure and the neuropathology of raised intracranial pressure

The brains from 56 patients whose ventricular fluid pressure had been continuously monitored during life have been subjected to a neuropathological analysis. This has shown that the morphological criterion of a significantly high intracranial pressure during life is pressure necrosis in one or both parahippocampal gyri. In patients known to have had a high ventricular fluid pressure, there is also a high incidence of pressure necrosis in the cingulate gyrus and infarction in the medial occipital cortex (‘calcarine infarction’), but these changes do not occur in the absence of pressure necrosis in the parahippocampal gyri. Conventional maeroscopic tentorial and supracallosal herniae may occur without the intracranial pressure having been high. There was no correlation between pressure necrosis in the parahippocampal gyri and hypoxic necrosis in the hippocampus: this suggests that a high intracranial pressure is not an important factor in the pathogenesis of such hypoxic necrosis. It is concluded that the neuropathologist can state with a high degree of accuracy post mortem if intracranial pressure has been significantly high, i. e. an increase associated with a pressure differential between the supratentorial and infratentorial compartments, even when it has not been monitored clinically.
ACCUMULATIONS OF NOR‐ADRENALINE ASSOCIATED WITH AXONAL CHANGES IN AUTONOMIC GANGLIA IN GRASS SICKNESS
Authors: GILMOUR J. S.
Published: May 2008

Stellate ganglia from cases of grass sickness and control horses were examined, using the formaldehyde‐induced fluorescence method, for the presence of catecholamines. Accumulations of a catecholamine, identified as nor‐adrenaline, were observed in nerve fibre tracts within ganglia of horses with grass sickness. On the grounds of site and morphology these accumulations conform with axonal lesions seen in silver‐stained sections. The changes were compared with the results of experimental trauma to adrenergic nerves, and it was deduced that there is a primary axonal lesion in grass sickness. It was further suggested that this lesion may be caused by the neurotoxin already implicated in the disease.
NEUROFIBRILLARY TANGLES AND THE PATHOGENESIS OF DEMENTIA: A QUANTITATIVE STUDY
Authors: BALL M. J.
Published: May 2008

A morphometric technique employing Congo red staining and scanning light microscopy with appropriate filters provided a sensitive sampling method for counting hippocampal neurons bearing neurofibrillary tangles in serially sectioned temporal lobes from mentally normal subjects of different ages as well as from demented patients. The number of tangled neurons per mm3 of cortex was compared with patients' ages. Tangle formation in controls increased only slightly with age; whereas the ‘Tangle Index’ of cases with the organic dementia of Alzheimer's disease exceeded by many times that of age‐matched controls. The posterior portion of the hippocampus was found to be more susceptible to this augmented neurofibrillary degeneration than the anterior part of the hippocampus of demented subjects.
EFFECTS OF UNDERNUTRITION DURING THE SUCKLING PERIOD ON GROWTH OF THE ANTERIOR AND POSTERIOR LIMBS OF THE MOUSE ANTERIOR COMMISSURE
Authors: STURROCK R. R. , SMART J. L. , DOBBING J.
Published: May 2008

The anterior and posterior limbs of the anterior commissure were examined quantitatively in normal mice, and mice undernourished during the suckling period. There was no change in the mean length of the anterior commissure in either group. The total number of axons, the percentage of myelinated axons, and the mean number of myelin lamellae remained unchanged between each group in both limbs. There was, however, a highly significant fall in the total number of cells in both the anterior (P<0·001) and posterior (P<0·001) limbs, mainly in the oligodendrocyte fraction of the population. There was no change in the relative proportion of cells in each limb. The cross‐sectional area of both the limbs was significantly less in the undernourished animals, with the posterior limb being affected more than the anterior limb. These differences were found to be due to a significant (P<0·001) fall in the mean diameter of myelinated axons in the anterior limb and to a significant (P<0·001) fall in the mean diameter of unmyelinated axons in posterior limb. The mean diameters of the unmyelinated axons in the anterior limb, and of the myelinated axons in the posterior limb remained unchanged. The possible reasons for these changes, and their place in the general pathology of deficits and distortions following early undernutrition are discussed.
ANTIGENICITY OF ETHYLNITROSOUREA INDUCED RAT SCHWANNOMAS ASSAYED BY IN VITRO LYMPHOCYTOTOXICITY
Authors: RAINBIRD SUSAN , RIDLEY A.
Published: May 2008

The antigenicity of six ENU‐induced schwannomas was investigated in two strains of rats using transplantation procedures and an in vitro lymphocytotoxicity assay. Onby one of the six tumours was sufficiently antigenic to give rise to tumour immunity as judged by transplantation. Lymphocytes from animals inoculated with this tumour were cytotoxic for tumour cells grown in culture. Of the remaining tumours, one showed some degree of lymphocytotoxicity but this was not associated with any transplantation immunity. The significance of these findings is discussed.
THE EFFECTS OF MITOMYCIN C ON THE PROCESS OF REGENERATION IN THE MAMMALIAN PERIPHERAL NERVOUS SYSTEM
Authors: HALL SUSAN M. , GREGSON N. A.
Published: May 2008

