bluuebunny/crossref_metadata_2025 huggingface dataset:
CHANGING PATTERNS OF AXONAL REACTION DURING NEURONAL DEVELOPMENT. A STUDY IN THE DEVELOPING CHICKEN NERVOUS SYSTEM
Authors: HOUTHOFF H. J. , DRUKKER J.
Published: May 2008

Houthoff H. J. & Drukker J. (1977) Neuropathology and Applied Neurobiology 3, 441–451

Changing patterns of axonal reaction during neuronal development: a study in the developing chicken nervous system

Age dependency of axonal reaction patterns was studied in the lumbosacral spinal cord and dorsal root ganglia following unilateral sciatic nerve section in grown chickens and in chick embryos, by histochemical and histological methods. A marked change in reaction pattern coincides with the onset of rapid neuronal growth and, after this the axonal reaction is comparable to the pattern in adult fowls. The axonal reaction thus appears not to be influenced by the degree of dendritic growth, by the type and size of the neurones, by glial and satellite cell proliferation or by the presence of myelination. Before this moment, axotomy leads to a massive loss of postmitotic neuroblasts, resulting in reduction in size of the ipsilateral motor column and the dorsal root ganglia. The time between the end of neuroblast proliferation and neuronal development is a highly vulnerable period in development. The hypothesis is brought forward that this highly vulnerable period is related to the initiation of axonal contacts between neuroblasts and their peripheral targets.
SCHWANN CELL RESPONSES DURING RECURRENT DEMYELINATION AND THEIR RELEVANCE TO ONION‐BULB FORMATION
Authors: RAINE C. S.
Published: May 2008

Raine C.S. (1977) Neuropathology and Applied Neurobiology 3, 453–470

Schwann cell responses during recurrent demyelination and their relevance to onion‐bulb formation

Morphological findings from the spinal nerve roots of six rabbits afflicted with chronic, relapsing EAE are presented. The fate of the Schwann cell subsequent to demyelination has been followed. It has been found that the original Schwann cell does not effect remyelination and that pockets of its cytoplasm are displaced by a new remyelinating cell. These pockets assume positions lateral to the main fibre, sometimes invested by cytoplasm from a separate, apparently healthy Schwann cell. At times during remyelination, difficulty was encountered in determining which profiles were axonal and which were Schwannian. However, plasmalemmal specialisations peculiar to Schwann cells, some of them described here for the first time, permitted positive identication in most cases. After several episodes of demyelination, each followed by rapid remyelination, supernumerary Schwann cells were common but, over the 24‐month period of study, profiles consistent only with primitive onion‐bulb formations were found. It is concluded that advanced (typical) onion‐bulb formation is not a feature of repeated demyelination per se but rather belongs to the hereditary, metabolic defects of the PNS, conditions in which the Schwann cell might be rendered impotent to form myelin.
HEMIPARKINSONISM WITH INFARCTION OF THE IPSILATERAL SUBSTANTIA NIGRA
Authors: HUNTER R. , SMITH J. , THOMSON T. , DAYAN A. D.
Published: May 2008

An elderly man suffering from dementia associated with hypertension developed right‐sided parkinsonism marked by rigidity and flexion. At autopsy the brain showed generalized vascular changes chiefly in the white matter, diffuse plaque and neurofibrillary tangle formation in the temporal cortex, and a discrete gliotic scar in the right substantia nigra. Hemiparkinsonism with a strictly unilateral lesion confined to the substantia nigra has, to our knowledge, not been described before, and the fact that it was ipsilateral adds to its theoretical interest.
THE CERVICAL CORD IN MULTIPLE SCLEROSIS
Authors: OPPENHEIMER D. R.
Published: May 2008

The spinal cords were examined in eighteen cases of multiple sclerosis, with special attention to the cervical enlargement. It was found that (1) lesions in the cervical cord are about twice as common as at lower levels, (2) in this region there is a striking preponderance of fan‐shaped lesions in the lateral columns. It is argued that both these findings are explicable on the theory that mechanical stresses play a part in determining the site of lesions; that such stresses are commonly transmitted to the cord via the denticulate ligaments during flexion of the spine; and that many of the lesions are attributable to vascular leakages due to tension in the denticulate ligaments. It is concluded that in patients with multiple sclerosis neck flexion is dangerous–especially in cases where Lhermitte's sign has occurred.
FINE STRUCTURAL CHANGES IN NERVE CELL BODIES OF THE ADULT RABBIT DORSAL MOTOR VAGAL NUCLEUS DURING AXON REACTION
Authors: ALDSKOGIUS H.
Published: May 2008

Counts of neuronal nucleoli were made in the dorsal motor vagal nucleus (DMV) of the adult rabbit 10, 18, 70 and 90 days following unilateral cervical vagotomy. The structural characteristics of nerve cell bodies in the DMV were studied electron microscopically 2–90 days after cervical vagotomy. The nucleolar counts indicated that 20% of the large DMV neurones had disappeared ipsilateral to the operation 10 days postoperatively (p. o.), 65% 18 days p. o. and 70% 70 and 90 days p. o. No loss of small neurones was found. Large neurones ipsilateral to the operation showed nuclear displacement, infoldings of the nuclear membrane and disappearance of granular endoplasmic reticulum beginning 4 days p. o. and being prominent 6–18 days p. o. At the peak of the response, 10–18 days p. o., reacting neurones showed nucleolar condensation and vacuolation, the appearance of intranuclear electron‐dense particles, extensive accumulation of intracytoplasmic lipid droplets, increased numbers of microtubules and neurofilaments, focal mitochondrial aggregates, and widespread mitochondrial degeneration. Ten to 21 days p. o. degenerating neurones were observed. After 30 days p. o. survival a partial recovery of surviving large DMV neurones seemed to have taken place. The findings are interpreted as indications of distubed protein metabolism, oxidative metabolism and intraneuronal transport in the axotomized DMV neurones. The unique response of these neurones compared to previously studied peripherally projecting neurones is emphasized.
THE MORPHOLOGY OF SPASTIC INTRACEREBRAL ARTERIOLES
Authors: CERVÓS‐NAVARRO J. , MATAKAS F. , ROGGENDORF W. , CHRISTMANN U.
Published: May 2008

