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PubMed2000

Murine macrophages stimulated with central and peripheral nervous system myelin or purified myelin proteins release inflammatory products.

Macrophage inflammatory products including tumor necrosis factor (TNF) and interleukin-12/p40 are implicated in demyelinating diseases such as multiple sclerosis (MS), Guillain-Barré syndrome, and animal models experimental autoimmune encephalomyelitis and neuritis. The macrophage product angiotensin converting enzyme (ACE) is released during inflammation. ACE can also be elevated in MS. We investigated the ability of central (CNS) and peripheral nervous system (PNS) myelin to stimulate TNF, interleukin-12, and ACE production by murine macrophages. Both CNS and PNS myelin and purified myelin basic protein and P2 protein induced release of these products. Direct stimulation by myelin may represent a mechanism of inducing release of macrophage products in inflammatory demyelination or neural injury.

Animals↗
PubMed2001

Constitutive expression of the 27-kDa heat-shock protein in neurons and satellite cells in the peripheral nervous system of the rat.

By use of reverse transcriptase-polymerase chain reaction, abundant expression of the mRNA of 27 kDa heat shock protein (Hsp27) was revealed in the sympathetic and parasympathetic ganglia as well as in the sensory ganglia of unstressed adult rats. In situ hybridization and immunohistochemistry further localized Hsp27 mRNA and protein to both neurons and satellite cells in all types of ganglia examined. Schwann cells in the ganglia and peripheral nerve fibers were devoid of Hsp27 signal. These results suggested that Hsp27 is constitutively expressed in neurons and satellite cells in the entire peripheral nervous system of the rat.

Animals↗
PubMed1993

Expression of high molecular weight tau in the central and peripheral nervous systems.

Using a novel PCR approach, we have cloned a cDNA encoding the entire high molecular weight tau molecule from rat dorsal root ganglia. The resulting 2080 bp cDNA differs from low molecular weight rat brain tau by the insertion of a novel 762 bp region (exon 4a) between exons 4 and 5. This cDNA clone is identical in sequence with a high molecular weight tau (HMW) cDNA from rat PC12 tumor cells and is closely related to a HMW tau cDNA from mouse N115 tumor cells. In vitro transcription/translation produces a protein that migrates on SDS-PAGE with the same apparent molecular weight as HMW tau purified from rat sciatic nerve. The HMW tau protein is generated from an 8 kb mRNA, which can be detected by northern blots in peripheral ganglia, but not in brain. A more sensitive assay using PCR and Southern blot analysis demonstrates the presence of exon 4a in spinal cord and in retina. In combination with immunohistochemical studies of spinal cord, these data suggest that HMW tau, though primarily in the peripheral nervous system, is also expressed in limited areas of the central nervous system, although its presence cannot be detected in the cerebral cortices.

Amino Acid Sequence↗
PubMed1997

Potentiation of organophosphorus compound-induced delayed neurotoxicity (OPIDN) in the central and peripheral nervous system of the adult hen: distribution of axonal lesions.

Clinical manifestations of mild organophosphorus compound-induced delayed neurotoxicity (OPIDN) produced by diisopropylphosphorofluoridate (DFP) in adult hens are potentiated by posttreatment with phenylmethanesulfonyl fluoride (PMSF). The purpose of this study was to assess whether potentiation of mild OPIDN produces a pattern of axonal lesions in the central and peripheral nervous system similar to that seen in severe OPIDN. Groups of 6 hens each were given the following priming/challenge doses sc at 0 and 4 h, respectively: 0.20 ml/kg corn oil/0.50 ml/kg glycerol formal (GF) (control); 0.50 mg/kg DFP/GF (low-dose DFP); 0.50 mg/kg DFP/60 mg/kg PMSF (potentiated DFP); 60 mg/kg PMSF/GF (PMSF alone); 60 mg/kg PMSF/1.5 mg/kg DFP (protected DFP); and 1.5 mg/kg DFP/GF (high-dose DFP). Two hens from each group were used to assay brain neurotoxic esterase (NTE) 24 h after the challenge dose, and the remaining hens were scored for deficits in walking, standing, and perching ability on d 18. Three hens from each group were perfusion-fixed on d 22 and neural tissues were prepared for histologic evaluation. DFP and/or PMSF caused > 88% brain NTE inhibition in all treated groups, compared to control. Protected DFP yielded no clinical deficits and a distribution and frequency of axonal lesions similar to control. PMSF alone produced a small increase in the frequency of lesions in the cervical spinal cord and peripheral nerves compared to control. Low-dose DFP caused minimal ataxia and increased frequency of axonal lesions in dorsal and lateral cervical spinal cord, ventral lumbar spinal cord, and inferior cerebellar peduncles (ICP) compared to control. Potentiated DFP and high-dose DFP produced maximal ataxia and essentially identical increases in the frequency of lesions in dorsal and ventral thoracic spinal cord, lateral lumbar spinal cord, and peripheral nerves compared to low-dose DFP. The results indicate that PMSF potentiation of mild OPIDN induced in adult hens by low-dose DFP results in an overall pattern of axonal degeneration like that produced by a threefold higher dose of DFP alone, and support the hypothesis that potentiation causes an increase in the frequency of axonal lesions in central and peripheral loci normally affected by OPIDN.