Schwann cell proliferation is a prominent feature of the normal response of a peripheral nerve fibre bundle to injury. In this report we have attempted to analyse the consequence of inhibiting this response using the cross‐linking alkylating agent mitomycin C. In the presence of the drug, Schwann cell division was inhibited within a region about the site of injection. In this region myelin breakdown was delayed relative to that occurring distally and in control fibres: even after 3 weeks many Schwann cells had failed to phagocytose their myelin. Regeneration subsequently took place—certain morphological features of the repaired mitomycin C‐treated zones are discussed. It is concluded that dilution of debris by successive Schwann cell divisions is necessary during the cellular response to injury in a peripheral nerve fibre bundle.
THE EVOLUTION OF ‘ONION BULBS’ IN THE HEREDITARY HYPERTROPHIC NEUROPATHY OF THE TREMBLER MOUSE
Authors: LOW P. A.
Published: May 2008

The evolution of ‘onion bulbs’ was studied ultrastructurally in the dominantly inherited hypertrophic neuropathy of the Trembler mouse. Demyelination was prominent in the peripheral nerves of mice aged 7 days to 4 weeks. Following demyelination, the Schwann cell divided. One Schwann cell captured the axon while the supernumerary Schwann cell produced many sprouts which were delimited by the original basement membrane which later became discontinuous. While the central (adaxonal) Schwann cell had abundant cytoplasm with a normal content of organelles, degenerative changes were evident in the supernumerary more peripheral Schwann cell sprouts. Cytoplasm degenerated from these, and left behind empty membrane configurations which assumed an approximately circumferential orientation. As more ‘onion bulb’ lamellae were added, a morphological gradation became evident; the outer lamellae were more degenerate than the inner ones. Pari passu with the formation of ‘onion bulbs’, endoneurial collagen fibrils increased in number and marked variations in calibre, and frequently islands of microfibrils, were seen in older Tremblers. The axon in older animals underwent changes in contour, with an increase in neurofilaments and decrease in neuro‐tubules.
THE GROWTH OF TWO SSPE VIRUSES IN ORGANOTYPIC CULTURES OF HAMSTER DORSAL ROOT GANGLIA
Authors: ECOB‐JOHNSTON MARION
Published: May 2008

Two isolates of subacute sclerosing panencephalitis virus (LEC and HallB) were used to infect organotypic cultures of hamster dorsal root ganglia. Virus replication was assessed using indirect immunofluorescence, histological staining, and virus production. Using these criteria, the LEC isolate did not infect the cultures, but the Hallé virus establihed a productive infection. Schwann cells appeared to be the initial site of infection from where virus spread to every cell in the culture by 11 days post‐inoculation (p.i.), except the neurons and their associated satellite cells, both of which contained no antigen and appeared histologically to be the same as controls even at 15 days p.i. The results are discussed with reference to the growth of measles virus in hamster dorsal root ganglia and the usefulness of this system as a model for subacute sclerosing panencephalitis.
POLYNEUROPATHIES AND CNS PROTEIN METABOLISM. I. DESCRIPTION OF THE ACRYLAMIDE SYNDROME IN RATS
Authors: GIPON L. , SCHOTMAN P. , JENNEKENS F. G. I. , GISPEN W. H.
Published: May 2008

Behavioural, histological and metabolic studies were performed on acrylamide‐intoxicated rats. Treated rats showed disturbed food and water consumption accompanied by loss of body weight. In addition, in an open field test they displayed less ambulation and rearing activity than controls, and had severe difficulties in balancing on a rotating rod. The last test gives a reliable indication of the acryla‐mide‐induced disorder before the onset of histological changes. In the discussion it is suggested that the data question the neurotoxic selectivity of acrylamide.
MECHANISMS INVOLVED IN THE ‘DYING‐BACK’ PROCESS—AN HYPOTHESIS IMPLICATING COENZYMES
Authors: SCHOENTAL R. , CAVANAGH J. B.
Published: May 2008

Annotation. Mechanisms involved in the ‘dying‐back’ process—an hypothesis implicating coenzymes

Attention is drawn to the occurrence of the ‘dying back’ type of neuronal degeneration in several vitamin deficiencies and in many toxic neuropathies. It is suggested, hypothetically, that these toxic substances may be inactivating or in other ways interfering with the function of cofactors in the axons of peripheral nerves. It is further suggested from this that the distal distribution of the axonal lesions in such toxic neuropathies may depend upon the distance from the source of materials and of enzymes that would normally be derived from the cell soma for the synthesis and supply of new cofactors upon which survival of the axon will depend. This hypothesis suggests a number of different experimental approaches to this basic neuronal lesion.
NEUROGLIA IN THE INTERNAL GRANULAR LAYER OF THE DEVELOPING RAT CEREBELLAR CORTEX
Authors: LEWIS P. D. , FüLÖP Z. , HAJÓS F. , BALÁZS R. , WOODHAMS P. L.
Published: May 2008

Neuroglia in the internal granular layer of the developing rat cerebellar cortex

In the first week after birth, a proliferating cell population identifiable as astrocytes is a prominent constituent of the developing internal granular Layer of the rat cerebellar cortex. This population becomes less prominent in the second postnatal week, and by 12 days proliferation within it has fallen to a low level. At 6 days, the dividing astrocytes of the internal granular layer have a cell cycle time of 19.5 h and an estimated turnover time of between 36 and 72 h. These figures are comparable to those obtained for other proliferating cell populations in the 6 day old brain, and contrast with previously published data suggesting much slower rates of neuroglial division in the early postnatal cerebellum.
EFFECTS OF METHYLMERCURY ON IN VIVO PROTEIN SYNTHESIS IN ISOLATED CEREBRAL AND CEREBELLAR NEURONS
Authors: SYVERSEN T. L. M.
Published: May 2008

