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PubMed1990

Genes involved in the development of the peripheral nervous system of Drosophila.

The development of the peripheral nervous system (PNS) requires the activity of a number of genes. The neurogenic and the proneural genes are necessary in the earliest phase; their mutations lead to hyperplasia and partial or total elimination of the PNS respectively. Some of these mutations also affect other developmental processes. Other mutations affect later events: cut transforms one type of sensory organ into another; numb alters the fate of the components of a single sensory organ. We will describe the effects of the best studied mutations on PNS development and discuss the possible role of the wild type genes.

Animals↗
PubMed1995

The cyclic AMP response element directs tyrosine hydroxylase expression in catecholaminergic central and peripheral nervous system cell lines from transgenic mice.

Enhancer elements regulating the neuronal gene, tyrosine hydroxylase (TH), were identified in TH-expressing peripheral nervous system PATH and central nervous system CATH cell lines. Mutational analysis in which rat TH 5'-flanking sequences directed chloramphenicol acetyltransferase (CAT) reporter gene expression demonstrated that mutating the cyclic AMP response element (CRE) at -45 base pair reduced expression by 80-90%. A CRE linked to an enhancerless TH promoter fully supported expression. Cotransfection of a dominant-negative CREB protein reduced expression 50-60%, suggesting that the CRE is bound by CREB or a CREB dimerization partner. Although mutating the AP1/dyad (AD) element at -205 base pair only modestly reduced CAT levels, AD minimal enhancer constructs gave 45-80% of wild type expression when positioned at -91 or -95. However, in its native context at -205, the AD could not support expression. In contrast, a CRE, moved from its normal position at -45 to -206, gave full activity. These results indicate that the CRE is critical for TH transcription in central nervous system CATH and peripheral nervous system PATH cells, whereas the AD is less important and its enhancer activity is context-and/or position-dependent. These results represent the first attempts to map regulatory elements directing TH expression in central nervous system cell lines.

Adrenal Gland Neoplasms↗
PubMed1980

Adult metachromatic leukodystrophy. IV. Ultrastructural studies on the central and peripheral nervous system.

Ultrastructural studies on the central and peripheral nervous system of 2 patients with adult onset metachromatic leukodystrophy (MLD), dead at the ages of 46 and 51 years, showed MLD-specific inclusions, tufaceous and prismatic structures, a wide spectrum of membranous arrangements within lysosomal residual bodies, and the intimate admixture of sulfatides and other membranous material with lipopigments. Oligodendrocytes and Schwann cells were foremost affected but membranous inclusions could also be verified in neuronal perikarya and astrocytes. The varying ultrastructural spectrum of lysosomal residual bodies in adult onset MLD and the association with lipopigments, chiefly in nerve cells, exceed the fine structural observations on late infantile and juvenile MLD and may reflect morphological differences between these subtypes of MLD that are also known from clinical and biochemical observations.

Adipose Tissue↗
PubMed1993

Effect of hypothyroidism on rat peripheral nervous system.

The function and structure of the peripheral nervous system of Sprague-Dawley rats, 3 months after the induction of hypothyroidism by administration of N-propylthiouracil in drinking water, has been studied. The motor action potential amplitude of the caudal nerve showed a significant reduction (p < 0.001) when compared with an age-matched control group of animals. Computer-assisted morphometric analysis of sciatic nerves of hypothyroid rats showed normal distribution and density of myelinated fibers, and a normal axon/myelin ratio. Electron microscopy revealed only minor alterations in axons of myelinated fibers characterized by a dissolution of neurotubules. After two months of substitution therapy these effects were reversed. The present data suggest that early impairment of nerves induced by hypothyroidism is rare and could be related to metabolic alterations rather than to structural changes and is reversible with hormone treatment.

Action Potentials↗
PubMed1986

Small basic proteins of myelin from central and peripheral nervous systems are encoded by the same gene.