Animals↗
PubMed1993

Expression of common acute lymphoblastic leukemia antigen (CD 10) by myelinated fibers of the peripheral nervous system.

The common acute lymphoblastic leukemia antigen (CALLA), CD10, is a 100-kDa surface glycoprotein endowed with neutral endopeptidase activity, shared by a number of hemopoietic and non-hemopoietic cells. In this report, immunohistochemical and Western blot techniques, using different anti-CD10 monoclonal antibodies, were utilized to demonstrate that CD10 is also expressed by myelin sheaths of the human peripheral nervous system (PNS), but not of the central nervous system. CD10-positive immunoreactivity appeared to be localized in the outer and inner borders of myelinated fibers, in nodes of Ranvier and in the Schmidt-Lantermann clefts, thus showing a distribution pattern very similar to that of myelin-associated glycoprotein (MAG). The above findings suggest that CD10 antigen, through its enzymatic activity, may have a functional role in the assembly and maintenance of PNS myelin. In addition, it is not known whether CD10, similarly to MAG, may be a target antigen in some PNS immune-mediated disorders.

Antibodies, Monoclonal↗
PubMed1996

Expression of type 1 inositol 1,4,5-trisphosphate receptor during axogenesis and synaptic contact in the central and peripheral nervous system of developing rat.

Release of intracellular Ca2+ is triggered by the second messenger inositol 1,4,5-trisphosphate, which binds to the inositol 1,4,5-trisphosphate receptor and gates the opening of an intrinsic calcium channel in the endoplasmic reticulum. In order to understand the importance of this mechanism in development, we have examined the distribution of the type 1 inositol 1,4,5-trisphosphate receptor during development, in some areas of the rat brain and spinal cord and in peripheral neurons, using in situ hybridization and immunohistochemistry. In brain, we find that type 1 inositol 1,4,5-trisphosphate receptor is expressed in neurons from very early in development; low levels of expression are first detected after the neurons have migrated to their final positions, when they start to differentiate and begin axonal growth. Increasing levels of expression are observed later in development, during the time of synaptogenesis and dendritic contact. Glial cells do not express type 1 inositol 1,4,5-trisphosphate receptor, except for a transient period of expression, probably by oligodendrocytes, in developing fibre tracts during the onset of myelination. In contrast with the brain, both grey and white matter of the spinal cord express type 1 inositol 1,4,5-trisphosphate receptor throughout development, and it remains present in the adult spinal cord. We also show, for the first time, that type 1 inositol 1,4,5-trisphosphate receptor is expressed in the peripheral nervous system. Strong labelling was observed in the dorsal root ganglia and during development this expression seems to coincide with the onset of axogenesis. These results suggest that type 1 inositol 1,4,5-trisphosphate may be involved in the regulatory mechanism controlling Ca2+ levels in neurons during the periods of cell differentiation, axogenesis and synaptogenesis.

Animals↗
PubMed1993

Tumor necrosis factor-alpha in immune-mediated demyelination and Wallerian degeneration of the rat peripheral nervous system.

