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PubMed1988

Long-term effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the peripheral nervous system. Clinical and neurophysiological controlled study on subjects with chloracne from the Seveso area.

This work was set up to investigate the possible presence of peripheral nervous system involvement as a long-term effect of the exposure to dioxin in 152 subjects with chloracne from the Seveso area; 123 age- and sex-matched subjects living in nearby towns with similar environmental pollution formed the control group. The accident in Seveso took place in July, 1976, and this study was carried out from October, 1982, to May, 1983. Although a peripheral neuropathy was not found in any of the subjects, a significant increase of the number of individuals presenting at least two bilateral clinical signs (p less than 0.05) or one abnormal electrophysiological parameter (p less than 0.02) was found in the Seveso group. Principal component analysis did not show any subdivision between these two groups. The Fisher approach to discriminant analysis reveals a clear subdivision between the group of the most exposed subjects and randomly selected subgroups of control subjects. In conclusion, clinical and electrophysiological signs of peripheral nervous system involvement occur with a statistically increased frequency in the Seveso population 6 years after the accident, although a peripheral neuropathy was not evident in any of the chloracne patients using the World Health Organization diagnostic criteria.

Accidents, Occupational↗
PubMed1992

Effects of catechol compound administration on nerve growth factor synthesis in the peripheral nervous system.

The effects of the intraperitoneal administration of catechol compounds on nerve growth factor (NGF) synthesis in the peripheral nervous system were examined in Wistar male rats. Five injections of 4-methylcatechol (4-MC) during a three-day period caused a threefold to fourfold increase in the NGF content of organs with sympathetic innervation (heart, submandibular gland) and the sciatic nerve. Next, we investigated time-dependent changes in the NGF content after a single injection of 2 micrograms of 4-MC. A transient increase in the NGF content was detected in the heart and submandibular gland at 16 hours after administration. In the sciatic nerve, a transient increase in the NGF content was noted at 20 hours in the nerve segments on the distal side, and at 24 hours in the segments on the proximal side. In the superior cervical ganglion and dorsal root ganglion, i.e., the locations of the sympathetic and sensory nerve cell bodies, an increase in the NGF content was detected between 32 and 40 hours. Therefore, catechol compounds stimulate NGF synthesis in the peripheral nervous system, and NGF induced by 4-MC is transported retrogradely in the axon to the soma in a physiological manner. Furthermore, in the dorsal root ganglion and superior cervical ganglion, the use of substance P and tyrosine hydroxylase activity as biochemical markers of sensory and sympathetic neurons has demonstrated the biological activity of newly-synthesized NGF induced by catechol compounds.

Animals↗
PubMed1990

The myelin-associated glycoprotein is phosphorylated in the peripheral nervous system.

Phosphorylation of the myelin-associated glycoprotein (MAG) in the peripheral nervous system is demonstrated by immunoprecipitation from myelin proteins radiolabeled in vivo, in nerve slices and in a cell-free system. Phosphoamino acid analysis of immunoprecipitated MAG revealed the presence of radioactivity in phosphoserine, but not in phosphothreonine or phosphotyrosine. Only the shorter isoform of MAG (S-MAG) was detected by immunostaining of nitrocellulose sheets with anti-MAG anti-serum after enzymatic deglycosylation of immunoprecipitated MAG labeled in nerve slices. Autoradiography of the same Western blots revealed that most of the radioactive phosphate was in S-MAG, demonstrating that the polypeptide backbone of S-MAG is phosphorylated in the PNS.

Animals↗
PubMed1991

Amyloid beta/A4 protein precursor is widely distributed in both the central and peripheral nervous systems of the mouse.

We studied the immunocytochemical distribution of amyloid beta/A 4 protein precursor (APP) in both the central and peripheral nervous tissues of the mouse. We used two different antisera against the synthetic peptides corresponding to the carboxyl- and the amino-terminal regions of APP, which are common to all isoforms of APP (APP695, APP714, APP751 and APP770). Both antisera recognized the same 106-122 kDa proteins from the mouse brain on immunoblotting. Immunocytochemically, in cortical and subcortical areas, reactivities of both antisera were located in neurons of all sizes. Immunoreactive neurons were widely distributed showing no particular pattern. Various neuron types in the spinal cord were also immunoreactive. In the peripheral nervous system, ganglion cells and their processes showed immunostaining. Immunoreactivity was also seen in the astrocytes, oligodendroglia and ependymal cells widely distributed in the brain and spinal cord, mantle cells in the ganglia, and Schwann cells in peripheral nerves. These results indicated that the full length of APP is distributed in almost all neurons and some glial cells in the mouse central and peripheral nervous systems.

Amyloid beta-Protein Precursor↗
PubMed2003

Stretch receptor-associated expression of alpha 3 isoform of the Na+, K+-ATPase in rat peripheral nervous system.