Pial and parenchymatous vessels of cat cerebral cortex were subjected to electrical stimulation by direct current by the application of a silver gel electrode to the vessel wall. A current of small intensity (5 V, 10 mA, 2 s) was sufficient to produce spastic constriction of the pial arteries. Arterial spasm was always segmental and lasted up to 20 min. Intracerebral vessels were stimulated by applying a DC of 20 to 100 V, 20 to 150 mA for 30 s to the brain. Intracerebral muscular vessels showed varying diameters and spastic segments in frozen sections and by electron microscopy. The lumen of spastic vessels was collapsed. The vessel wall was convoluted, indicating that the factors causing spastic constriction are different from those responsible for physiological vessel wall constriction. In many cases the perivascular tissue of moderately constricted or spastic arterial vessels was destroyed while the tissue around capillaries always remained intact. It is suggested that periarterial tissue destruction is the result of the sudden and powerful constriction in muscular arteries.
LYSOSOMAL STORAGE DISEASES
Authors: JOLLY R. D.
Published: May 2008

The majority of lysosomal storage diseases affect the central nervous system. Those that reflect a primary lysosomal disorder are associated with genetically determined deficiencies of specific lysosomal enzymes and storage of the relevant substrate. Autofluorescent lipopigments accumulate in the ceroid‐lipofuscinoses, a heterogeneous group of diseases in which lysosomal storage is thought to be a secondary event. In animals, there occurs a group of toxic storage diseases whose pathology mimics that of some of the genetic diseases. In humans some element of control may be achieved by heterozygote detection programmes and/or prenatal diagnosis of pregnancies at risk with elective abortion of an affected foetus. The outlook for specific therapy is not encouraging at this stage.
STUDIES OF CULTURED HUMAN AND SIMIAN FETAL BRAIN CELLS
Authors: OSTER‐GRANITE MARY LOU , HERNDON R. M.
Published: May 2008

Explant cultures of the cerebral subventricular zone and cerebellar external germinal layer were established from fetal human, rhesus and cynomolgus monkey brains. Using comparable gestational ages, the morphogenesis of the cultures from these three sources was almost indistinguishable. Four cell types were distinguished by electron microscopy. Germinal cells or neuroblasts were confined largely to the primary explant and extended into a transitional outgrowth region. Astrocytes, which stained for glial fibrillary acidic protein, grew out of the explants and these could be distinguished from the large, mesenchymal epithelioid cells. A fourth cell type, not identified in previous studies, had the ultrastructural characteristics of an oligodendrocyte, but did not produce myelin in these culture conditions.
PROGRESSION OF HERPES ENCEPHALITIS IN RABBITS FOLLOWING THE INTRA‐OCULAR INJECTION OF TYPE I VIRUS
Authors: NARANG H. K. , CODD A. A.
Published: May 2008

The injection of HSV type I into the vitreous body of the eye in the 18‐day‐old albino rabbits consistently induces herpes encephalitis with 90%, survival. The longterm observations up to 64 days post‐inoculation indicate that HSV travels slowly by cell‐to‐cell infection of neuroglia. The lesions follow a defined anatomical pathway producing a progressive disease not dissimilar to the natural human disease. Semiserial (1 μm) sections show that as the infection progresses tissue repair follows. It appears that HSV does not become latent, repeated episodes of viral activity cause further damage with which the repair does not keep pace. By the sixteenth day virus particles and lesions are found in contralateral side cf the chiasma, lateral geniculate body and both optic nerves, but not in the ipsilateral geniculate body. This suggests that the virus does not follow the axonal route.
A LIGHT AND ELECTRON MICROSCOPIC STUDY OF THE NEUROPATHY OF EQUINE IDIOPATHIC LARYNGEAL HEMIPLEGIA
Authors: DUNCAN I. D. , GRIFFITHS I. R. , MADRID R. E.
Published: May 2008

A study has been made of the pathological changes in the recurrent laryngeal nerves from horses with clinical and sub‐clinical idiopathic laryngeal hemiplegia. Qualitative and quantitative studies showed in clinical cases there was a progressive distal loss of large myelinated fibres in the left recurrent nerve. Regenerating clusters and onion bulbs were frequently seen in affected nerves both at proximal and distal levels. Degenerating axons were characterized by collections of organelles, and denervated bands of Bungner were common. Similar but less severe changes were seen in the left recurrent nerve of sub‐clinical cases, and in both the clinical and sub‐clinical cases the distal right recurrent nerve was also affected. Teased fibre studies showed evidence of chronic demyelination and remyelination. The aetiology of this chronic neuropathy remains uncertain but the possibility of nerve compression is discussed.
AXON SPROUTING INTO SEGMENTS OF RAT SPINAL CORD ADJACENT TO THE SITE OF A PREVIOUS TRANSECTION
Authors: MATTHEWS M. A. , ONGE M. F. ST. , FACIANE C. L. , GELDERD J. B.
Published: May 2008

Axon sprouting into segments of rat spinal cord adjacent to the site of a previous transection