Effects of methylmercury on in vivo protein synthesis in isolated cerebral and cerebellar neurons

A preparative method is described for the bulk isolation of two neuronal populations from cerebellum, namely the granule cell and Purkinje cell bodies. This isolation method was used for studying in vivo effects of methylmercury on protein synthesis. The experimental rats were given a single i.p. dose of 10 mg/kg methylmercury. Mercury levels are reported in blood, total brain, cerebral neurons and two cerebellar neuron populations. The methylmercury was shown to inhibit incorporation of radioactive leucine into protein. The time course and degree of inhibition were dependent on cell type. The highest inhibition was found in neurons which are morphologically the most mercury sensitive species of the cells tested.
PRIMARY AMYLOIDOSIS WITH INVOLVEMENT OF THE PERIPHERAL NERVOUS SYSTEM
Authors: HORDER JOAN M. , TREIP C. S.
Published: May 2008

Primary amyloidosis with involvement of the peripheral nervous system

An unusual case of primary amyloidosis with peripheral neuropathy, due to severe involvement of the peripheral nerves and posterior root ganglia, is described. The possible significance of the changes in the posterior root ganglia is discussed. The sympathetic nervous system was also severely involved, although disturbances of autonomic function were slight.
PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY: ULTRASTRUCTURAL FINDINGS IN TWO BRAIN BIOPSIES
Authors: MAZLO MARIA , HERNDON R. M.
Published: May 2008

Progressive multifocal leukoencephalopathy: ultrastructural findings in two brain biopsies

Cerebral biopsies from two patients with progressive multifocal leukoencephalopathy due to SV40 (Case 1) and JC viruses (Case 2) have been examined by light and electron microscopy. No features permitting the morphologic differentiation of the diseases caused by the two agents were found. In the first case, intranuclear viral inclusions were seen in satellite oligodendrocytes in the cerebral cortex as well as in oligodendrocytes in the white matter. In this case demyelination developed in the absence of an inflammatory response. Extensive oligodendrocyte proliferation was evident, and phagocytosed myelin debris was found in both oligodendrocytes and astrocytes. In the second case extensive perivascular and tissue infiltration with plasma cells and evidence of viral multiplication in astrocytes were found. Demyelination occurred in the absence of macrophages in the first case which supports the conclusion that the demyelination in PML is due to the cytolytic effect of the virus on oligodendrocytes and is not an immunopathologic process.
EFFECT OF UNDERNUTRITION DURING THE SUCKLING PERIOD ON THE INDUSIUM GRISEUM AND ROSTRAL PART OF THE MOUSE ANTERIOR COMMISSURE
Authors: STURROCK R. R. , SMART J. L. , DOBBING J.
Published: May 2008

Effect of undernutrition during the suckling period on the indusium griseum and rostral part of the mouse anterior commissure

The indusium griseum and rostral part of the anterior limb of the anterior commissure were examined quantitatively in normal mice and in mice undernourished during the suckling period and subsequently rehabilitated. Both groups were examined at 5 months of age. In the indusium griseum no significant difference was found between the number of neurons or neuroglia in the well‐nourished and undernourished animals. There was a large decrease in the number of glia in the rostral part of the anterior limb which also showed a decrease in length and cross‐sectional area. These results confirm that the effects of undernutrition are most marked in areas in which growth is maximum during the period of stress.
AXONAL AND DORSAL ROOT GANGLION CELL CHANGES IN EXPERIMENTAL ALLERGIC NEURITIS
Authors: KING R. H. M. , THOMAS P. K. , POLLARD J. D.
Published: May 2008

King R.H.M., Thomas P.K. & Pollard J.D. (1977) Neuropathology and Applied Neurobiology 3, 471486

Axonal and dorsal root ganglion cell changes in experimental allergic neuritis

Observations have been made on experimental allergic neuritis in guinea pigs induced by the inoculation of rabbit sciatic nerve combined with Freund's adjuvant. Axonal lesions were observed most often in the later stages of the acute disease and in animals with a chronic relapsing course. They consisted of axonal interruption and regeneration, and ‘reactive’ axonal changes in demyelinated and remyelinated fibres, and in fibres of normal appearance that may have possessed lesions at some other point along their course. Abnormalities were not detected in anterior horn cells. Loss of dorsal root ganglion cells was rare, but invasion of the cells by lymphocytes which were present within large intracellular vacuoles, was at times conspicuous. The axonal and dorsal root ganglion cell changes may represent a ‘bystander’ effect in a cell‐mediated delayed hypersensitivity reaction.
STUDY OF AXONAL DYSTROPHY. I. PATHOLOGY OF THE NEUROPIL OF THE GRACILE AND THE CUNEATE NUCLEI IN AGEING AND OLD RATS: A STEREOLOGICAL STUDY
Authors: FUJISAWA K. , SHIRAKI H.
Published: May 2008

