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At least 721 records · Page 40Linked to original sources
PubMed1999

Genetically-targeted and conditionally-regulated ablation of astroglial cells in the central, enteric and peripheral nervous systems in adult transgenic mice.

Ablation of tissue regions, specific genes, or specific cell types represent important means of studying function in the nervous system. Here we summarize recent experience using a strategy for the genetically-targeted and conditionally regulated ablation of astroglial cells in different parts of the nervous system. The strategy is based on the targeted expression of herpes simplex virus thymidine kinase to astroglial cells using the glial fibrillary acid protein promoter in transgenic mice, combined with treatment with the antiviral agent ganciclovir. Under different experimental conditions we find that transgene-expressing astroglial cells can be selectively ablated by ganciclovir in the enteric nervous system, or in the injured forebrain or sciatic nerve, providing models in which to study the functions of these cells.

Animals↗
PubMed2003

L-DOPA increases noradrenaline turnover in central and peripheral nervous systems.

The ability of L-3,4-dihydroxyphenylalanine (L-DOPA) to release noradrenaline (NA) from peripheral and CNS neurons was studied using isolated rat vas deferens and in vivo frontal cortex microdialysis. Application of L-DOPA (30 microM) to vas deferens increased basal NA efflux but not electrical field stimulation-evoked release of NA when the tissue was pretreated with an inhibitor of MAO-B (clorgyline 1 microM) or an inhibitor of MAO-A and MOA-B (AGN-1133 1 microM). No effect on NA efflux was seen when the tissue was treated with rasagiline (0.005 microM; selective inhibitor of MAO-B), but rasagiline, AGN-1133 and clorgyline increased basal efflux of dopamine (DA) following L-DOPA. In microdialysis experiments, systemic administration of L-DOPA/carbidopa combination (50/12 mg.kg(-1)) increased the efflux of 3,4-dihydroxyphenylglycol and 3-methoxy,4-hydroxyphenylglycol but reduced that of NA. Microdialysate levels of NA, however were increased following L-DOPA/carbidopa when desipramine (1 microM) was infused locally via the probe, or following systemic administration of yohimbine (2 mg.kg(-1)). The data are consistent with the hypothesis that administration of L-DOPA is followed by increased axoplasmatic levels of DA which release NA from storage sites into the free cytoplasmatic pool.

Animals↗
PubMed1977

Serotonergic neurons in the peripheral nervous system: identification in gut by immunohistochemical localization of tryptophan hydroxylase.

A specific antibody to tryptophan hydroxylase [L-tryptophan, tetrahydropteridine:oxygen oxidoreductase (5-hydroxylating), EC 1.14.16.4] has been used to localize the enzyme immunohistochemically in neurons of the mammalian gut. The enzyme was found in perikarya of intestinal neurons of mice, rats, and guinea pigs. Neurons containing the enzyme survived for up to 3 weeks in organotypic tissue culture and were intrinsic to the gut. These neurons are probably serotonergic and are the first such neurons to be found in the peripheral nervous system.

Animals↗
PubMed2000

Protective effect of Rolipram in experimental autoimmune neuritis: protection is associated with down-regulation of IFN-gamma and inflammatory chemokines as well as up-regulation of IL-4 in peripheral nervous system.

Rolipram, a phosphodiesterase type 4 inhibitor, is reported to have anti-inflammatory effects. It can markedly downregulate antigen-driven T cell proliferation and suppress TNF-(alpha and TNF-beta production in vitro and in vivo, which have led to its use in the treatment of a number of autoimmune disorders including experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune neuritis (EAN). EAN is a CD4+ T cell-mediated demyelinating autoimmune disease of peripheral nervous system (PNS) that represents an animal model for the study of the immunopathogenesis and immunotherapy of Guillain-Barré syndrome (GBS) in human. In the previous study, we reported that suppression of EAN by Rolipram was associated with down-regulated myelin antigen-induced T cell responses as well as downregulated IFN-gamma and TNF-alpha production. Here we report that EAN induced in Lewis rats by inoculation with the PNS P2 protein peptide 57-81 and Freund's complete adjuvant (FCA), was strongly suppressed by Rolipram administered twice daily intraperitoneally from day 9 post immunization (p.i.), i.e. after onset of clinical EAN to day 18 p.i. This clinical effect was associated with dose-dependent down-regulated production of IFN-gamma and the chemokines macrophage inflammatory protein-1 alpha (MIP-1 alpha, MIP-2 and monocyte chemotactic protein-1(MCP-1) as well as up-regulated IL-4 production in sciatic nerve sections from Rolipram-treated EAN rats at maximum of clinical EAN, i.e. on day 14 p.i.. These findings suggest that Rolipram may be useful in certain T cell-dependent autoimmune diseases and inflammatory neuropathies. These observations call for further studies on the potential role of Rolipram in the treatment of autoimmune diseases.