Transection of the spinal cord in adult Long‐Evans Hooded rats is followed by the formation of a connective tissue matrix in the lesion site and the rapid erosion of the neural elements above and below this zone particularly within the dorsal white columns. In the period between 15–45 days after operation two significant events begin to occur. First the injured surfaces of the divided cord become invested by a glial limiting membrane (glia limitans) and, concomitantly, large numbers of axons ensheathed by Schwann cells sprout into the scar matrix and along the eroded dorsal column region. The injured surface of the spinal cord is highly irregular with deep, collagen‐filled rifts into which the sprouting axons may probe and penetrate into the adjacent normal neuropil. Electron microscopic examination generally reveals the interposed glia limitans and that these fibres are usually restricted to the peripheral environment. However, as some axons approach the reconstituting glia limitans, they are enveloped by an astrocytic cytoplasmic process which may either displace the Schwann cell or encompass it together with the enclosed axons. This last phenomenon appears to precede the entry of some axons into the neuropil and suggests that the glia limitans may not necessarily represent an impenetrable barrier to the passage of regenerating nxons into the CNS. Apparent maintenance of most of these fibres for periods of up to 3 months may suggest that viable, functional synapses were established upon available neuronal elements, but clear evidence of this could not be documented.
ADULT METACHROMATIC LEUCODYSTROPHY: CLINICOPATHOLOGICAL REPORT OF TWO FAMILIAL CASES WITH SLOW COURSE
Authors: TAGLIAVINI F. , PIETRINI V. , PILLERI G. , TRABATTONI G. , LECHI A.
Published: May 2008

Tagliavini F., Pietrini V., Pilleri G., Trabattoni G. & Lechi A. (1979) Neuropathology and Applied Neurobiology5, 233–243

Abstract Case report. Adult metachromatic leucodystrophy: clinicopathological report of two familial cases with slow course

Two cases of adult metachromatic leucodystrophy in one family are reported. The main clinical features in both were predominantly psychiatric with alcoholism and an extremely long duration of the illness. Neuropathological examination revealed a similar distribution of the lesions in both, and scanty metachromatic accumulation in the CNS and not at all elsewhere. The great variability of the lengths of the courses is stressed. The duration in no way seems to be linked to the age of onset, except in the typical infantile form. The authors argue that different lengths of history correlate with distinct neuropathological findings, and may possibly be related to qualitative differences in the involved enzyme disturbance. Therefore, the authors suggest that the classification based on the age of onset be enlarged with a further one distinguishing between ‘rapid’ and ‘slow’ course types.
FOETAL THYROIDECTOMY AND BRAIN DEVELOPMENT IN THE SHEEP
Authors: McINTOSH G. H. , BAGHURST KATRINE I. , POTTER B. J. , HETZEL B. S.
Published: May 2008

Foetal thyroidectomy and brain development in the sheep

Sheep foetuses were surgically thyroidectomized at 50–60 days gestation, when thyroid function begins, and the pregnancy was then allowed to continue until 90, 120 or 150 days (term). At these times the foetuses were removed by caesarean delivery, exsanguinated, weighed and dissected. The central nervous system was divided—cerebral hemispheres, brain stem, cerebellum and spinal cord for subsequent analysis. Comparison was made with sham operations on seven foetuses. Thyroidectomy led to a fall in body weight (24.77;) and brain weight (11.7%) at 120 days and 150 days, 31.1% and 24.5% respectively. The hemispheres showed the greatest change and the cerebellum the least. DNA and protein contents were reduced in the hemispheres and cerebellum at 150 days, while in the brain stem and spinal cord the DNA content was not significantly affected. Protein content was, however, reduced indicating a reduced cell size, but not a reduced cell number as in the other two regions. Somatic changes included reduced wool growth, delayed osseous development in the limbs (X‐ray assessment) a reduced heart weight (39.1%) and an increased pituitary weight (48.1%). The thyroidectomized lambs failed to survive for more than a few hours after birth or caesarean delivery at 150 days. The findings indicate significant effects of foetal thyroidectomy on brain development in the sheep late in pregnancy along with other evidence of foetal hypothyroidism.
OBSERVATIONS ON FOCAL DEMYELINATING LESIONS IN CAT OPTIC NERVES
Authors: COOK R. D.
Published: May 2008

A demyelinating perivascular condition has been observed in the optic nerves of three cats, the lesions of which included the following features: thinly myelinated and demyelinated axons, few normal oligodendrocytes, astroglial scar tissue, lymphocytes, plasma cells, mononuclear phagocytic cells and lipid‐laden cells. Also present were tubular inclusion bodies which had morphological features similar to the nucleocapsids of some paramyxoviruses. These lesions are compared with some other demyelinating diseases of the central nervous system, and similarities to the lesions of multiple sclerosis are suggested.
A QUANTITATIVE LIFESPAN STUDY OF CHANGES IN CELL NUMBER, CELL DIVISION AND CELL DEATH IN VARIOUS REGIONS OF THE MOUSE FOREBRAIN
Authors: STURROCK R. R.
Published: May 2008

A quantitative lifespan study of changes in cell number, cell division and cell death in various regions of the mouse forebrain