Expression of the neuronal alpha(3) isoform of the Na(+),K(+)-ATPase (alpha(3) Na(+),K(+)-ATPase) was studied in the rat peripheral nervous system using histological and immunohistochemical techniques. Non-uniform expression of the alpha(3) Na(+),K(+)-ATPase was observed in L5 ventral and dorsal roots, dorsal root ganglion, sciatic nerve and its branches into skeletal muscle. The alpha(3) Na(+),K(+)-ATPase was not detected in nerve fibers in skin, saphenous and sural nerves. In dorsal root ganglion 12+/-2% of neurons were immunopositive for alpha(3) Na(+),K(+)-ATPase and all these neurons were large primary afferents that were not labeled by Griffonia simplicifolia isolectin B4 (marker of small primary sensory neurons). In dorsal and ventral roots 27+/-3% and 40+/-3%, respectively, of myelinated axons displayed immunoreactivity for alpha(3) Na(+),K(+)-ATPase. In contrast to the dorsal roots, strong immunoreactivity in ventral roots was observed only in myelinated axons of small caliber, presumably gamma-efferents. In the mixed sciatic nerve alpha(3) Na(+),K(+)-ATPase was detected in 26+/-5% of myelinated axons (both small and large caliber). In extensor hallicus proprius and lumbricales hind limb muscles alpha(3) Na(+),K(+)-ATPase was detected in some intramuscular axons and axonal terminals on intrafusal muscle fibers in the spindle equatorial and polar regions (regions of afferent and efferent innervation of the muscle stretch receptor, respectively). No alpha(3) Na(+),K(+)-ATPase was found in association with innervation of extrafusal muscle fibers or in tendon-muscle fusion regions. These data demonstrate non-uniform expression of the alpha(3) isoform of the Na(+),K(+)-ATPase in rat peripheral nervous system and suggest that alpha(3) Na(+),K(+)-ATPase is specifically expressed in afferent and efferent axons innervating skeletal muscle stretch receptors.

Animals↗
PubMed1983

[Effects of suloctidil on the central and peripheral nervous systems].

The effects of suloctidil (MY103) on the central (CNS) and peripheral nervous systems were investigated with single and consecutive administration. The general behavior in mice, awareness and motor activity were slightly depressed with the dose above 300 mg/kg, p.o. of MY 103. Soft stool was also marked in the dose above 100 mg/kg, p.o. in beagles and 1000 mg/kg, p.o. in mice. In beagles, vomiting was another syndrome with 100 and 300 mg/kg, p.o. of MY 103. Spontaneous motor activity was significantly decreased after MY 103 by p.o. administration in the dose above 100 mg/kg in mice and 300 mg/kg in rats. In sleep anesthesia studies, MY 103 and iproniazid did not potentiate the effect of a subthreshold dose of barbital, but those two drugs significantly prolonged the sleeping time of pentobarbital as chlorpromazine did. No anticonvulsive effect was observed with MY 103 in chemo- and electroshock seizure tests. My 103 of 300 mg/kg, p.o. significantly decreased the acetic acid induced writhing number, but no analgesic activity was found in the Haffner's method in mice. In the rotarod test, MY 103 of 30-300 mg/kg, p.o. inhibited the motor coordination dose-dependently. MY 103 antagonized the m-amphetamine group toxicity. A cataleptogenic effect was observed following the relatively high dose of MY 103 by an i.p. route. This effect was antagonized by atropine. The spinal reflexes in the immobilized cat, and spontaneous rabbit EEG were not affected by MY 103. The conditioned avoidance response (CAR) was also not changed with MY 103 in rats. In the isolated phrenic-nerve diaphragm preparation, 10(-4)M MY 103 irreversively inhibited the muscle twitches elicited by nerve and muscle stimulation, but suloctidil at 300 micrograms/kg, i.v., did not suppress the tibialis muscle twitches in vivo. In the consecutive administration study, MY 103 suppressed the CAR in rats and prolonged the thiopental-sleeping time in an administration period-related manner. These changes disappeared rapidly after drug withdrawal. Taking these evidences together, it can be concluded that MY 103 has little effect on the CNS with single administration, but the tendency to depress the CNS was observed after the repeated administration of MY 103.

Analgesics↗
PubMed1991

[Inflammatory demyelinating diseases if the peripheral nervous system: immunological concepts and experimental models].

Some inflammatory diseases of the peripheral nervous system, most prominently the Guillain-Barré syndrome, are currently regarded to be of autoimmune origin. Experimental models show clearly that the balance between cellular and humoral autoimmune reaction against peripheral myelin components significantly determines the appearance of the disease. Yet, important questions, such as target antigens of the antimyelin reaction are still unresolved.

