Metabolically inert proteins of the central and peripheral nervous system, muscle and tendon.
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Central Nervous System↗
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Genetic control of cell fate specification in Drosophila peripheral nervous system.
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Animals↗
[Pathology of paraneoplastic syndromes of the central and peripheral nervous systems and muscle ].
INTRODUCTION AND DEVELOPMENT: The paraneoplastic neurological syndromes are alterations associated with neoplasias. However, they are not caused by metastases or complications such as infections, vascular disorders, metabolic or nutritional alterations or secondary effect of treatment. The paraneoplastic syndromes are often associated with the creation of autoantibodies against antigens produced by the neoplastia, but also may be against other cells or target molecules of the patient. Sometimes, especially with antibodies directed against cell membrane proteins, there is a close relationship between the antibody and the target organ, as for example antibodies against the acetylcholine receptor in myasthenia gravis. On other occasions, especially when the antigen is intracellular, the mechanism of the autoantibody reaction is not known. Finally, in a third group, the antibody associated with a particular paraneoplastic neurological alteration has not been identified. In this paper we describe the main paraneoplastic neurological pictures and known antibodies, including the molecular aspects and the neoplasias most frequently related to them.
Adult↗
[Effects of inorganic lead exposure on the autonomic nervous system and on the variability of heart rate among workers at a battery plant].
Inorganic Lead can cause a toxic effect on Central Nervous System, Peripheral Nervous System and Autonomic Nervous System (ANS). A damage of the ANS can determine an heart rate variability (HRV) reduction. In this study 43 battery workers exposed to inorganic lead with mean PbB = 31.63 microg/dl (DS 14.77 microg/dl) and 35 not exposed subjects underwent to an evaluation of heart rate variability by specific tests. Heart rate variability in the exposed group was, for some tests (lying to standing, lying to standing-standing to lying) reduced compared with not exposed subjects and for other tests (Valsalva manouvre, lying to standing-standing to lying) correlated with PbB and Zinc Protoporphyrin (ZPP), but not with BMI, age and smoking habits. This study, like others conducted on similar populations, suggest an effect of occupational inorganic lead exposure on Autonomic Nervous System and heart rate variability
Adult↗
[Nasal hyperreactivity and neuropeptides].
The Authors define nasal-sinusal hyperreactivity and closely investigate the influence it has on the relationship existing among the Central Nervous System, Peripheric Nervous System, Immunitary System and Nasal Mucosa. Particular reference is made to neuropeptides that seem to be true "bridge" substances between the Nervous System and some components of the Immunitary System. Importance of the P-Substance is emphasized.
Humans↗
[Pathogenetic characteristics of diseases of the peripheral nervous system in workers having contact with chromium compounds].
When analyzing the results of clinical neurologic, neurophysiologic, psychologic and laboratory instrumental study of 105 chromium-exposed patients with lumbosacral diseases of the peripheric nervous system there were detected clinical and pathogenetic characteristics of this pathology: distinct manifestations of segmental (homolateral) and generalized vegetovascular disorders, deficiency of sympathetic activation, emotional shifts accompanied by disquieting, depressive and hypochondriac tendencies, elevation of the cerebrovascular tension, body sensitization to chromium, increase in its blood serum and urine content. The account of these characteristics is very important for the improvement of the diagnostic process and raising efficacy of treatment of diseases of the peripheric nervous system in chromium-exposed patients.
Adult↗
Histopathological findings in the central and peripheral nervous systems in neuroborreliosis. A report of three cases.
Very little is known about tissue changes and pathophysiological mechanisms in Garin-Boujadoux-Bannwarth syndrome. We report histopathological findings in the central and peripheral nervous systems of three typical cases. In the acute stage of the disease mononuclear perivascular infiltrations with mainly T-helper cells were the prominent finding, whereas after treatment there was no vessel involvement. The fibre changes in the peripheral nervous system consisted of axonal degeneration. No Borrelia burgdorferi-specific antigen could be detected by immunohistochemical methods. Thus vasculitis might be one of the primary pathophysiological mechanisms for the involvement of the nervous system.
Adult↗
Separation of the major proteins of central and peripheral nervous system myelin using reversed-phase high-performance liquid chromatography.