A quantitative study of changes in total cell number was carried out in the indusium griseum and anterior commissure from fetal life to old age in the mouse brain. The changes in the number of mitotic and pyknotic cells were recorded in the indusium griseum, anterior commissure, subependymal and ependymal layers over the same period. The number of neurons which are produced and which migrate to the indusium griseum are in excess of the number eventually required and the surplus neurons are lost by cell death in late gestation and early postnatal life while synapto‐genesis and neuronal differentiation is taking place. This neuronal loss is associated with a rapid turnover of glia. Most first generation glia, or their immediate precursors, are produced prenatally, in parallel but one day behind neurons. There is no large burst of mitotic activity in the postnatal brain which gives rise to the myelination gliosis which is probably largely a migratory phenomenon. Cell division continues throughout life in all parts of the brain studied. The greatest mitotic activity is centred in the subependymal layer where mitotic cells substantially outnumber pyknotic ones. There is a gradual decrease in mitotic activity in the subependymal layer up to 9 months of age with fairly constant mitotic activity thereafter. Mitotic activity in the indusium griseum levels out at 3 months post‐natum with mitotic and pyknotic cells present in roughly equal numbers thereafter. Mitotic activity in all parts of the anterior commissure levels out at 6 months postnatum and remains constant thereafter. Mitotic and pyknotic cells are present in similar numbers except for a peak in pyknotic cells at 9 months. Cell number in the indusium griseum and anterior commissure is fairly constant between 3 and 9 months, but glial number begins to decrease in all parts of the anterior commissure from 12 to 22 months. In the indusium griseum the number of glia increased slightly between 6 and 22 months. The number of neurons fluctuated during the first week after birth then remained constant until 18 months. There was a significant decrease in the number of neurons between 18 and 22 months.
SPIRAL MEMBRANE CYLINDERS IN THE SKELETAL MUSCLE OF A PATIENT WITH MELORHEOSTOSIS
Authors: McDOUGALL JENNIFER , WILES C. M. , EDWARDS R. H. T.
Published: May 2008

Case report. Spiral membrane cylinders in the skeletal muscle of a patient with melorheostosis

Spiral membrane cylinders have been found in the quadriceps muscle of a patient with melorheostosis. These structures were confined to type II fibres in the leg affected by the bone disease. The possible origins of such structures are discussed.
NEURONAL CHANGES IN EXPERIMENTAL GLIOMAS
Authors: LANTOS P. L. , PILKINGTON G. J.
Published: May 2008

Lantos P.L. & Pilkington G.J. (1980) Neuropathology and Applied Neurobiology 6, 255–266

Neuronal changes in experimental gliomas Gliomas were induced transplacentally by the administration of ethylnitro‐sourea to pregnant rats on the 15th day of gestation. The fine structure of neurones involved in these tumours was studied in order to assess the changes caused by neoplasia. The severity of the neuronal damage depended on their location, those within the tumours being more affected than those in the neighbouring brain. The histological type and grade of malignancy also influenced the changes: periventricular pleomorphic gliomas and ependymomas of high‐grade malignancy caused the most severe alterations. Neurones displayed a spectrum of appearances from apparent normality to complete necrosis. Both nucleus and cytoplasm were affected: of the cytoplasmic organelles the rough‐surfaced endoplasmic reticulum and mitochondria showed the most striking changes. There were many lipofuscin granules and autophagic vacuoles. Axons underwent advanced degeneration: swollen mitochondria, disrupted vesicles and vacuoles, disintegrated microtubules, irregular filaments and unidentified debris were sometimes seen. Disintegration of myelin sheaths frequently occurred with consequent engulfing of their debris by macrophages and reacting astrocytes. The neuronal satellites–mainly oligodendrocytes–were often replaced by neoplastic glial cells. Hydrolytic ‘marker’ enzymes were demonstrated in neurones at various stages of degeneration. In all cases neurones displayed low acid phosphatase activity, while thiamine pyrophosphatase activity decreased with increasing neuronal degeneration.
REMODELLING DURING REMYELINATION IN THE PERIPHERAL NERVOUS SYSTEM
Authors: BONNAUD‐TOULZE EVELYNE N. , RAINE C. S.
Published: May 2008

Bonnaud‐Toulze E.N. & Raine C.S. (1980) Neuropathology and Applied Neurobiology 6,279–290

Remodelling during remyelination in the peripheral nervous system

Morphologic analysis of longitudinal sections of lumbar anterior root tissue from rabbits at different stages of chronic experimental allergic encephalomyelitis has revealed new information on Schwann cell behaviour during early remyelination. Some short remyelinated internodes were displaced laterally towards nodes as other internodes elongated in a stepise fashion to occupy the vacated axonal segments. This suggests that a Schwann cell possesses the ability to remodel its myelin sheath after the initial establishment of the internode. Subaxolemmal densification was found to be formed wherever pairs of Schwann cells overlapped and gap junctions were observed between young Schwann cells.
THE CONTUSION INDEX: A QUANTITATIVE APPROACH TO CEREBRAL CONTUSIONS IN HEAD INJURY
Authors: ADAMS J. H. , SCOTT GRACE , PARKER LILIAN S. , GRAHAM D. I. , DOYLE D.
Published: May 2008

Adams J.H., Scott G., Parker L.S., Graham D.I. & Doyle D. (1980)

Neuropathology and Applied Neurobiology 6, 319–324

The contusion index: a quantitative approach to cerebral contusions in head injury

A quantitative means of assessing contusions of the brain (the ‘contusion index’) following head injury has been devised. Its derivation and application to a consecutive series of 151 cases are described.
MYELINATION OF THE MOUSE CORPUS CALLOSUM
Authors: STURROCK R. R.
Published: May 2008

Sturrock R. R. (1980) Neuropathology and Applied Neurobiology 6, 415–420

Myelination of the mouse corpus callosum

Myelination has been studied in the corpus callosum of the mouse brain between birth and 240 days‐of‐age. Myelin sheaths were first seen at 11 days. The most rapid phase of myelination occurred between 14 and 45 days when 13–5% of axons were myelinated, but myelination continued at a reduced rate up to 240 days when 28% of axons were myelinated. The mean diameter of unmyelinated axons was more or less constant throughout the study with an overall mean diameter of 0–25 ± 0–01 μn. Similarly myelinated axon diameter showed little variation with age with a mean diameter of 0–46 ± 001 μn. This suggests that in the corpus callosum axons do not increase in size until they begin to myelinate.
PERSISTENT MULTIPLICATION OF AXON‐ASSOCIATED CELLS IN THE SPINAL ROOTS OF DYSTROPHIC MICE
Authors: PERKINS C. S. , BRAY G. M. , AGUAYO A. J.
Published: May 2008