This study reports on the immunocytochemical localization of tumor necrosis factor-alpha (TNF alpha) in immune-mediated demyelination and Wallerian degeneration of the rat peripheral nervous system (PNS) using teased nerve fiber preparations. In experimental autoimmune neuritis induced by active immunization (EAN) or by adoptive transfer of autoreactive T cells (AT-EAN), macrophages passing blood vessels as well as macrophages adherent to nerve fibers were TNF alpha-positive. Large post-phagocytic macrophages at later stages of demyelination were TNF alpha-negative. Intraperitoneal application of an anti-TNF alpha antibody to EAN rats significantly reduced the degree of inflammatory demyelination, suggesting a pathogenic role for TNF alpha. After nerve transection only macrophages located within degenerating nerve fibers were TNF alpha-positive, while those entering and leaving nerves were negative. TNF alpha produced by macrophages seems to be involved in immune-mediated demyelination and non-immune myelin degradation after axotomy. While interferon-gamma (IFN gamma) is present in EAN nerves and may act as a local stimulus for TNF expression, the nature of this signal in Wallerian degeneration in the absence of IFN gamma is unknown.

Animals↗
PubMed1982

Migration and differentiation of neural crest cells and their derivatives: in vivo and in vitro studies on the early development of the avian peripheral nervous system.

After a period of extensive migration through the vertebrate embryo, neural crest cells differentiate into a great variety of cell types, including all the elements of the peripheral nervous system. We have studied crest cell migration in quail-chick chimeras in which quail cells can be identified by means of a stable natural nuclear marker. The results of interspecific grafts of neural primordium, performed systematically at different levels of the neuraxis, have established the sites of origin of the principal peripheral ganglia. In addition, they suggest that the cholinergic and adrenergic phenotypes are not predetermined in the neural crest before migration, but are the result of multiple cellular interactions. Furthermore, the phenotype expression of young differentiating autonomic ganglia is labile and can be modified if the latter are subjected to an appropriate cellular environment by grafting into a younger host embryo. The results of experiments in which fragments of neural crest, sensory and autonomic ganglia were transplanted are presented in terms of a model of crest cell-line segregation. As a step towards the analysis of the cellular interactions occurring during autonomic neuron differentiation, we have also studied neuronal development in tissue cultures of neural crest, taken from the cranial and trunk levels of quail embryos and grown in the presence or absence of other embryonic tissues. The results confirm that both levels of the crest are potentially able to give rise to cells that can make acetylcholine and catecholamines. However, whereas acetylcholine-synthesizing ability is apparently a very early feature of autonomic neuron precursors, the ability to produce catecholamines is acquired later as a result of interactions with other cell types, in particular with mesenchymal derivatives. Although production of both neurotransmitters can be considerably stimulated by associating crest with any of several young embryonic rudiments, only when trunk crest is cultured with the sclerotomal moiety of the somite is biochemical differentiation accompanied by extensive morphological and cytochemical neuronal maturation.

Acetylcholine↗
PubMed1984

Neuroaxonal pathology of central and peripheral nervous systems in cerebrotendinous xanthomatosis (CTX).

We studied three siblings and one unrelated patient with cerebrotendinous xanthomatosis (CTX). Of two unrelated patients, we examined biopsies of sural nerve, soleus muscle, and achilles tendon. We also performed neurophysiologic investigations. Another patient died, and a postmortem examination of both brain and spinal cord was made. It was concluded that both the central and the peripheral nervous system were involved in CTX, but the peripheral system only to a slight degree, and that the pathology was predominantly neuroaxonal rather than demyelinating in character.

Adult↗
PubMed1992

Impairment of peripheral nervous system in patients with non-Hodgkin's lymphomas treated with CBVPM/AVBP and CHOP schedules.

Clinical examination and conduction velocity measurements in peripheral nerves have been done on 56 patients with non-Hodgkin's lymphomas of high malignancy (NHL). It is suggested that: the evaluation of the influence of chemotherapy on peripheral nervous system (PNS) is possible by means of systematic neurological and electroneurographic studies; electroneurographic assessment is most important in the diagnosis of early subclinical stages of peripheral neuropathy; toxic influence of CBVPM/AVBP protocol on PNS is greater than CHOP schedule; impairment of PNS due to chemotherapy is reversible in patients during complete remission (CR).