A general method to separate the major proteins of rat central and peripheral nervous system myelin has been developed. The key step is the initial quantitative removal of the lipids under conditions where the proteins retain their solubility in HPLC solvents. Lipids are removed by a combination of solvent extraction and column chromatography on Sephadex LH-60 in 2-chloroethanol:10 mM HCl (9:1). Proteins are then separated by reversed-phase (RP) HPLC. Samples are applied to a wide pore reversed-phase C-3 column and eluted with a linear gradient of 10-70% 1-propanol in 0.1% trifluoroacetic acid (0-100% B) over a 60-min period. Myelin basic proteins elute between 25 and 30% B, Wolfgram and other high molecular weight proteins at 35-50% B, proteolipid protein at 65-80% B, and P0 glycoprotein at 55-65% B. This elution pattern is consistent with the known relative hydrophobicity of these proteins. Protein recovery for the entire procedure is greater than 74%. Proteolipid and P0 proteins isolated by HPLC contain 2.3 and 1.1 mol of covalently bound fatty acids, respectively. This fatty acid composition is similar to that previously reported using different isolation procedures. The analysis of central and peripheral nervous system myelin proteins by RP-HPLC permits the isolation of purified proteins for structural and metabolic experiments.
Animals↗
Evaluating the patient with peripheral nervous system complaints.
Patients commonly seek care from their family physicians for symptoms that are suggestive of peripheral nervous system (PNS) dysfunction. At some point in active practice, virtually all family physicians will be required to conduct at least an initial evaluation of a patient with PNS. The authors outline and describe common themes found in the symptoms and diagnoses of PNS dysfunctions. These themes may be useful to physicians when performing initial evaluations of patients with PNS dysfunctions. The authors also discuss diagnostic methods and effective therapeutic interventions for this population.
Algorithms↗
Ethanol-induced vacuolation in rat peripheral nervous system.
The effect of chronic (3-4 weeks), heavy ethanol exposure on neuronal vacuolation in rat peripheral nervous system was studied in male Wistar rats. The rats were force-fed with 25% ethanol 3 times a day, which resulted in blood ethanol levels of 53.1 +/- 18.8 mmol/l, i.e., marked intoxication. In the superior cervical ganglia (SCG), the ethanol exposure increased the proportion of vacuolated neurons c. 13-fold (0.2 +/- 0.0% in the control ganglia, 2.7 +/- 0.6% in the EtOH-ganglia, P < 0.001). A considerable population of vacuolated neurons (VN) was seen in the sensory inferior vagal (nodose) ganglia, and occasional neurons with large cytoplasmic vacuoles in the sensory dorsal root ganglia (DRG) of the EtOH-rats. In the hypogastric ganglia, where VN are regularly found in the adult rat, ethanol exposure did not affect the amount or the appearance of the vacuolated neurons. The number of VN in the SCG decreased significantly between 2 days and 1 week after cessation of the exposure, but did not return to control level by 1 month after ethanol withdrawal. In electron microscopy, most of the vacuolated SCG neurons showed normal ultrastructure, apart from the large cytoplasmic vacuoles. Some vacuolated neurons, however, showed neuropathologic changes, e.g., dilated endoplasmic reticulum, mitochondrial alterations and increased numbers of myelin figures. These degenerative changes were more frequent in the vacuolated DRG neurons than in the sympathetic ones. The occurrence of VN in rat peripheral ganglia may represent a reaction to increased stimulation during prolonged ethanol exposure and, especially, during repeated phases of ethanol withdrawal.
Animals↗
[Alcohol and central and peripheral nervous system disorders].
It belongs to the definition of chronic alcoholism that also clinically established lesions of the organs can be proved. As to the nervous system the case in question are multilocular defects which concern the central and peripheral nervous system. The local accentuation, the developmental speed and the intensiveness of the alcoholic defect of the cellular metabolism lead to different courses. The suggestion of their individuality must at the same time take into consideration the character of chronic alcoholism which on principle affects the whole nervous system.
Alcohol Amnestic Disorder↗
Infective endocarditis with inflammatory lesions in the peripheral nervous system.
