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Results for “Peripheral Nervous System”

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PubMed2002

Planarian cytochrome b(561): conservation of a six transmembrane structure and localization along the central and peripheral nervous system.

Cytochrome b(561) is a major transmembrane protein of catecholamine and neuropeptide secretory vesicles in the central and peripheral nervous systems of higher animals. We succeeded in cloning a full-length cDNA encoding planarian cytochrome b(561). The deduced amino acid sequence shows a very similar six transmembrane topology to those of cytochromes b(561) of higher vertebrates and contains both putative ascorbate- and monodehydro ascorbate-binding sites. Among the six totally-conserved His residues of cytochrome b(561) in higher vertebrates, one is substituted with an Asn residue, indicating that His88 and His161 of bovine cytochrome b(561) play roles as heme b ligands at the extravesicular side. Northern- and Western-blot analyses confirmed the expression of the mRNA and protein with the expected sizes in planarians. The distributions of the mRNA and apoprotein were analyzed by in situ hybridization and immunohistochemical staining, respectively, showing two morphologically distinct structures, a pair of ventral nerve cords and the cephalic ganglion cluster in the head region. The present results suggest that the usage of ascorbate to supply electron equivalents to neuroendocrine-specific copper-containing monooxygenases is likely to have originated in organisms with a very simple nervous system.

Amino Acid Sequence↗

PubMed1975

Histophysiology of the vegetative peripheral nervous system of skin.

Preterminal nerve fibers of the peripheral vegetative nervous system make inmediate contact (neuro-effector-areas) to interstitial cells (I.C.). This connection is characterized through a common glycocalyx with the nerve fiber. The I.C. are specific innervated cells and differ morphologically from Schwann-cells, fibrocytes, and histiocytes. The I.C. are able to come into morphologically different contacts with neighbouring cells by microvilli-like cell protrusions. These neighbouring cells then are able to contact other cells by themselves. The results are interpreted in the sense of electro-mechanical feed-back system of information processing in the vegetative periphery.

Animals↗

PubMed2002

Neuropathology of some hereditary conditions affecting central and peripheral nervous system.

Neuropathology plays a crucial role in the phenotypic individualization of hereditary disorders affecting the central and peripheral nervous system even if molecular genetics represents the most essential step in describing the genotypes. The neuropathological description of phenotypes and genotypes can be used for refining clinical skills and understanding many clinical, neurophysiological and neuroradiological features. It contributes to the diagnosis of such disorders. The use of immunohistochemical techniques in combination with molecular genetics improves also our knowledge of their pathogenesis and might participate to the future development of therapeutic strategies. We discuss new features of spino-cerebellar ataxia (SCA) type 7 and of a recently identified SCA17 in order to illustrate the significance of the neuronal intranuclear inclusions (NIIs) described in various CAG/polyglutamine repeat expansion diseases. In the field of the peripheral neuropathies we present data on a newly described autosomal recessive Charcot-Marie-Tooth disease (CMT4F) with mutations in the periaxin gene. We document a dysjunction between myelin loops and axolemma with disappearance of the septate-like junctions or transverse bands. The significance of this dysjunction is not yet elucidated. We hope to show by these examples that the combination of classical and new neuropathological methods is useful in the study of hereditary disorders of the nervous system.

Central Nervous System↗

PubMed1980

[Diseases of the lumbosacral division of the peripheral nervous system in children and adolescents].

The clinical picture and course of diseases affecting the lumbosacral division of the peripheral nervous system in 111 children and adolescents aged 8 to 18 years are described. It was found that in 40.5% of the patients the diseases developed in the presence of congenital anomalies in the development of the lumbosacral part of the vertebral column. Unlike adults, the pain syndrome in children and adolescents is less pronounced, and leading in the clinical picture are signs of reflectory-tonic protection of the vertebral column.

Adolescent↗

PubMedDate not supplied

[The naphthalan therapy of patients with gunshot trauma to the peripheral nervous system].

Naphthalan therapy was given to 48 patients with gun-shot injuries of peripheral nervous system. Clinico-electrophysiological assessment stated a regress of motor, sensitivity, vegetovascular and trophic damage after a course of naphthalan therapy, enhancement of regeneration, reinnervation, stimulation of repair in impaired nervous-muscular structures.

Adult↗

PubMed2001

Association of human herpesvirus 6 and human herpesvirus 7 with demyelinating diseases of the nervous system.