The changes with age in the neuropil of the gracile and the cuneate nuclei of rats were studied using stereological techniques, in relation to the occurrence of axonal dystrophy. The following were found: (1) significant difference in the volume fraction of presynaptic boutons between the gracile and the cuneate nuclei throughout the whole life span (17% and 13% respectively at 100 days of age); (2) progressive decrease in the volume fraction (34% decrease in the gracile nucleus between 100 and 800 days of age) and in the numerical density of presynaptic boutons, the decline being evident as soon as the animals reached maturity and before axonal dystrophy became manifest; (3) significant differences in the volume fractions of dendrites and of nerve cell bodies between the two nuclei throughout the whole life span of the animals, both being greater in the cuneate than in the gracile nucleus; an agerelated decrease in the volume fraction of dendrites was also suspected in the gracile nucleus; (4) progressive increase in the volume fraction of fibrous astrocytic processes (from 3% at 100 days to 10.5% at 800 days in the gracile nucleus); (5) the above described age‐related changes of presynaptic boutons and fibrous astrocytic processes were significant only in the gracile nucleus, not in the cuneate. The loss of boutons in ageing gracile nuclei was partially reflected in the appearance of degenerating nerve fibres in ageing gracile tract in the rostral cervical cord. Involutional loss of boutons and dystrophic formation of spheroids both appear and progress closely related in time and space. It was suggested that this set of changes can be understood as one integrated whole in which axonal dystrophy may represent only one side of the coin. The question of the causal mechanism of axonal dystrophy still remains unanswered.
GLIAL OUTGROWTH AND CENTRAL‐TYPE MYELINATION OF REGENERATING AXONS IN SPINAL NERVE ROOTS FOLLOWING TRANSECTION AND SUTURE: LIGHT AND ELECTRON MICROSCOPIC STUDY IN THE PIG
Authors: MEIER C. , SOLLMANN H.
Published: May 2008

Glial bundles growing out of the spinal cord were observed in spinal nerve roots in the pig after their section and surgical repair. The heterotopic occurrence of glial cells, most of which were identified as astrocytes, was more frequent and more pronounced in dorsal than in ventral roots. Several of the glial bundles contained regenerated myelinated axons. These were probably myelinated by cells which showed the typical cytological criteria for oligodendrocytes and the mode of myelination was clearly of central type. It was concluded that the glial outgrowth is induced by degeneration and regeneration of axons passing the central–peripheral transition zone.
PROGNOSTIC FACTORS IN RUPTURED ANEURYSMS OF THE CIRCLE OF WILLIS: THE SIGNIFICANCE OF SYSTEMIC HYPERTENSION
Authors: FRANKS A. J.
Published: May 2008

The incidence of essential hypertension has been retrospectively studied in a group of sixty‐four fatal cases of ruptured berry aneurysm, and compared with a non‐fatal group. Hypertension is more frequent in the fatal group, and is associated with a higher incidence of multiple aneurysms, a smaller size of aneurysm at rupture and a poorer survival after two haemorrhages when comparison is made with normotensive patients. The possible role of hypertension in the development and rupture of aneurysms is discussed, and it is concluded that it may contribute to both. Following rupture it carries a poor prognosis with a resulting over emphasis of its significance in autopsy series. Possible mechanisms for this effect include diffuse vascular disease, and an increased liability to oedema or spasm following rupture of an aneurysm.
THE SCHWANN CELL: A REAPPRAISAL OF ITS ROLE IN THE PERIPHERAL NERVOUS SYSTEM
Authors: HALL SUSAN M.
Published: May 2008

The Schwann cell is clearly essential for the maintenance of axonal integrityyet we know little of the regulatory mechanisms governing its behaviour at any point in its life cycle, or of the nature of its interaction with the axons with which each Schwann cell is associated. In this article, the involvement of the Schwann cell in myelinogenesis, aspects of Schwann cell‐axon recognition, the experimentally‐demonstrable ‘bipotentiality’ of the Schwann cell and the possible functional significance of the proliferative response of the Schwann cell that occurs after injury are discussed. The isolation and preparation of pure populations of Schwann cells which can be injected or implanted into a damaged nerve, coupled possibly with the localized application of drugs to manipulate the cellular responses to injury within the nerve, represent interesting areas of recent research which may be applied in planning methods of therapeutic intervention in the treatment of peripheral nerve injury.
CELLULAR REACTIONS TO SUBEPENDYMAL PLATE HAEMORRHAGE IN THE HUMAN NEONATE
Authors: SHERWOOD ANTHEA , HOPP ANN , SMITH J. F.
Published: May 2008

The most important cause of death in human premature babies at the present time is intraventricular haemorrhage consequent to haemorrhage in the subependymal plate. Lesser degrees of plate haemorrhage can also have serious effects. It was possible to observe the reaction to such haemorrhages in twenty‐seven cases whose range of gestational age extended from 23 to 36 weeks and survival from 4 to 59 days. The haemorrhage occurs in the first week of life, usually in the first few days. The earliest reaction at 4 days was the presence of mononuclear phagocytes around the haemorrhage, these evolved to iron pigment macrophages which were present in eighteen of the twenty‐two cases in which some reaction was detected. Subependymal astrocytic proliferation was seen at 11 days, related to ependymal disruption, but an astrocytic reaction around the haemorrhage and related to it was not seen until 14 days. Within the subependymal plate this reaction was scanty in fibril production and the cells were thought to be derived from differentiating astrocytes in the plate. In one case a more marked reaction was detected to hypoxic damage in the adjacent thalamus. The source of the phagocytes in these sites and the reasons for the rather slow astrocytic reaction are discussed.
INTRACELLULAR SERUM PROTEINS IN CEREBRAL GLIOMAS AND METASTATIC TUMOURS: AN IMMUNOPEROXIDASE STUDY
Authors: BRETT MARY , WELLER R. O.
Published: May 2008