A 64-year-old woman developed septicemia and a generalized peripheral neuropathy while being ventilated postoperatively. No cause for the neuropathy could be found during life. At autopsy she was found to have infective endocarditis and multifocal inflammatory lesions in the central and peripheral nervous systems, consistent with damage due to septic emboli. Infective endocarditis may be a cause of a generalized polyradiculoneuropathy and could be responsible for a proportion of cases of "critical illness polyneuropathy".
Endocarditis, Bacterial↗
Comparison of matrix metalloproteinase expression during Wallerian degeneration in the central and peripheral nervous systems.
The matrix metalloproteinases (MMPs) are a large family of zinc-dependent enzymes which are able to degrade the protein components of the extracellular matrix. They can be placed into subgroups based on structural similarities and substrate specificity. Aberrant expression of these destructive enzymes has been implicated in the pathogenesis of immune-mediated neuroinflammatory disorders. In this study we investigate the involvement of MMPs, from each subgroup, in Wallerian degeneration in both the central and peripheral nervous systems. Wallerian degeneration describes the process initiated by transection of a nerve fibre and entails the degradation and removal of the axon and myelin from the distal stump. A similar degenerative process occurs as the final shared pathway contributing to most common neuropathies. MMP expression and localisation in the peripheral nervous system are compared with events in the CNS during Wallerian degeneration. Within 3 days after axotomy in the peripheral nervous system, MMP-9, MMP-7 and MMP-12 are elevated. These MMPs are produced by Schwann cells, endothelial cells and macrophages. The temporospatial expression of activated MMP-9 correlates with breakdown of the blood-nerve barrier. In the CNS, 1 week after optic nerve crush, four MMPs are induced and primarily localised to astrocytes, not microglia or oligodendrocytes. In the degenerating optic nerve, examined at later time points (4, 8, 12 and 18 weeks), MMP expression was down-regulated. The absence of MMPs in oligodendrocytes and mononuclear phagocytes during Wallerian degeneration may contribute to the slower removal of myelin debris observed in the CNS. The low level of the inactive pro-form of MMP-9 in the degenerating optic nerve may explain why the blood-brain barrier remains intact, while the blood-nerve barrier is rapidly broken down. We conclude that the difference in the level of expression, activation state and cellular distribution of MMPs may contribute to the different sequence of events observed during Wallerian degeneration in the peripheral compared to the CNS.
Animals↗
Expression of corticotropin-releasing factor in the peripheral nervous system of the rat.
The occurrence and distribution of corticotropin-releasing factor (CRF) in the rat peripheral nervous system was studied by immunohistochemistry. CRF-positive nerve fibers were identified in the spleen, thymus, synovial membrane of the knee joint and adrenal gland. In general, CRF-positive fibers were seen predominantly in and around the blood vessels; however, many non-vascular thin varicose fibers were also observed. The neuronal character of the immunoreactive fibers was confirmed by staining consecutive tissue sections with a general neuronal marker, protein gene product 9.5. The finding of CRF-positive nerve fibers in the periphery demonstrates a strong anatomical link between the nervous, endocrine and immune systems, and may have pathophysiological implications in the inflammatory and stress-related disorders.
Animals↗
Development and organization of glial cells in the peripheral nervous system of Drosophila melanogaster.
We have used enhancer trap lines as markers to recognize glial cells in the wing peripheral nervous system of Drosophila melanogaster. Their characterization has enabled us to define certain features of glial differentiation and organization. In order to ask whether glial cells originate within the disc or whether they migrate to the wing nerves from the central nervous system, we used two approaches. In cultured wing discs from glial-specific lines, peripheral glial precursors are already present within the imaginal tissue during the third larval stage. Glial cells differentiate on a wing nerve even in mutants in which that nerve does not connect to the central nervous system. To assess whether peripheral glial cells originate from ectoderm or from mesoderm, we cultured discs from which the mesodermally derived adepithelial cells had been removed. Our findings indicate that peripheral glial cells originate from ectodermally derived cells. As has already been shown for the embryonic central nervous system, gliogenesis in the periphery is an early event during adult development: glial cells, or their precursors, are already present at stages when neurons are still differentiating. Finally, our results also suggest that peripheral glial cells may not display a stereotyped arrangement.
Animals↗
Peripheral nervous system alterations in small cell lung cancer. Clinico-pathological study.