Peripheral nervous system (PNS) and central nervous system (CNS) rodent myelins, which are produced by different cell types, share common morphological and functional characteristics although their major integral membrane proteins are completely different. Both types of myelin however, contain sets of four myelin basic proteins (MBPs), which share similar immunochemical and electrophoretic properties. We have isolated and characterized cDNA clones corresponding to the rat mRNAs encoding the small MBPs (SMBPs) found in both CNS and PNS myelin. Sequence analysis of these clones indicate that SMBPs in both divisions of the nervous system are encoded by the same nucleotide sequences, which suggests that they are the products of the same gene expressed in both oligodendrocyte and Schwann cells. In dot-blot hybridization experiments with the CNS SMBP cDNA as a probe, it was shown that there is a 20-fold higher level of MBP mRNA in a CNS myelin fraction than in total brainstem mRNA. It also was found that in optic and sciatic nerves, which contain oligodendrocytes and Schwann cells respectively, there are higher levels (4-fold and 2-fold, respectively) of MBP mRNA than in brainstem. Blot-hybridization experiments showed that a probe derived from the coding region of the rat SMBP cDNA hybridizes to an homologous mRNA (approximately equal to 2.6 kilobases) present in human optic nerve, which is not detectable with a probe derived from the 3' untranslated region. This conservation of coding-region sequences is in accord with the highly homologous amino acid sequences reported for the MBPs in the two species.

Animals↗
PubMed2003

Localization and modulation of calcitonin gene-related peptide-receptor component protein-immunoreactive cells in the rat central and peripheral nervous systems.

Calcitonin gene-related peptide (CGRP) is widely distributed in the central and peripheral nervous system. Its highly diverse biological activities are mediated via the G protein-coupled receptor that uniquely requires two accessory proteins for optimal function. CGRP receptor component protein (RCP) is a coupling protein necessary for CGRP-receptor signaling. In this study, we established the anatomical distribution of RCP in the rat central and peripheral nervous system and its relationship to CGRP immunoreactivity. RCP-immunoreactive (IR) perikarya are widely and selectively distributed in the cerebral cortex, septal nuclei, hippocampus, various hypothalamic nuclei, amygdala, nucleus colliculus, periaqueductal gray, parabrachial nuclei, locus coeruleus, cochlear nuclei, dorsal raphe nuclei, the solitary tractus nucleus and gracile nucleus, cerebellar cortex, various brainstem motor nuclei, the spinal dorsal and ventral horns. A sub-population of neurons in the dorsal root ganglia (DRG) and trigeminal ganglia were strongly RCP-IR. Overall, the localization of RCP-IR closely matched with that of CGRP-IR. We also determined whether RCP in DRG and dorsal horn neurons can be modulated by CGRP receptor blockade and pain-related pathological stimuli. The intrathecal injection of the antagonist CGRP(8-37) markedly increased RCP expression in the lumbar DRG and spinal dorsal horn. Carrageenan-induced plantar inflammation produced a dramatic bilateral increase in RCP expression in the dorsal horn while a partial sciatic nerve ligation reduced RCP expression in the ipsilateral superficial dorsal horn. Our data suggest that the distribution of RCP immunoreactivity is closely matched with CGRP immunoreactivity in most of central and peripheral nervous systems. The co-localization of RCP and CGRP in motoneurons and primary sensory neurons suggests that CGRP has an autocrine or paracrine effect on these neurons. Moreover, our data also suggest that RCP expression in DRG and spinal cord can be modulated during CGRP receptor blockade, inflammation or neuropathic pain and this CGRP receptor-associated protein is dynamically regulated.

Animals↗
PubMed1991

Serum antibodies against peripheral nervous system antigens in leprosy.