Perkins C. S., Bray G. M. & Aguayo A. J. 1980 Neuropathology and Applied Neurobiology 6, 83–91

Persistent multiplication of axon‐associated cells in the spinal roots of dystrophic mice

Axons which lack Schwann cells characterize the spinal roots of dystrophic mice. In these nerves, two types of cells are associated with large axons– typical Schwann cells which ensheath and myelinate individual axons and ‘uncommitted’ cells which closely contact some axons but do not unsheath them normally. Although neonatal Schwann cell multiplication in dystrophic spinal roots is less than normal, the ‘uncommitted’ cells continue to multiply in adult animals. Thus, these cells are presumably responsive to the mitogenic stimulus of axons, but are unable to extend radially and longitudinally to form a myelin sheath. This disorder of axon‐sheath cell interactions could be due to an intrinsic abnormality of Schwann cells or a failure of the mechanisms whereby axons induce Schwann cell differentiation.
A MORPHOLOGICAL LIFESPAN STUDY OF NEUROLIPOMASTOCYTES IN VARIOUS REGIONS OF THE MOUSE FOREBRAIN
Authors: STURROCK R. R.
Published: May 2008

Sturrock R.R. 1980 Neuropathology and Applied Neurobiology 6, 211–219

A morphological lifespan study of neurolipomastocytes in various regions of the mouse forebrain

The neostriatum, indusium griseum and anterior commissure of the mouse brain were examined by semithin light microscopy and electron microscopy in an attempt to identify and follow the development of the cells named neurolipomastocytes by Ibrahim et al. 1979. These cells were first seen at 5 dayspost natum in the indusium griseum and in the leptomeninges adjacent to it. Neurolipomastocytes were always associated with arterioles or venules almost invariably at the site of vessel branching. Their major feature was the presence of round osmiophilic granules. In older animals their cytoplasm contained large quantities of foamy vesicles. This foamy cytoplasm was restricted to neurolipomastocytes and was not a feature of ageing capillary pericytes which showed little morphological evidence of ageing apart from the occasional lipofuscin body.
PERMEABILITY OF THE PERINEURIUM OF SMALL NERVE FASCICLES: AN ULTRASTRUCTURAL STUDY USING FERRITIN IN RATS
Authors: OLDFORS A.
Published: May 2008

The permeability of the perineurial cells was studied with ferritin as a tracer. It was injected beneath the muscle fascia of the lateral aspect of the fore limb of rats. After various intervals the animals were killed and the distribution of ferritin in the nerves of the underlying muscle was observed. Two minutes after injection, ferritin was found surrounding nerve fascicles of various sizes. Some medium sized fascicles containing ten to twenty myelinated nerve fibres, were bounded by a single layer of perineurial cells. In the endoneurium of these fascicles only very occasional ferritin particles were observed. Ferritin was, however, found in perineurial micropinocytotic vesicles which communicated with the epineurial extracellular compartment and also in some vesicles which were entirely intracellular and in a few vesicles which had an opening towards the endoneurium. Occasionally two or more vesicles had fused with one another. Fifteen minutes after the injection of ferritin, numerous ferritin particles were seen in the endoneurium of all nerve fascicles covered by a single layer of perineurial cells. The vesicles of these cells then frequently contained numerous ferritin particles. Sixty minutes after injection of ferritin the tracer was observed within the endoneurium of fascicles of all sizes, including those with a multilayered perineurium. In the latter, ferritin was seen between all the perineurial cell layers as well as in micropinocytotic vesicles of the perineurial cells. The results of this study strongly indicate that the perineurium of small nerve fasicles is permeable to ferritin and that this permeability is due to pinocytosis in the perineurial cells.
LOCALIZATION OF S100 PROTEIN IN THE RAT CEREBELLUM: AN IMMUNOELECTRON MICROSCOPE STUDY
Authors: LEGRAND CH. , CLOS J. , LEGRAND J. , LANGLEY O. K. , GHANDOUR M. S. , LABOURDETTE G. , GOMBOS G. , VINCENDON G.
Published: May 2008

Immunoelectron microscopy has shown that, in adult rat cerebellum, S100 protein is localized exclusively in the astrocytes of both the cortex and the white matter. The labelling pattern was unaffected by the inclusion of glutaraldehyde in the primary paraformaldehyde fixative. The immunoperox‐idase reaction product is observed over both the perikaryal cytoplasm of astrocytes and their processes. S100 protein was not found in neuronal structures nor in oligodendrocytes.
SPONGIFORM POLIOENCEPHALOMYELOPATHY CAUSED BY A MURINE RETROVIRUS. II. ULTRASTRUCTURAL LOCALIZATION OF VIRUS REPLICATION AND SPONGIFORM CHANGES IN THE CENTRAL NERVOUS SYSTEM
Authors: SWARZ J. R. , BROOKS B. R. , JOHNSON R. T.
Published: May 2008

Swarz J.R., Brooks B.R. & Johnson R.T. (1981) Neuropathology and Applied Neurobiology 7, 365–380

Spongiform polioencephalomyelopathy caused by a murine retrovirus. II. Ultrastructural localization of virus replication and spongiform changes in the central nervous system