Small cell lung cancer (SCLC) is one of the most malignant tumors, especially often associated with nonmetastatic neurological disorders, corresponding to paraneoplastic neurological syndromes. The pathogenesis of which is unknown, however, mostly attributed to autoimmune processes. The aim of the study was to determine the pattern of the peripheral nervous system damage in SCLC. To provide further data contributing to the pathomechanism underlying these syndromes, immunocytochemical studies were initiated. Autopsy material was collected from 47 cases of SCLC. All these patients were examined clinically. The sections from the cervical, thoracic and lumbosacral segments of the spinal cord with spinal roots and dorsal root ganglia were taken. For immunohistochemistry following antisera were used: GFAP, MBP, IgG, IgM, ferritin, ubiquitin, alpha 1-antichymotrypsin, alpha 2-macroglobulin, C3 and C5b9 complement fractions. In 18 patients peripheral nervous system disturbances were diagnosed neurologically, 21 of cases presented neuromuscular disorders by emg. Among the nonmetastatic lesions most often a damage of dorsal root ganglia was observed (in 33 cases). Degeneration of the spinal roots was absent only in 8 cases. In 21 cases degenerative changes of motor neurons within anterior horn were present. In no case ubiquitin-positive inclusion bodies within the motor neurons could be found. In 8 cases extravasation of the IgG with diffuse labeling of the grey matter was observed. IgM immunoreactivity was markedly less frequently present, C5b9 complement fraction immunoreactivity was also confined only to cases with peripheral nervous system disturbances. Therefore, our preliminary data seem to confirm the participation of humoral immunity in paraneoplastic syndrome pathogenesis.
Adult↗
Mutations in the Drosophila neuroglian cell adhesion molecule affect motor neuron pathfinding and peripheral nervous system patterning.
We have identified and characterized three embryonic lethal mutations that alter or abolish expression of Drosophila Neuroglian and have used these mutations to analyze Neuroglian function during development. Neuroglian is a member of the immunoglobulin superfamily. It is expressed by a variety of cell types during embryonic development, including expression on motoneurons and the muscle cells that they innervate. Examination of the nervous systems of neuroglian mutant embryos reveals that motoneurons have altered pathfinding trajectories. Additionally, the sensory cell bodies of the peripheral nervous system display altered morphology and patterning. Using a temperature-sensitive mutation, the phenocritical period for Neuroglian function was determined to occur during late embryogenesis, an interval which coincides with the period during which neuromuscular connections and the peripheral nervous system pattern are established.
Animals↗
Association of the ecto-ATPase NTPDase2 with glial cells of the peripheral nervous system.
Cellular signaling via extracellular nucleotides appears to play a major role in the functioning of the peripheral nervous system. Information regarding the functional characterization of nucleotide P2 receptors or their expression pattern has been accumulating rapidly; however, very little is known regarding the distribution of ecto-nucleotidases in the periphery. The extracellular level of nucleotides is controlled by ecto-nucleotidases, whereby the three membrane-bound members of the ecto-nucleoside triphosphate diphosphohydrolase (E-NTPDase) family are of special functional importance. Using enzyme histochemistry and immunostaining, we demonstrate that NTPDase2 is associated with nonmyelinating Schwann cells of the rat sciatic nerve, whereas NTPDase1 is restricted to blood vessel walls. NTPDase2 immunoreactivity was detected from embryonic day E18 onward, suggesting that immature Schwann cells express the enzyme. With the onset of myelination, NTPDase2 immunoreactivity remained associated solely with nonmyelinating Schwann cells. NTPDase2 was absent from perisynaptic Schwann cells but was associated with fibroblasts covering the endplate at some distance. In addition, NTPDase2 immunoreactivity was associated with the satellite glial cells in dorsal root ganglia and sympathetic ganglia, and with the enteric glia surrounding the cell bodies of ganglionic neurons of the myenteric and the submucous plexus. In contrast to NTPDase1, NTPDase2 preferentially hydrolyzes nucleoside triphosphates over nucleoside diphosphates and thus can act either in inactivating or in producing P2 receptor ligands. Our results suggest that NTPDase2 plays an important role in the control of nucleotide-mediated activation of peripheral neurons or glia and in the dialogue between these two cell types.
Adenosine Triphosphatases↗