Since antibodies against peripheral nervous system (PNS) antigens may play a pathogenetic role in the mechanism of nerve damage in leprosy, sera from leprosy patients and contacts were investigated for anti-PNS antibodies by ELISA and immunoblot. In ELISA, elevated anti-PNS antibody levels were detected in 4 of 98 (4.1%) leprosy patients (4 of 52, 7.7%, lepromatous leprosy patients), in 1 of 28 (3.6%) contacts, and in 1 of 18 (5.6%) normal controls. There was no correlation between anti-PNS antibody levels and the bacterial index or neuropathy in leprosy. Immunoblot with a sample of six leprosy and five control sera showed that the antigenic binding pattern (mainly within the 100-200-kDa region) was very similar in patients and controls. Staining intensity, however, appeared to be higher with the leprosy sera than with the control sera. IgM and IgG were found to contribute to the staining pattern: IgM in the 150-200-kDa range, IgG with multiple bands between 25 kDa and 200 kDa. Thus, the presence and levels of serum anti-PNS antibodies in leprosy appear to be unrelated to parameters of disease activity, neuropathy in particular, and do not seem to be critically involved in the pathogenesis of nerve damage.

Antibody Specificity↗
PubMed1999

Effects of chronic lithium treatment on the peripheral nervous system.

BACKGROUND: Although lithium carbonate is widely used in the treatment of mood disorders, symptoms suggesting toxic effects on the peripheral nervous system may emerge even in subjects whose serum lithium levels remain within the recommended therapeutic range. METHOD: Electroneuronographic (ENG) parameters (motor nerve conduction velocity of peroneal and median nerves, sensory nerve conduction velocity of sural and median nerves, amplitude of motor potential of peroneal and median nerves, and amplitude of sensory action potential of the median nerve at the wrist and the sural nerve) were investigated in 2 groups (N = 34) of patients suffering from bipolar affective disorder (DSM-III-R, DSM-IV) undergoing maintenance treatment with lithium carbonate for at least 1 year (mean = 2.06 years) in monotherapy. For 12 patients, ENG results were compared with pretreatment values, whereas in the other 22 cases, only data relevant to posttreatment were available. Fifty-four healthy subjects and 20 patients with recurrent major affective disorder (unipolar and bipolar) never treated with lithium made up the comparison groups. RESULTS: Compared with the 2 comparison groups, patients on chronic lithium treatment showed significant reduction of motor nerve conduction velocity of peroneal and median nerves, sensory nerve conduction velocity of sural and median nerves, amplitude of motor potential of peroneal and median nerves, and amplitude of sensory action potential of the median nerve at the wrist and the sural nerve. The comparison with the assessment made prior to lithium treatment also showed significant changes; after a period of treatment with lithium varying from 2 to 8 years (mean = 5.2 years), significant reductions were found on motor and sensory nerve conduction velocity and on amplitude motor potentials and sensory action potentials. CONCLUSION: Chronic maintenance treatment with lithium affects the peripheral nerves, even if the impairment rarely is such as to warrant discontinuation of treatment. Monitoring of ENG results could be useful for the early detection of neurotoxicity of lithium.

Action Potentials↗
PubMed1996

Carcinoma and the peripheral nervous system.

An underlying carcinoma is an important differential diagnosis in peripheral neuropathy. While direct compression and infiltration of spinal roots or peripheral or cranial nerve trunks or branches can be identified easily when they occur in association with established malignancy, their diagnosis when they are presenting features may be difficult. In paraneoplastic sensory neuronopathy autoantibodies to neuronal antigens have become useful diagnostic markers for an underlying carcinoma, especially anti-Hu antibodies. Strong circumstantial evidence suggests that these antibodies form part of an autoimmune response which is responsible for the pathogenesis of some of these syndromes. Neuropathy appearing during the course of treatment of carcinoma may be due to radiation-induced damage or the neurotoxic effects of some chemotherapeutic agents. Neurotrophic factors are being investigated as a strategy for reducing the neurotoxic effects of these agents.

Combined Modality Therapy↗
PubMed1995

Neurosteroids: synthesis and functions in the central and peripheral nervous systems.