An immunoperoxidase technique was used to compare the presence of serum proteins in tumour cells in twenty cerebral gliomas and four intracerebral metastatic carcinomas, with the serum protein content of reactive astrocytes around four cerebral infarcts. Rabbit antiserum to human immunoglobulins and albumen was applied to paraffin sections of tumour biopsies and of infarcts from postmortem brains. All the reactive astrocytes surrounding infarcts stained positively for immunoglobulins and albumen. In the gliomas, a continuous range of staining was observed in plump astrocytic tumour cells varying from strongly positive to unstained. Very few poorly‐differentiated glioma cells stained for serum proteins; metastatic tumour cells, areas of capillary endothelial proliferation, and spindle cells in gliosarcomas remained unstained. These results suggest that the astrocytic function of serum protein uptake from the extracellular fluid is often lost in poorly‐differentiated glioma cells, but is retained to a variable degree by those tumour cells which histologically resemble reactive astrocytes.
CHANGES IN BRAIN CHOLINESTERASES IN SENILE DEMENTIA OF ALZHEIMER TYPE
Authors: PERRY ELAINE K. , PERRY R. H. , BLESSED G. , TOMLINSON B. E.
Published: May 2008

Acetyl‐ and butyryl‐cholinesterase activities have been measured biochemically in normal brain tissue, in senile dementia of Alzheimer type and in mental disorders without Alzheimer‐type abnormalities. Acetylcholinesterase was significantly reduced and butyrylcholinesterase significantly increased, compared with the normal, in the hippocampus and temporal cortex of the Alzheimer cases. No significant enzyme changes were seen in the other diseases investigated including multi‐infarct dementia, schizophrenia and depression. There was no correlation between age and acetylcholinesterase activity, but a significant positive correlation between the butyrylcholinesterase activities with increasing age (60–90 years) was found in the hippocampus. The possible connection between cholinergic system pathology and these cholinesterase abnormalities in Alzheimer dementia is discussed.
THE QUANTITATIVE ASSESSMENT OF LIPOFUSCIN PIGMENT, CYTOPLASMIC RNA AND NUCLEOLAR VOLUME IN SENILE DEMENTIA
Authors: MANN D. M. A. , SINCLAIR K. G. A.
Published: May 2008

Treatment of patients suffering from senile dementia with meclofenoxate has been reported to result in an improvement in mental performance. Furthermore meclofenoxate reduces the amount of lipofuscin pigment in nerve cells. We have shown that, although nerve cells in a group of demented patients have decreased amounts of cytoplasmic RNA and reduced nucleolar volume, they contain no more pigment than do cells of a control group. It seems, therefore, unlikely that removal of lipofuscin, per se, has any bearing on this reported improvement in intellectual capability, nor is it implicated in the aetiology of senile dementia.
THE FINE STRUCTURE OF THE CNS IN MULTIPLE SCLEROSIS. I. INTERPRETATION OF CYTOPLASMIC PAPOVAVIRUS‐LIKE AND PARAMYXOVIRUS‐LIKE INCLUSIONS
Authors: KIRK J. , HUTCHINSON W. M.
Published: May 2008

During an electron microscopic study of the white matter in multiple sclerosis (MS), spheroidal reticular particles were found both in MS and in control brains. These particles have previously been described in the brain in MS and in brain‐derived cell cultures in subacute sclerosing panencephalitis. In both cases they were interpreted as papovaviruses, but in size, morphology and distribution they are identical to the reticulosomes and related particles which occur as proteinaceous artefacts in a variety of tissues and in subcellular fractions. Inclusions in endothelial cell cytoplasm, previously reported from the CNS in MS as paramyxovirus similar to measles, have also been found in the present study. They were present both in MS and in control brains and are identified as ‘rod‐shaped tubular bodies’, normally occurring organelles of endothelial cells. The necessity for a cautious interpretation of virus‐like inclusions is emphasized.
PRIMARY DEMYELINATION IN CAT OPTIC NERVES ASSOCIATED WITH SURGICALLY INDUCED AXONAL DEGENERATION
Authors: COOK R. D.
Published: May 2008

Localized Wallerian degeneration was induced in cat optic nerves by the gentle scratching of the exposed retinas. At intervals ranging up to 103 days after operation, the cats were killed and microscopic examination of the optic nerves showed, in addition to axonal degeneration, the presence of both demyelinating and demyelinated normal axons. The tongues of oligodendroglial cytoplasm were still associated with these demyelinated axons. This phenomenon is considered to reflect a change in the homeostasis of the oligodendroglial cell imposed by degeneration of a few axons from a state of maintaining the myelin sheath to one of resorption from adjacent normal axons. No evidence for the involvement of microglia in this process was found. It is concluded also that oligodendrocytes alone can be responsible for the removal of myelin debris during Wallerian degeneration. This observation may be important to the understanding of certain demyelinating diseases of the central nervous system.
ULTRASTRUCTURE OF THE MUSCLE SPINDLE IN DYSTROPHIA MYOTONICA. I. THE INTRAFUSAL MUSCLE FIBRES
Authors: STRANOCK S. D. , DAVIS J. NEWSOM
Published: May 2008