Peripheral blood mononuclear cells and plasma of 113 patients with neurological disorders and 150 blood donors were analyzed for HHV-6 and HHV-7 sequences by PCR. The prevalence of HHV-6 was significantly higher in patients with multiple sclerosis (P < 0.01) than in cases of nondemyelinating diseases of the central and demyelinating diseases of the peripheral nervous systems and blood donors. HHV-6 viremia was found only in patients with multiple sclerosis, predominantly in the active phase of the disease. A significantly higher frequency of HHV-7 reactivation in patients with demyelinating diseases of the peripheral nervous system suggests also its association with demyelinating processes.

Adolescent↗

PubMed1991

Pharmacological studies with the alpha 2-adrenoceptor antagonist midaglizole. Part II: Central and peripheral nervous systems.

Pharmacological properties of midaglizole (DG-5128, CAS 66529-17-7) on central and peripheral nervous systems were investigated in comparison with those of tolbutamide. 1. Central nervous system: Midaglizole showed little or no effects on general behavior (mouse), spontaneous motor activity (mouse), hexobarbital anesthesia (mouse), conditioned avoidance response (rat) and body temperature (rabbit) at an oral dose of 100 mg/kg. It also produced little or no changes in electroencephalogram (cat) and spinal reflex (cat) after intravenous dosing of 10 mg/kg. The drug lacked anticonvulsant and analgesic activities (mouse). Midaglizole produced clonic convulsion, mydriasis, lacrimation, increase in pinna reflex, decrease in spontaneous motor activity, increase in pain threshold (mouse) and rise in body temperature (rabbit) at oral dose of 300 mg/kg. Tolbutamide showed similar effects except that it potentiated hexobarbital anesthesia, slightly decreased convulsion and tended to decrease body temperature. 2. Autonomic nervous system: Midaglizole potentiated the pressor response to norepinephrine and inhibited the depressor response to acetylcholine at an intravenous dose of 10 mg/kg (anesthetized dogs). Similar results were observed after dosing of tolbutamide. Midaglizole potentiated the contractile response of nictitating membrane to pre- and post-ganglionic cervical sympathetic nerve stimulation after intravenous dosing of 1 mg/kg (cat). Tolbutamide lacked the activity on the contraction elicited by both stimulations. Midaglizole and tolbutamide had little or no effect on pupil size (rabbit). 3. Skeletal muscle contraction (neuromuscular junction): Midaglizole (3-10 mg/kg i.v.) slightly potentiated the tibialis anterior muscle contraction induced by peroneal nerve stimulation, but did not potentiate the contraction by direct (muscle) stimulation (rabbit). On the other hand, tolbutamide increased the contraction induced by both nerve and muscle stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1987

Activated neu oncogene sequences in primary tumors of the peripheral nervous system induced in rats by transplacental exposure to ethylnitrosourea.

Neurogenic tumors were selectively induced in high incidence in F344 rats by a single transplacental exposure to the direct-acting alkylating agent N-ethyl-N-nitrosourea (EtNU). We prepared DNA for transfection of NIH 3T3 cells from primary glial tumors of the brain and from schwannomas of the cranial and spinal nerves that developed in the transplacentally exposed offspring between 20 and 40 weeks after birth. DNA preparations from 6 of 13 schwannomas, but not from normal liver, kidney, or intestine of tumor-bearing rats, transformed NIH 3T3 cells. NIH 3T3 clones transformed by schwannoma DNA contained rat repetitive DNA sequences, and all isolates contained rat neu oncogene sequences. One schwannoma yielded a transformant with rat-specific sequences for both neu and N-ras. A point mutation in the transmembrane region of the putative protein product of neu was identified in all six transformants and in the primary tumors from which they were derived as well as in 5 of 6 schwannomas tested that did not transform NIH 3T3 cells. Of 59 gliomas, only one yielded transforming DNA, and an activated N-ras oncogene was identified. The normal cellular neu sequence for the transmembrane region, but not the mutated sequence, was identified in DNA from all 11 gliomas surveyed by oligonucleotide hybridization. Activation of the neu oncogene, originally identified [Schechter, A.L., Stern, D.F., Vaidyanathan, L., Decker, S.J., Drebin, J.A., Greene, M.I. & Weinberg, R.A. (1984) Nature (London) 312, 513-516] in cultured cell lines derived from EtNU-induced neurogenic tumors that by biochemical but not histologic criteria were thought to originate in the central nervous system in BD-IX rats, appears specifically associated with tumors of the peripheral nervous system in the F344 inbred strain.

