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At least 19 recordsLinked to original sources
PubMed1991

[The transition zone of the central nervous system-peripheral nervous system of the adult rat; ultrastructural and immunocytochemical studies: a new function of the astroglia?].

At the transition between central nervous system (CNS) and peripheral nervous system (PNS), the CNS compartment forms cone-shaped incursions into the peripheral part of the dorsal root. The ultrastructural study of the CNS-PNS transitional zone shows that this region is particularly rich in astrocyte processes. In an attempt to investigate the possible role of the CNS-PNS interface astrocytes in myelin formation, a photonic microscopy immunocytochemical study has been done with anti-GFAP and anti-MBP sera. The CNS glial expansion shows an important GFAP immunoreactivity with intimate association between astrocyte processes and myelinated axons. This may indicate that the transitional myelin originates from astrocytes. The same region is also MBP-positive. Two explanations are considered: some astrocytes form transitional myelin sheathes and express MBP epitopes, or oligodendrocytes, with cell bodies distant from the CNS-PNS interface, send myelinating cytoplasmic expansions which are not shown by the techniques we used.

Animals↗
PubMed1994

Effects of lymphoma on the peripheral nervous system.

Peripheral nervous system abnormalities occur in 5% of patients with lymphoma and have a wide differential diagnosis. Herpes zoster is the commonest cause. Vinca alkaloids are the only drugs used in lymphoma which commonly cause neuropathy. Compression or infiltration of nerve roots by lymphoma is a rare presenting feature but becomes more common with advanced disease. Radiation plexopathy does not usually develop until at least 6 months after irradiation and can be difficult to distinguish from neoplastic infiltration. Either multifocal infiltration of nerves or lymphoma-associated vasculitis may present as a peripheral neuropathy. The incidence of Guillain-Barré (GBS) syndrome, and possibly chronic idiopathic demyelinating polyradiculoneuropathy, appears to be increased in association with lymphoma, especially Hodgkin's disease. Subacute sensory neuronopathy and subacute lower motor neuronopathy have both been reported as paraneoplastic syndromes associated with Hodgkin's disease. Treatment of the underlying lymphoma is only rarely followed by recovery of the associated neuropathy.

Antineoplastic Agents↗
PubMed1984

Fast axonal transport in central nervous system and peripheral nervous system axons following axotomy.

After axotomy, changes in the composition of fast axonally transported proteins ( FTP ) within the peripheral nervous system (PNS) axons have been reported. The most significant and reproducible changes involved polypeptides found within the molecular weight range of 31.0 to 14.5 kilodaltons ( Bisby , 1980). We wished to determine whether similar changes following axotomy occur in axons of the central nervous system (CNS). Intracranial axotomy of the left optic tract was performed stereotaxically in rats. Six days post axotomy 50 muCi 35[S]-methionine was injected into the vitreous body of both eyes. FTP were isolated within the optic nerves 2 h after isotope injection. The nerve segments were processed for SDS-PAGE, fluorography, and compared to similarly prepared fluorographs of normal and eight day post-axotomy sciatic nerve segments. The labelling of 5 major polypeptide bands (S1, MW congruent to 28,000; S2a , MW congruent to 25,000; S2b , MW congruent to 23,000; T1, MW congruent to 20,200; and T2, MW congruent to 17,000) was studied by laser densitometry. Band S2b showed a highly significant (p less than 0.001) increase in concentration, while bands S1 and T1 demonstrated highly significant decreases in concentration following axotomy of the sciatic nerve. In contrast, after axotomy of the retinal ganglion cell axons the only significant change was a decrease (p less than 0.05) in T1. We suggest that failure of CNS axons to respond similarly to PNS axons following axotomy may be related to the failure of CNS axons to regenerate.

Animals↗
PubMed1999

Characterization of peripheral myelin protein 22 in zebrafish (zPMP22) suggests an early role in the development of the peripheral nervous system.

Peripheral myelin protein 22 (PMP22) is a component of compact myelin of the peripheral nervous system (PNS). Mutations affecting PMP22 are associated with hereditary neuropathies in humans and rodents. Although mammalian PMP22 is expressed in several tissues, the disease pathology is restricted to the PNS. We describe the characterization of a PMP22-related cDNA from zebrafish and the distribution of its cognate mRNA. Phylogenetic considerations and mRNA expression in cranial nerves are consistent with the interpretation that the encoded protein is the orthologue of mammalian PMP22. In situ hybridization analysis during development showed zebrafish PMP22 expression in embryonic sclerotome cells, in neural crest cells, and in migratory derivatives of both populations. Based on this specific expression pattern prior to the onset of myelination, we hypothesize that zebrafish PMP22 may play a role in early PNS development and that disturbance of such functions may contribute to the PNS-restricted defects caused by mutations in the mammalian PMP22 gene.