Animals↗
PubMed1996

Sequential study of central and peripheral nervous system involvement in an infant with merosin-deficient congenital muscular dystrophy.

Diffuse white matter changes on brain imaging and peripheral neuropathy are associated features of merosin-deficient congenital muscular dystrophy (CMD). In this report we describe the early manifestation and evolution of brain changes, and the involvement of the peripheral nervous system in a female infant with merosin-deficient CMD diagnosed in the neonatal period who had sequential clinical, neurophysiological and magnetic resonance imaging (MRI) assessment. Both MRI and nerve conduction velocity in the first week of life failed to demonstrate any abnormality. By 6 months of age both nerve conduction and MRI were abnormal. White matter changes became more evident on a further scan at 1 yr of age and this pattern remained unchanged on the following scan performed at 17 months of age. Our findings suggest a failure in the physiological maturation process of myelination of both the central and peripheral nervous system.

Central Nervous System Diseases↗
PubMed1996

Expression and distribution of CD9 in myelin of the central and peripheral nervous systems.

CD9 is a member of the newly identified tetra-membrane-spanning protein family. We show here that CD9 is a constituent of myelin in the central and peripheral nervous systems. Expression of CD9 was detected in human cerebral white matter and sciatic nerve by Northern and Western blotting. Myelin in the central and peripheral nervous systems was strongly stained with a monoclonal antibody against human CD9 antigen in paraffin-embedded sections. CD9 was detected in adult nervous tissue but not in developing brain at less than 20 weeks of gestation. Immunohistochemical studies indicated that expression of CD9 is correlated with myelination and is somewhat delayed compared with expression of myelin basic protein, a major component protein of myelin. In the central nervous system, CD9 was detected along the outermost membrane of compact myelin but not inside compact myelin or the periaxonal region. Although the membrane-anchored form of heparin-binding epidermal-growth-factor-like growth factor (proHB-EGF), which is identical to the diphtheria toxin receptor, forms a complex with CD9 in some human and monkey cell lines, proHB-EGF was not detected in myelin immunocytochemically. The distribution of CD9 in the outer surface of myelin and its relatively late developmental appearance suggest that CD9 may interact with the extracellular matrix or cell adhesion molecules and participate in the maintenance of the entire myelin sheath.

Aging↗
PubMed1988

Stage-specific cell-surface antigens of oligodendrocytes in the peripheral nervous system. Expression during development and regeneration and in myelin-deficient mutants.

Monoclonal antibodies to stage-specific cell surface antigens of oligodendrocytes have been used to investigate the expression of antigens 05 through 011 in the peripheral nervous system of the mouse by immunohistology. In the adult sciatic nerve antigens 05 through 09 and 011 were diffusely positive. 010 antigen was not detectable in the peripheral nervous system at any age tested. During development antigens 05, 06 and 07 were first detectable at birth in tracts at the proximal part of the sciatic nerve. At day 2 the whole diameter of the nerve was positive for 05 antigen, while antigens 06 and 07 were detectable only in part of the nerve and antigens 08 and 09 were just about to appear. At day 4 antigen 011 was the last to appear. At day 7 all antigens were strongly detectable throughout the nerve. After transection of adult sciatic nerve expression of antigens 05 through 09 and 011 was studied at the proximal and distal ends of the cut. Three days after transection all antigens were fully detectable in the degenerating myelin and its debris. After 15 days residual debris was still distinctly positive, while Schwann cells in the bands of Bünger were antigen-negative. At approximately two weeks a connecting bridge between proximal and distal ends of the cut nerve had developed, but the 0 antigens were not detectable in this bridge until day 21. At day 42 all antigens were again fully detectable in the regenerating nerve. In hypomyelinating mouse mutants no difference to the normal control littermates was seen in staining pattern and intensity for jimpy and shiverer, while quaking showed an increase in staining intensity for 05 through 08 antigens. In trembler antigens 05, 06 and 07, but not 08, 09 and 011 appeared associated with non-myelin-forming Schwann cells, while the few recognizable myelin-forming Schwann cells expressed all antigens. These observations show that we have characterized 4 new monoclonal antibodies as further reagents to look at developmentally distinct steps in myelination of the peripheral nervous system.

Animals↗
PubMed2001

Role of integrins in the peripheral nervous system.

Integrins, a subgroup of adhesion receptors, are transmembrane glycoproteins that mediate interactions between cytoplasm and the extracellular environment. These interactions influence, among others, events such as cell migration, proliferation, and differentiation. Differential expression of integrins is developmentally regulated in the peripheral nervous system (PNS) and is associated with crucial events in both physiological and pathological processes. Preliminary studies suggest that integrin expression influences neural crest cell migration, axonal outgrowth, and Schwann cell differentiation. Similarly, the abnormal expression of integrins or their ligands, is associated with degenerative, inflammatory, and malignant disorders of the PNS. Finally, integrins participate in the complex interactions that promote repair of the PNS. A better comprehension of the role of integrins in the PNS, their protein interactions and transducing signals is being achieved by selected biochemical and genetic experiments. Here we review a large bias of evidence suggesting the key functions for integrins in the PNS.