Animals↗
PubMed1993

Microglial involvement in experimental autoimmune inflammation of the central and peripheral nervous system.

Microglial cells form a network of potential antigen presenting cells throughout the nervous system. Much progress has recently been made towards a better understanding of their immunological properties. This study examines their activation in 2 models of T cell-mediated autoimmune inflammation of the nervous system, experimental autoimmune encephalomyelitis (EAE) and its peripheral counterpart, experimental autoimmune neuritis (EAN), induced by the transfer of antigen-specific T cell lines. In both models microglial activation occurs at early stages of the disease. Activated microglial cells show an increased expression of MHC class I and II antigens. In EAE ultrastructural analysis revealed that MHC antigen expression is pronounced on perivascular microglial cells, suggesting this cell population may be important for antigen presentation at a site close to the blood-brain barrier. In contrast to EAE, the microglial reaction in EAN occurs at sites remote from the inflammatory response in the peripheral nerve, not only in the spinal cord but also in the terminal projection fields of primary sensory neurons in the lower brainstem. This early microglial activation in EAN suggests that a rapid and remote signaling mechanism can operate following peripheral inflammation. Immuno-electron microscopy revealed that activated microglial cells are also involved in the synaptic deafferentation of spinal cord motoneurons during autoimmune reactions. The rapid involvement of microglial cells in experimental autoimmune inflammation of the nervous system further points to their role as the main intrinsic immuneffector cell population of the central nervous system.

Animals↗
PubMed2000

The role of matrix metalloproteinases in autoimmune damage to the central and peripheral nervous system.

Members of the family of matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of inflammatory demyelination. MMPs apparently mediate important steps in the genesis of inflammatory demyelination, such as cell migration, blood-brain/nerve barrier breakdown, demyelination, and cytokine activation. This review will highlight in vitro as well as in vivo findings, which support the importance of this group of proteases in the pathogenesis of inflammatory demyelinating disorders of the central and peripheral nervous system.

Guillain-Barre Syndrome↗
PubMed2001

Gene array analysis reveals changes in peripheral nervous system gene expression following stimuli that result in reactivation of latent herpes simplex virus type 1: induction of transcription factor Bcl-3.

The earliest events within the peripheral mammalian nervous system that cause herpes simplex virus type 1 (HSV-1) to reactivate from latency are unknown but are highly likely to include altered regulation of cellular transcription factors. Using gene array analysis, we have examined the changes that occur in cellular mRNA levels in mouse trigeminal ganglia following explantation, a stimulus that results in HSV-1 reactivation from latency. We have detected both increased and decreased expression levels of particular cellular transcripts, which include RNAs encoding neuronal factors, transcription factors, and factors involved in the cell cycle. Among the transcription factors that are upregulated is Bcl-3, a coactivator for NFkappaB. We have confirmed these increases in Bcl-3 transcription levels using reverse transcription-PCR and S1 nuclease protection assays. In addition, we have shown Bcl-3 upregulation at the protein level. Importantly, Bcl-3 RNA levels were found to increase specifically in neuronal cells within the trigeminal ganglia. We discuss a potential role for this factor in upregulating ICP0 transcription, which is an important viral event for initiation of HSV-1 reactivation.

Animals↗
PubMed1992

Somatosensory conduction delay in central and peripheral nervous system of diabetic patients.

Fifty-four diabetic patients with or without clinical evidence of neuropathy and with no clinical evidence of CNS dysfunction were studied by somatosensory-evoked potentials after electrical stimulation of the median nerve at the wrist and recorded from the scalp electrode against a noncephalic reference. Peripheral conduction index, calculated as the distance from the wrist to the C7 spinous process divided by the P9 latency, was significantly decreased (P less than 0.01) in diabetic patients (69.81 +/- 6.47 m/s) compared with 28 age-matched nondiabetic subjects (76.85 +/- 5.65 m/s). The P11-P13 interpeak latency, representative of the transit time from the dorsal column at the level of the sensory input into the cervical cord to the brain stem along the somatosensory pathways (CCT1), and the P13-N19 interpeak latency, representative of the transit time from the brain stem to the somatosensory cortex (CCT2), were significantly increased in diabetic patients (CCT1, 2.51 +/- 0.63 ms; CCT2, 5.76 +/- 0.92 ms) compared with nondiabetic subjects (CCT1, 2.28 +/- 0.36 ms, P less than 0.05; CCT2, 5.18 +/- 0.51 ms, P less than 0.01). We conclude that, in diabetic patients, neurophysiological abnormalities may be present in two distinct parts of the CNS and the peripheral nervous system.