Amino Acid Sequence↗
PubMed1999

Mechanisms of immune regulation in the peripheral nervous system.

The peripheral nervous system (PNS) is a target for heterogenous immune attacks mediated by different components of the systemic immune compartment. T cells, B cells, and macrophages can interact with endogenous, partially immune-competent glial cells and contribute to local inflammation. Cellular and humoral immune functions of Schwann cells have been well characterized in vitro. In addition, the interaction of the humoral and cellular immune system with the cellular and extracellular components in the PNS may determine the extent of tissue inflammation and repair processes such as remyelination and neuronal outgrowth. The animal model experimental autoimmune neuritis (EAN) allows direct monitoring of these immune responses in vivo. In EAN contributions to regulate autoimmunity in the PNS are made by adhesion molecules and by cytokines that orchestrate cellular interactions. The PNS has a significant potential to eliminate T cell inflammation via apoptosis, which is almost lacking in other tissues such as muscle and skin. In vitro experiments suggest different scenarios how specific cellular and humoral elements in the PNS may sensitize autoreactive T cells for apoptosis in vivo. Interestingly several conventional and novel immunotherapeutic approaches like glucocorticosteroids and high-dose antigen therapy induce T cell apoptosis in situ in EAN. A better understanding of immune regulation and its failure in the PNS may help to develop improved, more specific immunotherapies.

Animals↗
PubMed1989

Marchi-positive myelinoid bodies at the transition between the central and the peripheral nervous system in some vertebrates.

The CNS-PNS (central nervous system-peripheral nervous system) transitional region of cranial and spinal nerve roots in some vertebrate species was analysed with respect to the occurrence and the distribution of myelinoid Marchi-positive bodies. Both cranial and spinal nerve roots contained more Marchi-positive bodies in their CNS than in their PNS segments. An accumulation of Marchi-positive bodies was usually noted just central to the CNS-PNS borderline. Comparisons between calibre spectra and Marchi index in the cat revealed a particularly high number of Marchi-positive bodies in nerve roots with a high content of myelinated fibres with diameters greater than or equal to 5 microns. Marchi-positive bodies were absent in CNS tissue lacking myelinated nerve fibres. CNS borderline internodes measuring between 200 and 300 microns in length were noted in fibres as thick as 15 microns in feline S1 ventral and dorsal roots. The general picture was similar in all analysed species. Noteworthy however, was the small difference in number of Marchi-positive bodies between CNS and PNS tissue in Xenopus. The chicken contained many myelinoid bodies of similar size and texture as the Marchi-positive bodies but without the Marchi-positive staining properties. The results show that normally occurring Marchi-positive bodies in the CNS are more numerous along paranodal segments than along mid-internodal segments of myelinated nerve fibres and thus support the hypothesis that Marchi-positive bodies are preferentially derived from paranodal myelin.

Animals↗
PubMed1988

General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 2nd communication: effect on the peripheral nervous system and peripheral organs.

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the peripheral nervous system and peripheral organs were studied in various laboratory animals in comparison with those of disopyramide and mexiletine, and the following results were obtained. 1. Large doses (50 or 100 mg/kg p.o.) of SUN 1165 as well as mexiletine had little effects on the pilocarpine-induced hypersalivation and the pupil size in mice. At higher concentration (10(-5) g/ml), SUN 1165 had no effects on the various spasmogen acetylcholine (ACh)-, histamine- or BaCl2-induced contractions in the isolated guinea pig ileum, tracheal smooth muscle and urinary bladder. Disopyramide caused mydriasis, inhibited the pilocarpine-induced hypersalivation at antiarrhythmic doses (10-30 mg/kg p.o.), and suppressed ACh-induced contractions in the various organs. 2. SUN 1165, like disopyramide and mexiletine, decreased the contractile amplitude and diastolic tone of the isolated rabbit ileum. SUN 1165 as well as disopyramide had no effect on the intestinal propulsion even at a large dose (100 mg/kg p.o.). Mexiletine inhibited it at antiarrhythmic doses (10-30 mg/kg p.o.). SUN 1165 only at a large dose (100 mg/kg i.d. or p.o.) inhibited volume of pepsin output in the gastric juice in pylorus-ligated rats and caused a damage to the gastric mucosa. 3. SUN 1165, like disopyramide and mexiletine, slightly potentiated the norepinephrine-induced contraction of the rat vas deferens in vitro. Moreover, SUN 1165 as well as disopyramide and mexiletine slightly potentiated the serotonin-induced contraction of the rat isolated fundus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

How do the migratory and adhesive properties of the neural crest govern ganglia formation in the avian peripheral nervous system?