The development of murine retrovirus induced spongiform polioencephalomyelopathy was studied sequentially by electron microscopy. During the initial 30 days, viral infection of the central nervous system, as evidenced by viral budding from membranes, was limited to endothelial cells and pericytes. Viral particles were observed in the lumen of blood vessels, extracellular spaces and astrocytic endfeet surrounding blood vessels, but no morphological evidence of productive infection was found in astrocytes or neurons during early development of vacuolation. The earliest lesions in the neuropil consisted of swelling of astroglia followed by vacuolation, initially in axons and dendrites and later in neuronal and astrocytic soma, where vacuoles appeared to arise from dilated cisternae of the Golgi apparatus. Vacuoles contained only amorphous debris and fragments of membranes. Virions budding aberrantly into vacuoles were seen only in mice surviving beyond 35 days. Numerous reactive astrocytes were observed, but inflammatory cells were absent. The ultrastructural changes were remarkably similar to those described in scrapie, Kuru, and Creutzfeldt‐Jakob disease.
IMMUNOCYTOCHEMICAL STUDY OF P0 GLYCOPROTEIN, P1 AND P2 BASIC PROTEINS, AND MYELIN‐ASSOCIATED GLYCOPROTEIN (MAG) IN LESIONS OF IDIOPATHIC POLYNEURITIS
Authors: SCHOBER R. , ITOYAMA Y. , STERNBERGER NANCY H. , TRAPP B. D. , RICHARDSON E. P. , ASBURY A. K. , QUARLES R. H. , WEBSTER H. DEF.
Published: May 2008

Schober R., Itoyama Y., Sternberger N.H., Trapp B.D., Richardson E.P., Asbury A.K., Quarles R.H. & Webster H. deF. (1981) Neuropathology and Applied Neurobiology 7, 421–434

Immunocytochemical study of P0 glycoprotein, P1 and P2 basic proteins, and myelin‐associated glycoprotein (MAG) in lesions of idiopathic polyneuritis

To investigate the mechanism of myelin breakdown in idiopathic polyneuritis, paraffin and Epon sections of lesions were immunostained with antisera to four proteins in myelin sheaths. Three of these (P0, P2, and BP) are constituents of compact myelin whereas myelin‐associated glycoprotein (MAG) is restricted to membranes near Schwann cell cytoplasm in periaxonal and paranodal regions and in Schmidt‐Lanterman clefts. In early lesions, there were focal abnormalities in P2, P0, and BP immunostaining of paranodal and intemodal myelin. No single protein was affected selectively and lesions occurred in fibres of all sizes, not just in larger fibres selectively stained by P2 antiserum. Early changes in MAG immunostaining occurred only in regions where myelin immunostaining also was abnormal. More severe, later changes in the distribution of P0, P2, BP and MAG were consistent with the sequence of myelinated fibre alterations seen in segmental demyelination and Wallerian degeneration. In regenerating fibres, MAG antiserum stained periaxonal regions intensely; thin regenerating myelin sheaths were stained by P0 and BP antisera, but not by P2 antiserum. The results show that myelin sheath changes are identified more easily in immunostained sections than in conventional histological preparations. Our data also suggest that in idiopathic neuritis, myelin sheaths are the primary target and that the breakdown of myelin and its proteins is not secondary to Schwann cell damage.
EOSINOPHILIC FASCIITIS: AN ULTRASTRUCTURAL AND IMMUNOHISTOCHEMICAL STUDY OF THE INTERMEDIATE FILAMENT PROTEIN SKELETIN IN REGENERATING MUSCLE FIBRES
Authors: THORNELL L.‐E. , BJELLE A.
Published: May 2008

Thornell L.‐E. & Bjelle A. (1981) Neuropathology and Applied Neurobiology 7, 435–449

Eosinophilic fasciitis: an ultrastructural and immunohistochemical study of the intermediate filament protein skeletin in regenerating muscle fibres

In a case of eosinophilic fasciitis with pronounced muscle involvement non‐specific ultrastructural signs of degeneration were observed in areas of perifascicular atrophy. By combined immunohistochemical and electron microscopical techniques intermediate skeletin filaments were demonstrated. These filaments, when found in combination with nuclei with large nucleoli and an abundance of polyribosomes are a sign of regeneration of muscle fibres. This finding is a useful indicator in assessing the prognosis and therapy of muscle involvement in eosinophilic fasciitis.
MUSCLE FIBRE SIZE AND SHAPE IN DUCHENNE MUSCULAR DYSTROPHY
Authors: WATKINS S. C. , CULLEN M. J.
Published: May 2008

Watkins S.C. & Cullen M.J. (1982) Neuropathology and Applied Neurobiology 8, 11–17

Muscle fibre size and shape in Duchenne muscular dystrophy

A method for measuring fibre area and shape which obviates variabilities inherent in diameter measuring techniques was applied to dystrophic and normal human muscle. It was seen that the mean fibre area in patients with Duchenne muscular dystrophy (DMD) increases with age at a greater rate than that of the controls until approximately 5 years‐of‐age, when it decreases rapidly. This is due to an increasing population of small regenerating, regenerated or split fibres. The shape of fibres was expressed as a form factor and it was seen that the fibres measured from DMD biopsies were less regular in shape than the controls due to constraints placed on the normal growth of regenerating fibres by the proliferation of connective tissue.
CHRONIC RELAPSING EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN THE GUINEA‐PIG: IN‐VITRO ANALYSIS OF MENINGEAL INFLAMMATORY CELLS
Authors: ALLSOPP GRETA , TURK J. L.
Published: May 2008

Allsopp G. & Turk J. L. (1982) Neuropathology and Applied Neurobiology 8, 63–70

Chronic relapsing experimental allergic encephalomyelitis in the guinea‐pig: in‐vitro analysis of meningeal inflammatory cells