Animals↗

PubMed1984

An immunohistochemical study of human central and peripheral nervous system tumors, using monoclonal antibodies against neurofilaments and glial filaments.

Monoclonal antibodies that recognize either neurofilaments or glial filaments were used with the peroxidase-antiperoxidase (PAP) method to retrospectively study 100 tumors of the central and peripheral nervous systems in paraffin-embedded sections. Only neoplasms of putative neuronal origin or with presumed neuronal differentiation (paraganglioma, ganglioglioma, ganglioneuroblastoma, ganglioneuroma, neuroblastoma, ovarian teratoma and pheochromocytoma) contained tumor cells with immunoreactive neurofilament, but such cells were more common in the more differentiated or benign neoplasms in this category. Glial filament immunoreactivity was observed in tumor cells of glial origin and in tumor cells with foci of glial differentiation arising within the central nervous system, consistent with findings from previous studies using anti-glial-filament antisera. With the exception of a benign cystic teratoma, no glial filament immunoreactivity was observed outside the central nervous system. Some immunoreactive neurofilaments, but not glial filaments, were arranged in presumably abnormal balls, cords, or clumps within tumor cells, possibly reflecting cytoskeletal alterations related to neoplastic transformation. These findings indicate that monoclonal antibodies against intermediate filament proteins such as neurofilaments and glial filaments retain their specificity and sensitivity when employed in paraffin sections in conjunction with the peroxidase-antiperoxidase method. They suggest that such reagents are useful probes for the evaluation of the histogenesis or degree of differentiation in human nervous system tumors. Finally, they permit the speculation that the analysis of the intermediate filaments of tumor cells, as contrasted with those in normal cells, may provide new insights into the biology of neoplasms.

Antibodies, Monoclonal↗

PubMed1983

Sympathetic postganglionic unmyelinated axons in the rat peripheral nervous system.

We determined the contribution made to the unmyelinated axon population of the rat peripheral nervous system by sympathetic paravertebral ganglion cells. Sympathectomy, achieved by administration of guanethidine to neonatal rats, led to atrophy of the sympathetic paravertebral ganglion chain, a 95% decrease in peripheral nerve norepinephrine, and loss of 20 to 26% of the unmyelinated axons in a cutaneous nerve (sural), a muscular nerve (nerve to soleus), and a mixed nerve (sciatic). These data indicate that up to a quarter of the total population of peripheral nerve unmyelinated axons are sympathetic ganglia-derived.

Animals↗

PubMed1991

A member of the RXR nuclear receptor family is expressed in neural-crest-derived cells of the developing chick peripheral nervous system.

Retinoic acid (RA) affects differentiation and morphogenesis in various developmental systems and is believed to act through nuclear RA receptors that belong to the steroid/thyroid hormone family of ligand-binding transcription factors. Three closely related receptors, RAR-alpha, -beta and -gamma, with distinct expression patterns, have been identified and a fourth receptor, hRXR-alpha, which responds to RA but which has low homology to RAR-alpha, -beta and -gamma, was recently discovered. Here we report the isolation of a cDNA clone encoding a chicken homologue of hRXR-alpha (cRXR) and show that a cRXR transcript of 2.5 kb is expressed in a range of embryonic chick tissues. By in situ hybridization to sections from stage 24 and stage 27 chick embryos, we show that cRXR transcripts are expressed at high levels in the liver and in elements of the developing peripheral nervous system derived from the neural crest, including dorsal root ganglia, cranial ganglia, enteric ganglia and peripheral nerve tracts. At stage 16, in the posterior trunk region, cRXR transcripts are expressed by cells in the neural crest and in neural crest cells migrating into the sclerotome, indicating that neural crest cells express cRXR transcripts before overt differentiation into peripheral nervous tissue. This distribution suggests a novel role for RA in the developing peripheral nervous system, mediated by cRXR. In addition, it identifies cRXR as a marker for a specific population of neural-crest-derived cells.

Amino Acid Sequence↗

PubMed1999

Syntaxin 1A and 1B display distinct distribution patterns in the rat peripheral nervous system.