The abnormal intrafusal muscle fibres of four spindles located in extensor indicis biopsies from two patients with dystrophia myotonica have been examined by electron microscopy. In all cases, the fibres had undergone severe longitudinal fragmentation in their equatorial, proximal‐polar and mid‐polar zones. It was not possible to differentiate the fibres into nuclear bag and nuclear chain types. Many of the fragments were arranged in clusters, each cluster being bounded by a single basement membrane. Numerous partially divided fibres were seen in mid‐polar sections, and a morphological picture of the fragmentation process has been presented. The ultrastructural appearance of individual fibre fragments ranged from normality through to severe atrophy. Intrafusal satellite cells showed an increase in numbers, presumably in response to the pathological processes affecting the muscle fibres. The nature of this response is discussed.
ULTRASTRUCTURE OF THE MUSCLE SPINDLE IN DYSTROPHIA MYOTONICA. II. THE SENSORY AND MOTOR NERVE TERMINALS
Authors: STRANOCK S. D. , DAVIS J. NEWSOM
Published: May 2008

The normal pattern of innervation was lost in the four dystrophia myotonica muscle spindles examined. There had been a proliferation of both sensory and motor nerve terminals, and many endings showed varying degrees of structural abnormality. The changes seen in the sensory nerve endings were an incomplete contact relationship between the terminal and the muscle fibre, the association of Schwann cell processes with the nerve ending, abnormal shape of the terminal, multiple sensory endings, and changes in the ultrastructural organization of the terminal axoplasm. Remnants of degenerated sensory terminals, and isolated sensory endings were also seen. Motor nerve terminals varied in size and shape. In general, they contained a normal complement of vesicles and mitochondria. Junctional folding was often absent or simplified, and sarcoplasmic specialization was, at the most, rudimentary. The relationship between these changes and intrafusal muscle fibre fragmentation is discussed.
THE CELLULAR ORIGIN OF LYSOSOMAL ENZYMES IN THE PLAQUE IN MULTIPLE SCLEROSIS: A COMBINED HISTOLOGICAL AND BIOCHEMICAL STUDY
Authors: McKEOWN STEPHANIE R. , ALLEN INGRID V.
Published: May 2008

Using a combined biochemical and histological approach certain conclusions can be drawn as to the origin of the increase in lysosomal enzymes in white matter from MS brains. Firstly, there is a gradient of lysosomal enzyme activity, plaque> periplaque > macroscopically normal white matter, which appears to be independent of the stage of evolution of the plaque. The most consistent change in cellular composition within and around all plaques is a marked astrocytosis. It thus appears that the increases in lysosomal enzymes can be mainly attributed to reactive astrocytes; macrophages and the cells of the perivascular infiltrate making only a limited contribution. Secondly, only one of the enzymes tested was significantly elevated in histologically normal white matter, i. e. n‐acetyl‐β‐D‐glucosaminidase. Since this enzyme appears to be a particularly sensitive marker for astrocytes this may be indicative of proliferation of astrocytes in so‐called normal white matter.
VACUOLATION IN THE HUMAN CEREBRAL CORTEX AND ITS RELATIONSHIP TO THE INTERVAL BETWEEN DEATH AND AUTOPSY AND TO SYNAPSE NUMBERS: AN ELECTRONMICROSCOPIC STUDY
Authors: GIBSON P. H. , TOMLINSON B. E.
Published: May 2008

Gibson P.H. & Tomlinson B.E. (1979) Neuropathology and Applied Neurobiology5, 1–7

Vacuolation in the human cerebral cortex and its relationship to the interval between death and autopsy and to synapse numbers: an electron microscopic study

Vacuolation in the human cerebral cortex resulting from swelling of cell processes after death was measured in electron micrographs in material obtained up to 69 hours post mortem from subjects with no known neurological abnormality. Vacuolation was found to increase significantly up to 30–35 hours after death and then to decrease. Accompanying this change was a significant reduction in the numbers of recognizable synapses which probably resulted from compression due to the vacuolation rather than from post‐mortem disintegration.
RESTITUTION OF BROMODEOXYURIDINE‐INDUCED CHANGES IN CEREBELLAR DEVELOPMENT
Authors: YU WAN‐HUA AMY
Published: May 2008

Yu W‐H. A. (1979) Neuropathology and Applied Neuropathology5, 41–48

Restitution of bromodeoxyuridine‐induced changes in cerebellar development

Previously, it was shown that bromodeoxyuridine (BrdU) in 2‐day‐old rats caused hypoplasia of the external cerebellar granular layer. Significant restitution was achieved after removal of BrdU by an increase in the rate and duration of prolifer‐ative activity of the EGL cells, but abnormal cerebellar cytoarchitecture remained detectable at 35 days of age due mainly to polarity changes in the regenerated cells. The present report concerns repair of the EGL after giving BrdU to 7‐day‐old rats i.p. (15 mg/100 g body weight) twice daily for 3 days and killed at 15 days‐of‐age. Now, the regenerative capacity of the EGL was severely curtailed. The proliferative activity of the EGL of the treated animals was similar to normal controls and there was no change in the orientation of either the EGL cells or the parallel fibers. The only noticeable differences were a decrease in the width of the molecular layer and the presence of unusually elongated primary dendrites in many Purkinje cells of the BrdU treated rats. It was concluded that lengthening of the cell cycle time had slowed down the removal of BrdU and thus reduced the regenerative potential of the EGL at this age.
PSEUDO‐INTRACELLULAR COLLAGEN TANGLES IN HUMAN SPINAL GANGLIA
Authors: KOGA M. , OYANAGI S. , OYAKE Y.
Published: May 2008