Blood Pressure↗
PubMed1984

Fetal mesencephalic neurons survive and extend long axons across peripheral nervous system grafts inserted into the adult rat striatum.

In adult rats whose nigrostriatal dopamine (DA) pathway had been chemically damaged we implanted a fetal mesencephalic graft over the superior colliculus and joined it to the denervated striatum by means of an approximately 2 cm long segment of heterologous sciatic nerve. Monoaminergic neurons within the implant extended axons along the entire length of the nerve bridges and of these fibers extended into the striatum, which is the normal target of nigral projections. Thus, combinations of fetal neuronal and peripheral nervous system grafts can be used in vivo to provide both a source and a substrate for lengthy axonal growth.

Animals↗
PubMed1991

High molecular weight tau: preferential localization in the peripheral nervous system.

Using epitope mapping we have demonstrated that a high molecular weight protein (Mr approximately 115 x 10(3)) present in brain and spinal cord is a member of the tau family of microtubule-associated proteins. Antibodies directed against the amino-terminal, middle and carboxyl-terminal portions of tau recognize this protein. A limited survey of neuronal tissues has shown that this high molecular weight tau protein is present in brain, spinal cord, dorsal root ganglia, dorsal and ventral roots and peripheral nerves. High molecular weight tau protein is expressed at higher levels in spinal cord than in brain and is the only form of tau detected in the adult peripheral nervous system.

Animals↗
PubMed2005

Adult onset metachromatic leukodystrophy without electroclinical peripheral nervous system involvement: a new mutation in the ARSA gene.

BACKGROUND: Metachromatic leukodystrophy (MLD) is a lysosomal storage disease caused by the deficiency of arylsulfatase A (ARSA). Clinically, the disease is heterogeneous with respect to the age of onset, affection of peripheral and central nervous systems, and progression. OBJECTIVES: To analyze mutations in the ARSA gene of a patient with adult-onset MLD with no signs of peripheral polyneuropathy and to emphasize the clinical, neuroradiologic, neuropathologic, and genetic features of the disease. DESIGN: Case study of a patient clinically presenting with rapidly progressive dementia and behavioral abnormalities. We report the findings of clinical evaluation and neurophysiologic and neuropathologic studies of peripheral nerves; we also performed DNA sequence analysis, transfections, metabolic labeling, and immunoprecipitation of mutant ARSA polypeptides. SETTING: Genetic research and clinical unit, university hospital. RESULTS: Genetic analysis revealed homozygosity for a novel mutation in exon 3 of ARSA (F219V). This substitution leads to a misfolded unstable enzyme with a specific activity less than 1% of normal. There were no clinical or neurophysiologic signs of peripheral nervous system dysfunction. Typical neuropathologic signs for MLD were absent from nerve biopsy specimens. CONCLUSIONS: This novel mutation is associated with progressive psychocognitive impairment without clinical or electrophysiologic signs and only minor morphologic signs of peripheral nerve affection. The F219V substitution causes reduction in enzyme activity to an extent unexpected for an adult patient with MLD.

Adult↗
PubMed1976

Reduction of folate levels in the rat: Difference in depletion between the central and the peripheral nervous system.

1. Rats were deprived of dietary folate for 12 and 9.5 months in two experiments; one with and one without succinylsulfathiazole added to the diet. Folate levels decreased faster in the former experiment and the final blood values were lower. Tissue folate was examined in the latter experiment only. 2. The animals were repeatedly examined with neurological tests and compared with a control group supplemented with folic acid. Every test proved normal. Measurement of motor nerve conduction velocities after 12 months in the experiment where succinylsulfathiazole was given revealed lower velocities in the non-supplemented group. There was no difference between the groups in the experiment without succinylsulfathiazole. 3. In the latter experiment brain folate was reduced by only 16% in the non-supplemented animals compared with the controls, whereas whole blood folate fell by 60%, liver folate by 50% and sciatic nerve folate by 59%. 4. The central nervous system is resistant to systemic folate depletion, whereas the peripheral nerves are depleted to the same degree as the extra-neural tissues.

Animal Nutritional Physiological Phenomena↗
PubMed1991

Neurophysiologic studies of the peripheral nervous system in nephropathic cystinosis.

Cystinosis is an autosomal recessive metabolic disorder in which nonprotein cystine accumulates within most body tissues due to a defect in lysosomal cystine transport. Neurologic declarations are only recently being recognized. We studied 13 cystinotic subjects (aged 5 to 21 years old), determining median motor and sensory nerve conduction velocities, F waves, peroneal motor nerve conduction velocities, sural sensory nerve conduction velocities, median sympathetic skin response, electrocardiogram R-to-R variability, and blink reflex analysis. The results were normal. We conclude that neurophysiologic testing suggests relative sparing of the peripheral nervous system in nephropathic cystinosis.

Adolescent↗