Adolescent↗
PubMed2004

Embryogenesis of the peripheral nervous system.

Embryogenesis is a complex, wide-ranging event. Key processes may proceed simultaneously in different portions of the embryo, or sequentially, with phase offsets as waves of maturation pass outward from an initial point toward the periphery. The molecular signals used to pattern the body commonly serve multiple functions and reiterate as the body plan progresses. This article therefore presents first the anatomic model of the peripheral nervous system, so that the final goal is clear. It then reviews the terminology needed to describe embryogenesis. The article's first section reviews neural development. The main portion of the article addresses the maturation of the fetal nervous system in terms of the evolving gross morphology and the molecular signals that pattern these changes.

Embryonic and Fetal Development↗
PubMed1985

The distribution of indium in the central and peripheral nervous system of the young rat.

A subtoxic quantity of radioactive 111indium and stable indium was injected once into young rats. Subsequently pairs of these rats were killed at intervals of 15 minutes to 3 days after the injection. Tissues from the central (CNS) and peripheral nervous system (PNS) and blood were removed from each rat and the amount of 111indium was measured in the tissues. Cryostat sections of the cerebrum, cerebellum, spinal cord, sciatic nerve, a blood smear and a kidney control from each rat were examined with an analytical ion microscope (secondary ion mass spectrometry analysis) and the presence of 113 and 115 indium was localized in the tissues. These observations show that indium penetrates all neural tissues and that the brain resists the entry of indium - a very toxic element - much more effectively than the sciatic nerve.

Animals↗
PubMed2006

GABA receptor-mediated effects in the peripheral nervous system: A cross-interaction with neuroactive steroids.

Gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the adult mammalian central nervous system (CNS), exerts its action via an interaction with specific receptors (e.g., GABAA and GABAB). These receptors are expressed not only in neurons but also on glial cells of the CNS, which might represent a target for the allosteric action of neuroactive steroids. Herein, we have demonstrated first that in the peripheral nervous system (PNS), the sciatic nerve and myelin-producing Schwann cells express both GABAA and GABAB receptors. Specific ligands, muscimol and baclofen, respectively, control Schwann-cell proliferation and expression of some specific myelin proteins (i.e., glycoprotein P0 and peripheral myelin protein 22 [PMP22]). Moreover, the progesterone (P) metabolite allopregnanolone, acting via the GABAA receptor, can influence PMP22 synthesis. In addition, we demonstrate that P, dihydroprogesterone, and allopregnanolone influence the expression of GABAB subunits in Schwann cells. The results suggest, at least in the myelinating cells of the PNS, a cross-interaction within the GABAergic receptor system, via GABAA and GABAB receptors and neuroactive steroids.

Animals↗
PubMed1988

Reactivity of circulating antineuronal antibodies (CANA) on peripheral nervous system structures.

The appearance of circulating antineuronal antibodies (CANA) in patients with malignant tumors has been correlated with the occurrence of paraneoplastic neurological syndromes. However, the effect of CANA on the peripheral nervous system is poorly understood. The reactivity of sera from CANA-positive and -negative patients were investigated on cryostat sections of peripheral nerves and skeletal muscle, and on nerve tease-fiber preparations. Only CANA-positive sera showed staining of Schwann cell nuclei on cryostat sections, whereas nerve tease-fiber preparations and sections of skeletal muscle remained negative. Positive direct immunofluorescence of small cell lung cancer (SCLS) cells was confined to CANA-positive patients only. These findings suggest the existence of a common antigen between SCLC and Schwann cells.

Autoantibodies↗
PubMed1999

Liquid chromatographic-mass spectrometric measurement of the endogenous cannabinoid 2-arachidonylglycerol in the spinal cord and peripheral nervous system.

AIM: To develop a sensitive method for measuring the putative endocannabinoid 2-arachidonylglycerol (2-AG) in the peripheral and central nervous system. METHODS: A method using atmospheric pressure chemical ionization (APCI) liquid chromatography/mass spectrometry (LC/MS) was developed to determine the levels of 2-AG in methanol extracts of the rat lumbar spinal cord, dorsal root ganglion (DRG), and sciatic nerve. RESULTS: 2-AG was detected with high sensitivity and minimal sample preparation. The levels in the tissues analyzed were < or = pmol/mg wet weight. Similar levels were found in the spinal cord and the DRG, whereas approximately 7-fold lower levels were observed in the sciatic nerve. CONCLUSION: 2-AG is present in the peripheral nervous system, and the levels are markedly higher in cell bodies than those in axons.