Pseudo‐intracellular collagen tangles in human spinal ganglia

A new structure was found in the spinal ganglia of 6 out of 215 human autopsy cases with various disorders. It was composed of ballooned cells fully packed with fibrillar structures showing the same staining properties as collagen. Ultrastructurally the fibrillar structures were bundles of collagen fibres with a striation of about 70nm periodicity, and they were enclosed by the cell membrane invaginated in a very complex manner into the cytoplasm. This structure, which we named ‘pseudo‐intracellular collagen tangle’, was considered to result from a disturbance in the releasing process of collagen fibre from fibroblasts. The aetiology of the structure is unknown, but it might represent one of regressive or senile changes in human spinal ganglia.
THE DENSITY OF NEURONS IN THE HUMAN HIPPOCAMPUS
Authors: DAM A. MOURITZEN
Published: May 2008

Mouritzen Dam A. (1979) Neuropathology and Applied Neurobiology5, 249–264 The density of neurons in the human hippocampus

The aim of this study was to determine the density and pattern of distribution of the neurons in the human hippocampus, and twenty‐nine brains of healthy individuals were examined. The cells counted in each unit area were the pyramidal cells in the H‐fields and the granule cells. Difference in density was found between all H‐fields. The neuronal density was highest in the H2‐fields. The density decreased through the transitional area H1–2 and H1, with the lowest density in H3. The neuronal density increased in all H‐fields in the antero‐posterior direction, while the granule cells decreased in density. In the individual brain there was a positive correlation found respectively between high and low cell density in the different H‐fields. The pyramidal cell density decreased in persons more than 68 years old. No difference was found between neuronal cell density in the two sides of the brain. Sex did not influence the neuronal cell density.
A QUANTITATIVE STUDY OF CELL PROLIFERATION IN EPENDYMA AND CHOROID PLEXUS IN THE POSTNATAL RAT BRAIN
Authors: CHAUHAN A. N. , LEWIS P. D.
Published: May 2008

A quantitative study of cell proliferation in ependyma and choroid plexus in the postnatal rat brain

Proliferative activity in forebrain ependyma and choroid plexus epithelium was studied in rats aged up to 42 days by means of autoradiography after injection cf [3H]‐thymidine. Labelling indices were higher in the lateral than in the third ventricle, while values for choroid plexus epithelium were lower than those for ependyma. In all areas examined, labelling indices showed a similar pattern of decline in the first two postnatal weeks reaching by day 12 a level about 20–30% of that on day 1. This low level, corresponding to a turnover time of 130 days for ependyma, was maintained thereafter up to day 42, indicating the persistence of proliferation in the young adult.
WIDESPREAD INTRANUCLEAR NEURONAL CORPUSCLES (MARINESCO BODIES) ASSOCIATED WITH A FAMILIAL SPINAL DEGENERATION WITH CRANIAL AND PERIPHERAL NERVE INVOLVEMENT
Authors: JANOTA I.
Published: May 2008

Case report. Widespread intranuclear neuronal corpuscles (Marinesco bodies) associated with a familial spinal degeneration with cranial and peripheral nerve involvement

Widespread intranuclear, paranucleolar, acidophilic corpuscles, known as Marinesco bodies, were found in association with degeneration of the posterior columns of the spinal cord, posterior root ganglia and cranial nerves. The patient was a man dying at the age of 45 years. Neurological examination of his sister (aged 51 years) indicates that she is suffering from the same disease. The cases appear to belong to the predominantly spinal form of spino‐cerebellar degenerations or Friedreich's ataxia. This report, which includes an electron microscope examination, considers the pathological significance of Marinesco bodies.
CHRONOLOGICAL STUDY OF ULTRASTRUCTURAL CHANGES IN THE PERIPHERAL NERVES IN MAREK'S DISEASE
Authors: LAWN A. M. , PAYNE L. N.
Published: May 2008

Chronological study of ultrastructural changes in the peripheral nerves in Marek's disease

A chronological study was made of the ultrastructural changes in peripheral nerves following inoculation of 1‐day‐old chicks with a neurogenic strain of Marek Disease virus. No virus particles were found in nerves. Cellular infiltration of nerves was detected as early as 5 days after inoculation and by 3 weeks some nerves contained proliferative lesions which possessed many of the ultrastructural features characteristic of normal, reactive lymphoid tissue. About 4 weeks after inoculation, coinciding with the onset of neurological signs, areas of widespread demyelination appeared within these lesions; lymphocytes and macrophages penetrated and destroyed the myelin sheath, but spared Schwann cells and most axons. Later oedematous, sparsely infiltrated B type lesions were observed, some of which contained demyelin‐ated nerve fibres undergoing repair; these were therefore a stage in the regression of the proliferative lesions. Our observations do not favour the hypothesis that cellular infiltration of nerves in Marek's disease is the direct result of auto‐sensiti‐zation to normal myelin. They are consistent with the hypothesis that demyelination is a secondary feature and that the primary lesions are preferential sites for immune demyelination.
A BASIC PROGRAM TO CORRECT FOR SPLIT CELL ERROR IN PARTICLES CLASSIFIED BY THE LOGARITHM OF THEIR PROFILE AREAS
Authors: MILLER A. K. H.
Published: May 2008

A BASIC program to correct for split cell error in particles classified by the logarithm of their profile areas