The peripheral nervous system derives mainly from the neural crest both in the head and trunk. Using markers such as fibronectin (FN), neural cell-adhesion molecule (NCAM), the nucleolar marker for quail cells in chimaeric embryos, and NC-1, a monoclonal antibody specific to crest cells and their neural derivatives, we have attempted to reconstruct the processes that lead to the formation of peripheral ganglia. Our observations allow us to propose a model of the formation of ganglia based on morphogenetic movements and on variations of crest cell adhesiveness. In most cases, crest cells migrate in morphologically defined and transient pathways that lead them to their final site of arrest; these pathways are always associated with FN, which appears necessary for crest cell attachment and movement in vitro. The directionality of crest cell migration is probably dictated by the cells' motile properties and population pressure in restricted areas suitable for cell movement. The disappearance of the pathways and of the substrate necessary for migration while the population is rapidly dividing may be responsible for the aggregation of crest cells in the case of the sensory ganglia. To the contrary, the aggregation of crest cells into autonomic ganglia (sympathetic, enteric, and ciliary ganglia) does not seem to obey the same rules, no disappearance of the substratum or of the pathways being obvious; rather, their formation seems correlated with the de novo synthesis of adhesive molecules such as NCAM.

Animals↗
PubMed1996

Cell lineage analysis of the Drosophila peripheral nervous system.

The peripheral nervous system (PNS) of Drosophila provides a very well-characterized model system for studying the genes involved in basic processes of neurogenesis. Because of its simplicity and stereotyped pattern, each cell of the PNS can be individually identified and the phenotypic consequences of mutations can be studied in detail. Thus, some of the genetic mechanisms leading to the formation of type I sensory organs, the external, bristle-type sensory organs (es), and the internal, stretch-receptive chordotonal organs (ch) have been elucidated. Each sensory organ seems to be generated by a stereotyped pattern of cell division of individual ectodermal precursor cells. Recent advances in cell lineage analysis of the PNS have provided a detailed picture of almost all the lineages in the PNS, including those giving rise to the type II sensory neurons, also known as multiple dendritic (md) neurons. This knowledge will be instrumental in the precise characterization of the phenotypes associated with mutations in known and new genes and their interactions which determine cell fate decisions during neurogenesis. Here, we describe and compare three recently developed methods by which cell lineages have been assessed: single cell transplantation, bromodeoxyuridine (BrdU) incorporation studies, and the flp/FRT recombinase system from yeast. In the light of a more complete knowledge of the PNS lineages, we will discuss the effects of known mutations that alter neuronal cell fates.

Animals↗
PubMed1986

Immunological nonidentity of 19K protein and TP0 in peripheral nervous system myelin.

Peripheral nervous system myelin contains as the major structural protein a glycoprotein known as P0. Another glycoprotein present in smaller amounts, known as the 19K or X protein, has been previously identified as derived from P0 and identical with the main tryptic degradation product of P0 (TP0). Although both P0 and 19K protein incorporated fucose in vitro and stained on polyacrylamide gels with the periodic acid-Schiff stain for carbohydrate, only the P0 blotted to nitrocellulose paper showed immunoreactivity to an antibody to P0, whereas the 19K protein did not. Furthermore, when P0 was hydrolyzed with trypsin or elastase, the main degradation products reacted with P0 on immunoblots, whereas the 19K protein showed no immunoreactivity. From these studies and those of others, it may be concluded that the 19K protein shows some similarities to TP0, but probably has a different structure. P0 and 19K protein do not appear to be related as shown by lack of cross-immunoreactivity.

Amino Acids↗
PubMed1988

Remyelination in the central nervous system and the peripheral nervous system.

Remyelination in the PNS is efficient, quick, and consistently found in all demyelinating diseases. Schwann cell proliferation in response to demyelination is rapid and prolific, and the numbers of Schwann cells generated are in excess of those required for adequate remyelination. This cell poses no limit to regenerative potential, and it can divide and remyelinate following numerous repetitive episodes. The Schwann cell generally has easy access to the denuded axons. The limiting factor to remyelination is the persistence of the demyelinating agent, be it directed at the myelin or secondarily through axonal disease. CNS remyelination differs in some respects. Although it has now become clear that it may occur in a variety of clinical and experimental situations, it is slower and often less complete than in the PNS. The limiting factors here include the nature of the demyelinating process, the regenerative potential of the oligodendrocyte, and the accessibility of the latter to the demyelinated axon. It is apparent that the oligodendrocyte is capable of some proliferation, but the time frame in which this can occur is more constrained than for the Schwann cell. Nevertheless the demonstration that the process occurs leads to increasing hope that clinically useful remyelination may be encouraged in the future either by more carefully controlling the extent of demyelination or by finding ways of stimulating oligodendrocyte proliferation and access to the axon.