Some steroids are synthesized within the central and peripheral nervous systems, mostly by glial cells. These are known as neurosteroids. In the brain, neurosteroids have been shown to act directly on membrane receptors for neurotransmitters. For example, progesterone inhibits the neuronal nicotinic acetylcholine receptor, whereas its 3 alpha,5 alpha-reduced metabolite 3 alpha,5 alpha-tetrahydroprogesterone (allopregnanolone) activates the type A gamma-aminobutyric acid receptor complex. Besides these effects, neurosteroids also regulate important glial functions, such as the synthesis of myelin proteins. Thus, in cultures of glial cells prepared from neonatal rat brain, progesterone increases the number of oligodendrocytes expressing the myelin basic protein (MBP) and the 2',3'-cyclic nucleotide-3'-phophodiesterase (CNPase). An important role for neurosteroids in myelin repair has been demonstrated in the rodent sciatic nerve, where progesterone and its direct precursor pregnenolone are synthesized by Schwann cells. After cryolesion of the male mouse sciatic nerve, blocking the local synthesis or action of progesterone impairs remyelination of the regenerating axons, whereas administration of progesterone to the lesion site promotes the formation of new myelin sheaths.

Animals↗
PubMed1999

Myelin deficiencies in both the central and the peripheral nervous systems associated with a SOX10 mutation.

We describe an unique patient presenting with severe leukodystrophy compatible with Pelizaeus-Merzbacher disease and peripheral neuropathy consistent with Charcot-Marie-Tooth disease type 1 in addition to Waardenburg-Hirschsprung syndrome. A novel mutation was identified in her SOX10 gene, which encodes a transcription factor preferentially expressed in the late embryonic glial cell lineage and in mature myelin-forming cells of both the central nervous system and peripheral nervous system, as well as in the early neural crest cells. Heterozygous SOX10 loss-of-function mutations have been reported in patients with Waardenburg-Hirschsprung syndrome and its murine model, Dominant megacolon. However, neither Waardenburg-Hirschsprung syndrome patients nor Dominant megacolon mice have dysmyelinating features, suggesting the question of how SOX10 acts in the glial lineage in vivo. The novel mutation described herein does not disrupt the coding region but extends the peptide and hence is likely to act as a dominant-negative allele. Our findings indicate that dysfunction of SOX10 may lead to deficiency of myelination in the central nervous system and peripheral nervous system as well as hypopigmentation and enteric aganglionosis.

Alleles↗
PubMed2005

Involvement of the peripheral nervous system in human prion diseases including dural graft associated Creutzfeldt-Jakob disease.

OBJECTIVE: To investigate abnormal prion protein (PrP) deposition in the peripheral nervous system (PNS) in human prion diseases. METHODS: Eight patients with prion diseases were examined: three with sporadic Creutzfeldt-Jakob disease (sCJD), two with dural graft associated CJD (dCJD), one with Gerstmann-Straussler-Scheinker disease (GSS) with a PrP P102L mutation (GSS102), and two with a P105L mutation (GSS105). An atypical case of sCJD with PrP plaques in the brain presented clinically with peripheral neuropathy, and showed demyelination in 12% of the teased fibres of the sural nerve. The PNS was investigated by immunohistochemical and western blotting analyses of PrP. RESULTS: In immunohistochemical studies, granular PrP deposits were detected in some neurones of dorsal root ganglia and a few fibres of peripheral nerves and spinal posterior roots in one sCJD and two dCJD patients, but not in GSS102 or GSS105 patients. The atypical case of sCJD with peripheral neuropathy showed no obvious PrP deposition in the nerves. Western blotting analysis of the PNS from the dCJD patients revealed a small amount of protease K resistant PrP in the dorsal root ganglia and peripheral nerves. CONCLUSIONS: Abnormal PrP deposition occurs in the dorsal root ganglia and peripheral nerves in sCJD and dCJD. The PrP deposits in the PNS are not correlated with clinical manifestation of peripheral neuropathy in CJD.

Adult↗