A program is presented, written in the BASIC computer language, to correct the errors which occur when cell profiles are counted in thin sections of tissue. Given the numbers of profiles in each of M size classes, and the thickness and area of the sections examined, the program calculates the number of cells in each of these classes per mm3 of tissue. The mathematical method is briefly described and it is shown that a useful level of accuracy may be obtained when the correction procedure is used in the study of non‐spherical cells.
ATYPICAL AXON‐SCHWANN CELL RELATIONSHIPS IN THE COMMON PERONEAL NERVE OF THE DYSTROPHIC MOUSE: AN ULTRASTRUCTURAL STUDY
Authors: JAROS E. , BRADLEY W. G.
Published: May 2008

Abstracts Jaros E. & Bradley W.G. (1979) Neuropathology and Applied Neurobiology 5, 133–147

Atypical axon‐Schwann cell relationships in the common peroneal nerve of the dystrophic mouse: an ultrastructural study

Several atypical features of myelination of the peripheral nervous system are reported in common peroneal nerve of dystrophic mice (129 Re J dy/dy): (i) central nervous system‐like contact between myelin sheaths of adjacent nerve fibres; (ii) nodes and internodes of myelinated fibres enwrapped with cytoplasmic processes of Schwann cells from adjacent nerve fibres; (iii) Schwann cells of adjacent nerve fibres co‐operating in formation of a single myelin sheath; and (iv) a single Schwann cell myelinating two separate axons. In view of the presence of similar features of myelination in the central nervous system, where the myelin producing cells lack basement membrane, we suggest that in the dystrophic peripheral nerves the development of these features can be attributed to the partial deficiency of the Schwann cell basement membrane. Two types of widened nodes of Ranvier are also identified: (i) nodes with paranodal damage; and (ii) nodes without paranodal damage. In addition, abnormal features of myelination are described which are likely to represent altered Schwann celliaxon relationships during demyelination and remyelination and/or decreased myelinating ability of Schwann cells. We interpret these findings as indicating a metabolic disorder of Schwann cells. They provide an experimental model for the investigation of factors involved in the origin and maintenance of the structural organization of peripheral nerve.
THYROID DEFICIENCY AND CELL DEATH IN THE RAT CEREBELLUM DURING DEVELOPMENT
Authors: PATEL A. J. , RABIÉ A.
Published: May 2008

Thyroid deficiency and cell death in the rat cerebellum during development.

The [3H]‐DNA content of the cerebellum remained constant during a period from 4 h to 8–9 days after the administration of [3H]‐thymidine both to normal rats at 6 and 12 days of age and to thyroid deficient rats at 6 days. On the other hand, when [3H]‐thymidine was given to 12‐day‐old thyroid deficient rats, a progressive decrease in the cerebellar content of [3H]‐DNA was observed during the first 4 days after the injection. These findings, together with previous results showing a markedly elevated pyknotic index in the internal granular layer of the 12‐day‐old hypothyroid cerebellum, are consistent with there being an increased death of newly formed and differentiating granule cells in thyroid deficiency towards the end of the second week of postnatal life.
NUCLEAR INCLUSIONS IN ALZHEIMER'S DISEASE
Authors: TOPER S. , BANNISTER C. M. , LINCOLN J. , MANN D. M. A. , YATES P. O.
Published: May 2008

Toper S., Bannister CM., Lincoln J., Mann D.M.A. & Yates P.O. (1980)

Neuropathology and Applied Neurobiology 6, 245–253

Nuclear inclusions in Alzheimer's disease

Biopsy samples of parietal cortex from seven patients undergoing atrio‐ven‐tricular shunt operations have been examined electron microscopically. Five were suffering from Alzheimer's disease, while two were subjects with normo‐tensive hydrocephalus following previous head injuries. Intranuclear neuronal, inclusions of three types were found. Most frequent was the intranuclear rodlet, which was commonly observed in four of the patients with Alzheimer's disease, but in one block only from one of the hydrocephalus cases. The other two types, namely the spherical inclusion body and the vermicellar‐like inclusion, were found less commonly and in only two cases. No inclusions were seen in glial nuclei.
CYTOPLASMIC INTERMEDIATE FILAMENTS IN CULTURED GLIAL CELLS
Authors: SOTELO J. , TOH B. H. , LOLAIT S. J. , YILDIZ A. , OSUNG O. , HOLBOROW E. J.
Published: May 2008

Sotelo J., Toh B.H., Lolait S.J., Yildiz A., Osung O. & Holborow E.J. (1980) Neuropathology and Applied Neurobiology 6, 291–298

Cytoplasmic intermediate filaments in cultured glial cells

Monolayer cultures of rat glial cells derived from 12 to 14 day fetal spinal cords and rat C6 glioma cells were examined for immunofiuorescent reactivity with human or rabbit autoantibodies to intermediate filaments and with rabbit antibody to GFAP. The embryonic glial cells and C6 glioma cells reacted identically with both. Protoplasmic astrocytes gave immunofiuorescent staining of an intricate network of cytoplasmic filaments while fibrous astrocytes and C6 glioma cells gave diffuse cytoplasmic staining of the cell body and cell processes. Cells, pretreated with colchicine or vinblastine, showed staining of thick coils of peri‐nuclear, circum‐nuclear, or juxta‐nuclear filaments. The observations suggest that intermediate filaments in glial cells contain unique antigenic determinants as well as antigenic determinants shared with intermediate filaments in other cell types.