Animals↗
PubMedDate not supplied

Intravascular lymphoma involving the central and peripheral nervous systems in a dog.

A 5-year-old, castrated male mixed-breed dog was presented for paraparesis, ataxia, hyperesthesia, and thrombocytopenia of 5 months' duration and recurrent seizures during the preceding 2 weeks. Multifocal neurological, ophthalmological, pulmonary, and cardiac diseases were identified. Magnetic resonance imaging and cerebrospinal fluid analysis supported a tentative diagnosis of neoplastic or inflammatory disease. A computed tomography-guided biopsy provided both cytopathological and histopathological evidence of intravascular lymphoma. The disease progressed despite chemotherapy with prednisone, L-asparginase, and vincristine. Postmortem histopathological examinations suggested intravascular lymphoma in the central and peripheral nervous systems as well as in multiple other organ systems. This is the first description of an antemortem diagnosis and treatment of intravascular lymphoma involving the central nervous system of a dog.

Animals↗
PubMed1993

Characterization of glial trkB receptors: differential response to injury in the central and peripheral nervous systems.

In situ hybridization on sections from the adult rat peripheral and central nervous systems demonstrated that trkB mRNA was expressed not only by neurons but also by cells in central nervous system white matter as well as by Schwann cells in the sciatic nerve. In situ hybridization with an oligonucleotide complementary to the trkB tyrosine kinase domain could only demonstrate mRNA in neurons, indicating expression of truncated trkB receptors lacking the tyrosine kinase domain by glial cells. RNA blot analysis was performed on separately cultured central nervous system glial cells to study which cell types express trkB mRNA. Several transcripts encoding truncated trkB receptors were expressed at high levels in O-2A progenitors, astrocytes, and oligodendrocytes, but not trkB mRNA could be detected in microglia. The expression of trkB mRNA by glial cells in vivo was also investigated after injury; strongly elevated levels of mRNA encoding truncated receptors were detected in the glial scar formed after an incision in the spinal cord dorsal funiculus. In contrast, in the cut sciatic nerve, trkB mRNA decreased distal to the transection, and by 3 weeks only very low levels of mRNA could be detected. Immunoelectron microscopy located trkB-like immunoreactivity to axons and Schwann cells in the sciatic nerve. The expression of truncated trkB receptors by astrocytes, oligodendrocytes, and Schwann cells and the altered levels in response to injury indicate that glial trkB receptors may serve an important function in the intact and injured nervous system.

Animals↗
PubMed2005

Tumor necrosis factor-alpha-converting enzyme is expressed in the inflamed peripheral nervous system.

Tumor necrosis factor-alpha (TNF-alpha) is considered to play a critical role in the pathogenesis of immune-mediated inflammatory demyelinating disorders of the peripheral nervous system (PNS). Processing of membrane-bound inactive pro-TNF-alpha into the active soluble cytokine is mediated by a sheddase, the so-called TNF-alpha-converting enzyme (TACE), a member of the A Disintegrin and Metalloproteinase (ADAM) family. We explored the expression of TACE (ADAM-17) in sciatic nerves from Lewis rats with experimental autoimmune neuritis (EAN), an animal model of the Guillain-Barré syndrome (GBS), an immune-mediated polyradiculoneuropathy. To extend our study to human disease, sural nerve biopsies from GBS patients were investigated by immunohistochemistry. In EAN, T lymphocytes could be defined as the cellular source of ADAM-17 with peak expression levels at maximum clinical disease severity. Similarly, in human sural nerves, ADAM-17-expressing T cells could be localized primarily within the epi- and perineurium, whereas in control sections from patients with non-inflammatory neuropathies, no expression could be depicted. Our findings indicate that ADAM-17 is upregulated during EAN and expressed in nerves of GBS patients and thus may contribute to the pathogenesis of inflammatory demyelination of the PNS.

ADAM Proteins↗