Animals↗
PubMed2001

Central and peripheral nervous system complications following allogeneic bone marrow transplantation.

Although graft vs. host disease (GvHD) is a frequent complication of allogeneic bone marrow transplantation (BMT), involvement of the central and peripheral nervous systems (CNS and PNS, respectively) has not been demonstrated conclusively. Here, we report of a patient who, following allogeneic BMT for lymphoblastic T-cell lymphoma, suffered a syndrome characterized by self-remitting cerebellar and pyramidal signs associated with a progressive involvement of the peripheral nervous system (PNS). Clinical course and laboratory findings correlated with relapses of systemic GvDH, thus suggesting the possibility that involvement of CNS and PNS may be sustained by a similar pathogenic mechanism.

Adult↗
PubMed1989

Type I collagen preparations inhibit DNA synthesis in glial cells of the peripheral nervous system.

The mechanisms underlying cessation of glial proliferation in the developing peripheral nervous system are obscure. One possibility, as yet little explored, is that mitotic inhibitory signals play a part in regulating glial cell numbers. In this study we demonstrate that type I collagen preparations from several different sources can inhibit the rate of DNA synthesis in purified populations of enteric glia and both short-term and long-term secondary Schwann cells in dissociated cell cultures. When these cells are grown on gelled or dried type I collagen substrata, they proliferate at substantially lower rates than on polylysine substrata. In contrast, type III or V collagen preparations do not inhibit glial DNA synthesis and laminin, fibronectin, type IV collagen, and secreted matrix from bovine corneal endothelial cells all stimulate thymidine incorporation. The inhibitory effect is not observed with heat denatured type I collagen preparations, but is seen equally in serum-containing medium, in medium containing fibronectin-free serum, or in serum-free medium, suggesting that the interaction of collagen with the cells requires structurally intact collagen molecules and does not occur via intermediary linkage to fibronectin. The inhibition on collagen is accompanied by a shape change from a more flattened morphology to a narrow spindle form. The labeling index of a rat Schwannoma cell line, 33B, is not inhibited on type I collagen substrata. These results demonstrate that type I collagen preparations inhibit the DNA synthesis levels of early postnatal peripheral glial cells in vitro. It remains to be determined whether this effect occurs via direct collagen-cell membrane interactions or whether it depends on accessory molecules, perhaps present in the collagen preparations themselves, since these are not purified to absolute homogeneity.

Animals↗
PubMed1975

[Structure of the perineurium of the peripheral nervous system].

The structure of the perineurium in different parts of the peripheral nervous system of rats, rabbits and cats was studied by light-optical and electron microscopic methods. The structure of the perineurium in all the animals studied is sim8lar and consists of different number of the epithelial type layers of the perineural cells, with bundles of cooagnous fibres between them. The greatest anount of layers is found in the perineurium of the sensory and vegetative ganglia, their amount being less between the nerve trunks and bundles. Solitary sensory mielinated nerve fibres are surrounded with a perineural etui consisting of one or two cellular layers. The thickness of the perineural cells varies from 300 to 1500 A and only in the nucleus field it is equal to 1-2 mu. Every layer of the perineural cells is surrounded by a basal membrane. In their cytoplasm there are many pinocytic vesicles in addition to main organells. Between the perineural cells there exist close contacts. The internal layer of the perineurium is the place of origin of intraganglionic septa and in certain distance surrounds the vessels entering the ganglion. Ultrastructurally the perineural cells are similar to the endothelium of the vessels.

Animals↗
PubMed1996

A syndrome of concurrent central and peripheral nervous system involvement due to Epstein-Barr virus infection.

Epstein-Barr virus infection can affect both the central and peripheral nervous system. In some patients this occurs concurrently. Two patients are presented with encephalopathy and acute quadriparesis with diminished reflexes. Positive serology for Epstein-Barr virus was found in both patients. Both patients had a cerebrospinal fluid pleocytosis in the setting of progressive weakness. Electrophysiologic studies early in the course of their illness demonstrated abnormal F-wave latencies with normal distal conduction. Electromyographic studies demonstrated prominent spontaneous activity in affected limbs. As both the encephalopathy and weakness improved, the electrophysiologic abnormalities improved. This presentation is characteristic of acute Epstein-Barr virus infection. Pathologic studies in other patients have documented both anterior horn cell degeneration and edema as well as cellular infiltration of nerve roots which are responsible for the paralysis with diminished reflexes and electrophysiologic findings. The prognosis for these patients is generally good.

Adult↗