Inflammatory cells from the meninges of guinea‐pigs with chronic relapsing experimental allergic encephalomyelitis (CREAE) have been isolated and compared to a similar cell population obtained from guinea‐pigs with acute EAE. A mean of 6.2 × 106 cells were recovered from the brains of animals with CREAE while a similar number of cells (8.0 × 106) was obtained from animals with acute EAE. Only 5.3% of the cells from animals with CREAE were found to be phagocytic in contrast with 28% of the cells obtained from animals with acute EAE. The meningeal inflammatory cells from guinea‐pigs with CREAE did not respond, in the lymphocyte transformation test, to specific antigens or to mitogen. Peritoneal exudate cells (PECs) from these animals did, however, proliferate in the presence of tuberculin and of mitogen, but not with the brain antigen myelin basic protein (MBP). In contrast, the meningeal inflammatory cells from animals with acute EAE did respond to mitogen and PECs from the same animals responded to both the specific antigens and to the mitogen. The meningeal inflammatory cells and PECs from the guinea‐pigs with CREAE did, however, behave in a similar manner to similar cell populations obtained from guinea‐pigs fully protected against clinical signs of acute EAE.
FACTORS WHICH AFFECT THE FUSION OF ALLOGENEIC MUSCLE PRECURSOR CELLS IN VIVO
Authors: WATT DIANA J.
Published: May 2008

Watt D.J. (1981) Neuropathology and Applied Neurobiology 8, 135–147

Factors which affect the fusion of allogeneic muscle precursor cells in vivo

keletal muscle allografts in mice have been used to study the factors which promote the fusion in vivo of muscle precursor cells derived from different strains of mice. Tolerance of host mice to allogeneic donor tissues has been induced either by the injection of donor spleen cells into newborn recipients, or by the irradiation and reconstitution, with donor bone marrow cells, of the haemopoietic system of the thymectomized recipient. The isoenzymes of glucose‐6‐phosphate isomerase (GPI) have been used as markers to distinguish the contribution of host and donor tissues to these allografts. In 174 of 204 such grafts evidence of both host and donor tissues was found. In 57 grafts which yielded a ‘hybrid’ isoenzyme of GPI, it was inferred that host and donor muscle cells had fused to form mosaic fibres. The following factors appear to influence the fusion of muscle precursor cells: a the presence within grafts of adequate numbers of precursor cells of both the host and the donor strains; b the particular strain‐combinations used; c the immunological state of the host.
IDPN NEUROPATHY IN THE CAT: COEXISTENCE OF PROXIMAL AND DISTAL AXONAL SWELLINGS
Authors: GRIFFIN JOHN W. , GOLD BRUCE G. , CORK LINDA C. , PRICE DONALD L. , LOWNDES HERBERT E.
Published: May 2008

Griffin J.W., Gold B.G., Cork L.C., Price D.L. & Lowndes H.E. 1982 Neuropathology and Applied Neurobiology 8, 351–36

IDPN neuropathy in the cat: coexistence of proximal and distal axonal swellings

Administration of β, β'‐iminodipropionitrile (IDPN) to rodents has previously been shown to produce neurofilament‐filled axonal swellings in the proximal regions of motor and sensory nerve fibers. Because of the distinctive distribution of these swellings, IDPN has been classed as a proximal axonopathy and thereby distinguished from other disorders in which similar axonal swellings occur in the distal parts of the axon (distal axonopathies). This report describes the pathology in the peripheral nerves of cats which received intermittent injections of IDPN and calls attention to two previously undescribed pathological changes. First, in addition to the typical proximal swellings associated with IDPN, these animals developed numerous axonal swellings within the distal branches of the sciatic nerve. Distal swellings were present as early as 23 days after initiation of intoxication, indicating that they formed locally (rather than developing in the proximal axon and undergoing transport into the distal regions). The second finding was Wallerian‐like degeneration within the affected nerve branches.

These changes in the distal sciatic nerve and its branches closely resembled the pathology of the distal axonopathies produced by agents such as the neurotoxic hexacarbons and carbon disulfide. The pathological similarities suggest that IDPN may share with these agents pathogenetic mechanisms to an extent not previously suspected.
ELECTRON MICROSCOPIC OBSERVATIONS ON MALIGNANT CHOROID PLEXUS PAPILLOMA
Authors: MOSS T. H.
Published: May 2008

Biopsy material from two cases of histologically proven malignant choroid plexus papilloma was studied by electron microscopy. Both tumours differed from benign papillomas in showing poorly differentiated areas with numerous mitoses. Even in such areas, however, a number of ultrastructural features characteristic of normal choroid plexus tissue were observed in both the cases, including cilia, microvilli, a continuous basement membrane and capillary endothelial fenestration. Such findings may be helpful in establishing the primary origin of malignant tumours in the choroid plexus, especially where light microscopy of poorly differentiated biopsy samples makes diagnosis uncertain.
PLASMA MEMBRANE PORES OF THE SCHWANN CELL IN WALLERIAN DEGENERATION: A MORPHOMETRIC ANALYSIS
Authors: ABRAHAMS P. H. , ALLT A. DAY AND G.
Published: May 2008

Using the freeze‐fracture technique, myelinated fibres were examined from the rabbit sciatic nerve at 48 h after a proximal nerve crush. Employing computer‐aided morphometric techniques the distribution of Schwann cell plasma membrane pores was analysed. In both normal control and crushed nerves membrane pores were restricted to the cytoplasmic circumferential bands and longitudinal columns, which characterize the surface of the myelinated nerve fibre, and were absent from the flat plaque‐like areas delimited by the bands and columns. In approximately half of the myelinated fibres from the crushed nerves there was a five‐fold increase in the density of plasma membrane pores. This response of the Schwann cell was interpreted in terms of an increase in pinocytosis and related to regenerative phenomena in the peripheral nerve.
IMMUNIZATION AGAINST WHOOPING COUGH: A NEUROPATHOLOGICAL REVIEW
Authors: CORSELLIS J. A. N. , JANOTA I. , MARSHALL A. K.
Published: May 2008