Animals↗
PubMed1979

Immunocytochemical localization of rat peripheral nervous system myelin proteins: P2 protein is not a component of all peripheral nervous system myelin sheaths.

Specific antibodies have been developed against P1, P2, and P0 myelin proteins and were used to study the localization of these proteins in the rat peripheral nervous system. Both peripheral and central nervous system myelin sheaths contain P1 protein. P0 and P2 proteins are found exclusively in peripheral nervous system myelin sheaths. Antisera to P1 and P0 proteins stain all peripheral nervous system myelin sheaths uniformly. P2 protein is not a component of all peripheral nervous system myelin sheaths. In sheaths that do contain P2 protein, it is concentrated in the area of the Schmidt-Lanterman incisures.

Animals↗
PubMed1998

Cholinergic neurons and terminal fields revealed by immunohistochemistry for the vesicular acetylcholine transporter. II. The peripheral nervous system.

The peripheral sympathetic and parasympathetic cholinergic innervation was investigated with antibodies directed against the C-terminus of the rat vesicular acetylcholine transporter. Immunohistochemistry for the vesicular acetylcholine transporter resulted in considerably more detailed visualization of cholinergic terminal fields in the peripheral nervous system than reported previously and was well suited to also identify cholinergic perikarya. Vesicular acetylcholine transporter immunoreactivity completely delineated the preganglionic sympathetic terminals in pre- and paravertebral sympathetic ganglia, and in the adrenal medulla as well as postganglionic cholinergic neurons in the paravertebral chain. Cholinergic terminals of sudomotor and vasomotor nerves of skeletal muscle were optimally visualized. Mixed peripheral ganglia, including periprostatic and uterovaginal ganglia, exhibited extensive preganglionic cholinergic innervation of both noradrenergic and cholinergic postganglionic principal neurons which were intermingled in these ganglia. Varicose vesicular acetylcholine transporter-positive fibres and terminals, representing the cranial parasympathetic innervation of the cerebral vasculature, of salivary and lacrimal glands, of the eye, of the respiratory tract and of the upper digestive tract innervated various target structures including seromucous gland epithelium and myoepithelium, respiratory epithelium, and smooth muscle of the tracheobronchial tree. The only macrovascular elements receiving vesicular acetylcholine transporter-positive innervation were the cerebral arteries. The microvasculature throughout the viscera, with the exception of lymphoid tissues, the liver and kidney, received vesicular acetylcholine transporter-positive innervation while the microvasculature of limb and trunk skeletal muscle appeared to be the only relevant somatic target of vesicular acetylcholine transporter innervation. Vesicular acetylcholine transporter immunoreactivity was particularly useful for identification of parasympathetic intrinsic ganglia, and their terminal fields, in heart, uterus, and other peripheral organs receiving parasympathetic innervation. Extensive vesicular acetylcholine transporter-positive terminal fields were apparent in both atrial and ventricular tissues of the heart targeting cardiomyocytes as well as cardiac microvessels. Pericardiac brown adipose tissue was also supplied by vesicular acetylcholine transporter-positive varicose fibres. The enteric ganglia of the myenteric and submucous plexus, their synaptic junctions with circular and longitudinal smooth muscle, and terminal fields of the lamina propria of the stomach and intestine and of the local microvasculature were intensely vesicular acetylcholine transporter positive. Vesicular acetylcholine transporter-positive innervation was delivered to the exocrine and endocrine pancreas originating from vesicular acetylcholine transporter-positive intrapancreatic ganglia. Vesicular acetylcholine transporter immunoreactivity in urogenital organs revealed the patterns of terminal cholinergic fields arising from the sacral parasympathetic innervation of these structures. Components of the cholinergic nervous system in the periphery whose existence has been controversial have been confirmed, and the existence of new components of the cholinergic nervous system has been documented, with vesicular acetylcholine transporter immunohistochemistry. Visualization of vesicular acetylcholine transporter will allow documentation of changes in synaptic patency during development, in disease, and during changes in neurotransmission accompanying injury and dystrophy, in the peripheral nervous system.

Acetylcholine↗
PubMed1986

Cell line segregation during peripheral nervous system ontogeny.

The peripheral nervous system of vertebrates arises from the neural crest and the ectodermal placodes. Construction of quail-chick chimaeras has provided significant information on the migration and fate of the neural crest and placodal cells. Transplantation of neural crest tissue to various sites in these chimaeras has demonstrated that the differentiation of neural crest cells is controlled by environmental influences during their migration and, particularly, during gangliogenesis. Experiments with in vitro and monoclonal antibody techniques have shown that these environmental cues act on a heterogeneous population of neural crest cells whose developmental potencies are partly restricted to definite differentiation pathways.

Animals↗