Syntaxin 1 has been shown to play an outstanding role in synaptic vesicle exocytosis. Two isoforms of this protein are expressed in neurons, syntaxin 1A and 1B. However, the physiological significance of the occurrence of such closely related isoforms is not still understood. Here, by means of isoform-specific immunocytochemistry, we show that syntaxin 1A and 1B display different patterns of expression in the rat peripheral nervous system. Nerve terminals of sensory neurons reaching the spinal cord were clearly enriched in immunoreactive syntaxin 1A. Both isoforms were detected in cell bodies of sensory neurons at the dorsal root ganglia, although specific immunolabelling displayed very different patterns at the cellular level. Motor endplates and muscle spindles were only immunostained for syntaxin 1B. Syntaxin 1A was mainly associated with nerve fibres reaching small blood vessels. In addition, nerve plexuses of the enteric nervous system showed immunostaining for both syntaxin isoforms. The different distribution pattern of the two neuronal syntaxin isoforms in the rat peripheral nervous system could be related to isoform-specific biochemical properties involved in the exocytotic process.

Animals↗

PubMed2005

Insulin therapy protects the central and peripheral nervous system of intensive care patients.

OBJECTIVE: To investigate the effectiveness of maintaining blood glucose levels below 6.1 mmol/L with insulin as prevention of secondary injury to the central and peripheral nervous systems of intensive care patients. METHODS: The authors studied the effect of intensive insulin therapy on critical illness polyneuropathy (CIPNP), assessed by weekly EMG screening, and its impact on mechanical ventilation dependency, as a prospectively planned subanalysis of a large randomized, controlled trial of 1,548 intensive care patients. In the 63 patients admitted with isolated brain injury, the authors studied the impact of insulin therapy on intracranial pressure, diabetes insipidus, seizures, and long-term rehabilitation at 6 and 12 months follow-up. RESULTS: Intensive insulin therapy reduced ventilation dependency (p = 0.0007; Mantel-Cox log rank test) and the risk of CIPNP (p < 0.0001). The risk of CIPNP among the 405 long-stay (> or =7 days in intensive care unit) patients was lowered by 49% (p < 0.0001). Of all metabolic and clinical effects of insulin therapy, and corrected for known risk factors, the level of glycemic control independently explained this benefit (OR for CIPNP 1.26 [1.09 to 1.46] per mmol blood glucose, p = 0.002). In turn, prevention of CIPNP explained the ability of intensive insulin therapy to reduce the risk of prolonged mechanical ventilation (OR 3.75 [1.49 to 9.39], p = 0.005). In isolated brain injury patients, intensive insulin therapy reduced mean (p = 0.003) and maximal (p < 0.0001) intracranial pressure while identical cerebral perfusion pressures were obtained with eightfold less vasopressors (p = 0.01). Seizures (p < 0.0001) and diabetes insipidus (p = 0.06) occurred less frequently. At 12 months follow-up, more brain-injured survivors in the intensive insulin group were able to care for most of their own needs (p = 0.05). CONCLUSIONS: Preventing even moderate hyperglycemia with insulin during intensive care protected the central and peripheral nervous systems, with clinical consequences such as shortening of intensive care dependency and possibly better long-term rehabilitation.

Adult↗

PubMed1998

The vestigial gene of Drosophila melanogaster is involved in the formation of the peripheral nervous system: genetic interactions with the scute gene.

The vestigial (vg) gene of Drosophila melanogaster encodes a novel nuclear protein which is required for wing formation but its function is not restricted to this developmental process. In this report, we have examined the possible role of vestigial in the formation of the peripheral nervous system. We found that most vestigial mutants display ectopic or missing macrochaetae. We also show that vestigial interacts in a dose dependant manner with different alleles of the scute gene and with the extramacrochaetae gene and that mis-expression of the vestigial gene in the wing disc increases the domain of scute expression and allows the formation of supernumerary ectopic bristles. From these results, we conclude that vestigial affects scute expression and plays a role in the differentiation of the peripheral nervous system.

Alleles↗

PubMed1991

Autonomic and peripheral nervous system dysfunction in workers exposed to mixed organic solvents.