The neuropathological aspects of vaccination against pertussis have been analysed. This has been done partly by considering the previous literature and partly by searching for data on any child whose death since 1960 has been thought to have a possible relationship to the vaccination. Twenty‐nine in due course were identified on whom a post‐mortem examination had been made. Eighteen had died within 3 weeks of inoculation ‐ the remaining eleven had survived the initial illness but had remained retarded, epileptic and disabled. Although a variety of cerebral abnormalities were found, neither those recorded in the present study nor those abstracted from previous case reports, have demonstrated a recurring pattern of inflammatory or other damage which could be accepted as a specific reaction to immunization against whooping cough. Those reactive changes that were occasionally found appear to be indistinguishable from those seen in many other infantile encephalopathies occurring as the result of a hypoxic/ischaemic state supervening on a complex of respiratory complications, fever and convulsions.
LIGHT MICROSCOPE AND IMMUNOHISTOLOGICAL INVESTIGATIONS ON THE BRAIN OF BORNA DISEASE VIRUS‐INFECTED RABBITS
Authors: ROGGENDORF W. , SASAKIAND S. , LUDWIG H.
Published: May 2008

We studied the distribution and composition of perivascular cellular infiltrates and the distribution of the virus‐specific antigen of Borna disease in the brains of rabbits inoculated either intracerebrally or intraperitoneally with infectious virus suspensions. Using standard histopathological and immunofluorescence techniques, there was, in all animals, a meningeal inflammatory reaction together with perivenous cellular infiltrates which were most numerous in the sti actures of the limbic system and basal ganglia, but also prominent in the spinal ganglia and area postrema. Studies with fluorescent anti‐IgG antibody (direct technique) showed IgG in 20–25% of the cells in any one perivascular cuff, suggesting that most of the infiltrating cells were T‐cells and that B‐cells were fewer. Studies with virus‐specific antibody showed that, in the early stages of the infection, there was evidence of a globular antigen mainly in neurons, while, at later stages, virus antigen was also demonstrated in oligodendrocytes and microgliocytes. The route of inoculation of the virus had no determining effect on the character or distribution of the cellular infiltrates or on the distribution of virus‐specific antigen in the nervous system.
NEURONAL DEATH IN THE DEVELOPMENT AND AGING OF THE CEREBRAL CORTEX OF THE MOUSE
Authors: HEUMANN D. , LEUBA G.
Published: May 2008

The numbers of neurons and glial cells in the cerebral cortex of the mouse have been estimated during its whole life‐span (5 to 720 days), taking into account both the cellular densities of several areas and the cortical volumes. The results clearly demonstrate that there is a massive neuronal loss in the cerebral cortex during early postnatal development, greater in layers II‐IV than in layers V‐VI. In contrast, aging is characterized by a discrete neuronal loss in the cerebral cortex, purely restricted to layers II‐IV. The number of glial cells increases continuously from 5 to 720 days. We emphasize here the need to obtain volumetric measure together with cellular densities in order to get interpretable quantitative data on cellular death and proliferation.
EFFECT OF MYOCRISIN (SODIUM AURO‐THIO‐MALATE) ON THE MORPHOGENESIS OF AVIRULENT SEMLIKI FOREST VIRUS IN MOUSE BRAIN: AN ELECTRON MICROSCOPICAL STUDY
Authors: PATHAK SNEHLATA , WEBB H. E.
Published: May 2008

Adult mice, infected intracerebrally or intraperitoneally with avirulent Semliki Forest virus, do not show mature virus or advanced stages of viral replication in the brain. If myocrisin is given intraperitoneally 3 h before the virus there is enhancement of all stages of viral replication and budding of virus and mature virions are seen. Compared with controls many intracytoplasmic smooth membrane vesicles were seen in the parenchymal cells of the brain treated with myocrisin or with myocrisin and virus. Myocrisin was visible in the brain and has a membrane proliferating effect which may enhance viral synthesis in the early stages of replication, as well as help in the assembly and budding of mature virus. Increased numbers of infiltrating cells were observed in myocrisin treated mice infected with SFV. The formation of mature virus, and its virulence, appears to be related to the degree of membrane proliferation of the brain cells. The inflammation associated with the increased number of infiltrating cells is secondary to this, the whole process promoting the death of the animals rather than survival.
NEUROTOXICITY OF VINCRISTINE AFTER THE OSMOTIC OPENING OF THE BLOOD‐BRAIN BARRIER
Authors: TOMIWA K. , HAZAMA F. , MIKAWA H.
Published: May 2008

The direct effect of intravascularly injected vincristine on the rat brain was investigated after the osmotic opening of the blood‐brain barrier. This was opened unilaterally by injecting 2–5 ml of 1–4 molal mannitol solution into the right carotid artery through a cannula inserted in the external carotid artery in retrograde fashion. Vincristine (0–75 mg/kg) was then injected into either the carotid artery or into a vein. Animals, thus treated, developed left hemiparesis and choreo‐athetoid head motion within several days. Microscopical analysis revealed 1 intracytoplasmic eosinophilic inclusions at an early period, 2 neuronal argyrophilic change and axonal thickening with spheroid formation at later times, and 3 glial mitotic arrest, a finding not reported in the previous studies with intrathecal injection of vincristine. Neuronal changes were usually confined to the selected area in the midbrain, whereas glial mitotic figures were seen in the hippocampus, midbrain and cerebellum. These changes are thought to be direct effects of the vincristine binding with cellular microtubules, including mitotic spindle tubules and neurotubules. The transient opening of the blood‐brain barrier seems to be a useful technique for studying the experimental neurotoxicology of drugs to which the blood‐brain barrier is impermeable.