To assess possible solvent-induced dysfunction of the autonomic and peripheral nervous systems, 11 solvent-exposed workers and 11 age-matched unexposed controls were examined using the coefficient of variation in electrocardiographic R-R intervals (CVRR) and the distribution of nerve conduction velocities (DCV). Two components of CVRR, i.e., the C-CVRSA and C-CVMWSA, were also examined, which are considered to reflect parasympathetic and sympathetic activities, respectively. The workers had been occupationally exposed to toluene and/or solvent mixtures such as thinners, for 35-360 months. In the solvent-exposed workers, the CVRR and C-CVRSA were significantly reduced compared with unexposed controls. Similarly, the faster velocities of the DCV and median nerve conduction velocities were significantly slowed. The reduction in the CVRR was significantly correlated with duration of exposure in the solvent-exposed workers. These data, despite the small sample size and the variety of organic solvents, suggest that organic solvents may affect both the faster myelinated nerve fibers and autonomic nervous activity (principally, parasympathetic component).

Adult↗

PubMed1998

Carboplatin toxic effects on the peripheral nervous system of the rat.

BACKGROUND: The most striking of carboplatin's advantages (CBDCA) over cisplatin (CDDP) is its markedly reduced rate of neurotoxic effects. However, the use of CBDCA higher-intensity schedules and the association with other neurotoxic drugs in polychemotherapy may cause some concern about its safety with respect to peripheral nervous system damage. MATERIALS AND METHODS: Two different schedules of CBDCA administration (10 mg/kg and 15 mg/kg i.p. twice a week for nine times) were evaluated in Wistar rats. Neurotoxicity was assessed for behavioral (tail-flick test), neurophysiological (nerve conduction velocity in the tail nerve), morphological, morphometrical and analytical effects. RESULTS: CBDCA administration induced dose-dependent peripheral neurotoxicity. Pain perception and nerve conduction velocity in the tail were significantly impaired, particularly after the high-dose treatment. The dorsal root ganglia sensory neurons and, to a lesser extent, satellite cells showed the same changes as those induced by CDDP, mainly affecting the nucleus and nucleolus of ganglionic sensory neurons. Moreover, significant amounts of platinum were detected in the dorsal root ganglia and kidney after CBDCA treatment. CONCLUSIONS: CBDCA is neurotoxic in our model, and the type of pathological changes it induces are so closely similar to those caused by CDDP that it is probable that neurotoxicity is induced in the two drugs by the same mechanism. This model can be used alone or in combination with other drugs to explore the effect of CBDCA on the peripheral nervous system.

Animals↗

PubMed1992

[Morbidity of the peripheral nervous system among the crew of fishing vessels and their treatment under shipboard conditions].

The incidence of diseases of the peripheral nervous system was studied during the voyage in different groups of sea sailors. The diseases due to overcooling and overexercise (cervico-thoracic and lumbosacral radiculosis) appeared to predominate. Methods of electroneurostimulation of acupuncture points and reflexogenic zones, lymphotropic therapy were used in the treatment administered on board the ship.

Absenteeism↗

PubMed1995

N-acetylated alpha-linked acidic dipeptidase is expressed by non-myelinating Schwann cells in the peripheral nervous system.

N-acetylated alpha-linked acidic dipeptidase is a membrane-bound brain peptidase which cleaves the neuropeptide N-acetyl-aspartyl-glutamate to N-acetyl-aspartate and glutamate. In the present study, we have determined the localization of N-acetylated alpha-linked acidic dipeptidase in the peripheral nervous system. Using enzyme assays and immunoblotting, we demonstrate that sciatic nerve, phrenic nerve, cervical dorsal root ganglion and superior cervical ganglion contain N-acetylated alpha-linked acidic dipeptidase activity as well as an N-acetylated alpha-linked acidic dipeptidase-like protein. Furthermore, we show that N-acetylated alpha-linked acidic dipeptidase-like immunoreactivity is extensively co-localized in peripheral nerves with immunoreactivity for glial fibrillary acidic protein, a known marker for non-myelinating Schwann cells. Using electron microscopy, we demonstrate N-acetylated alpha-linked acidic dipeptidase-like immunoreactivity in cell membranes of non-myelinating Schwann cells in the superior cervical ganglion. These results show that N-acetylated alpha-linked acidic dipeptidase is expressed in the peripheral nervous system by non-myelinating Schwann cells. This cellular localization suggests that N-acetylated alpha-linked acidic dipeptidase may be involved in the signalling between axons and Schwann cells, for example during development or regeneration.

Animals↗