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PubMed1992

[Hypomagnesemia associated with hypocalcemia after undetected parathyroidectomy].

A case is reported of hypomagnesaemia and hypocalcaemia occurring postoperatively in a 59-year-old man operated on for hypopharyngeal carcinoma which had extended to the upper extremity of the oesophagus. Surgery consisted in total pharyngolaryngectomy, ganglion curage, jejunal transplant, thyroidectomy and tracheostomy. Total parathyroidectomy was not mentioned in the surgical report. Hypocalcaemia was first noticed on the day following the procedure. On the tenth postoperative day, the patient became agitated and had myoclonia and muscle fasciculations. Nystagmus and orthostatic hypotension also occurred. There were no cardiac signs. Treatment with calcium alone was insufficient. These symptoms only disappeared once magnesium sulphate had been added.

Calcium Gluconate↗
PubMed2000

Atypical effect of some spin trapping agents: reversible inhibition of acetylcholinesterase.

N-tert-butyl-alpha-phenylnitrone (PBN), a widely used nitrone-based free radical trap was recently shown to prevent acetylcholinesterase (AChE) inhibitors induced muscle fasciculations and brain seizures while being ineffective against glutamergic or cholinergic receptor agonist induced seizures. In the present study we compared the effects on AChE activity of four free radical spin traps PBN, alpha-(4-pyridil-1)-N-tert-butyl nitrone (POBN), N-tert-butyl-alpha-(2-sulfophenyl)-nitrone (S-PBN) and 5-diethoxyphosphoryl-5-methyl-1-pyrroline-N-oxide (DEPMPO). The kinetics of AChE inhibition were studied in vitro using a spectrophotometric kinetic assay with AChE from rat brain, diaphragm, electric eel and mouse brain. Spin trapping compounds S-PBN and DEPMPO, in concentrations up to 3 mM did not inhibit hydrolysis of ACh, while PBN and POBN inhibited hydrolysis of ACh in a reversible and concentration-dependent manner. Double reciprocal plots of the reaction velocity against varying ACh concentrations at each inhibitor concentration were linear and generally indicated mixed type inhibition. PBN was the most potent inhibitor of mouse AChE with Ki and Ki' of 0.58 and 2.99 mM, respectively, and the weakest inhibitor of electric eel AChE. In contrast, POBN showed the highest affinity for electric eel enzyme, with Ki and Ki' values of 1.065 and 3.15 mM, respectively. These findings suggest that the effect of PBN and POBN on AChE activity does not depend on trapping of damaging reactive oxygen and that in addition to their antioxidant action other pharmacological effects of these compounds should be considered when neuroprotective actions of PBN or POBN are investigated.

Acetylcholinesterase↗
PubMedDate not supplied

Effects of cholinesterase inhibitors on a two-component chained schedule performance in rats.

The acetylcholinesterase (AChE) inhibitors physostigmine (PHY), tacrine (THA), and heptylphysostigmine (HEP) have been evaluated as potential therapeutics for treatment of Alzheimer's disease (AD) and as prophylactics against organophosphate (OP) poisoning. The above medical applications are based upon the neurochemical principles of elevation of transient levels of acetylcholine (ACh) in brain and reversible inhibition of AChE in blood and brain, respectively. The present study was undertaken to evaluate the effects of these drugs on performance of a two-component chained schedule of differential-reinforcement-of-high-rate (DRH) reward/differential-reinforcement-of-low-rate (DRL) nonreward contingencies, for water reinforcement in 2-h experimental sessions in rats. Both PHY (0.031-0.25 mg/kg, SC) and HEP (0.625-10.0 mg/kg, SC) decreased overall reinforcement rate and nonreinforced response in a dose-related and parallel manner, whereas THA (0.625-5.0 mg/kg) decreased the overall reinforcement rate in a dose-related manner, but did not significantly affect nonreinforced response. The least significant doses of PHY (0.625 mg/kg), THA (1.25 mg/kg), and HEP (1. 25 mg/kg) on the behavioral performance were associated with oral movements and/or muscle fasciculation. Moderate to high doses of these drugs (i.e., PHY >/= 0.624, THA >/= 1.25, and HEP >/= 1.25 mg/kg) produced behavioral suppression, which resulted mostly from the cessation of responding in the presence of cholinergic adverse events. The ED(50) values of the behavioral disruption (as documented by overall reinforcer loss) for PHY, THA, and HEP were 0. 081, 3.87, and 2.89 mg/kg, respectively, and the behavioral-deficit-free (BDF) doses were 0.031, 0.625, and 0.625 mg/kg, respectively. Preclinical data revealed that the BDF doses of both PHY and HEP have moderate inhibition of AChE, which leads to an efficacious elevation of ACh level in the brain, whereas the BDF dose of THA shows no significant AChE inhibition or elevation of brain ACh level; however, they all have cognition enhancing effects at their respective safety doses. The above data suggest that the BDF doses of PHY and HEP may have prophylactic efficacy against OP poisoning, whereas THA may not. The BDF doses of these three drugs are comparable to the maximum tolerated doses in clinical practice, suggesting that the present rat model may have potential value in predicting the clinical safety of AChE inhibitors developed for therapy of AD and prophylaxis against OP poisoning as well.

Animals↗
PubMed1998

Neurotactin functions in concert with other identified CAMs in growth cone guidance in Drosophila.

We have isolated and characterized mutations in Drosophila neurotactin, a gene that encodes a cell adhesion protein widely expressed during neural development. Analysis of both loss and gain of gene function conditions during embryonic and postembryonic development revealed specific requirements for neurotactin during axon outgrowth, fasciculation, and guidance. Furthermore, embryos of some double mutant combinations of neurotactin and other genes encoding adhesion/signaling molecules, including neuroglian, derailed, and kekkon1, displayed phenotypic synergy. This result provides evidence for functional cooperativity in vivo between the adhesion and signaling pathways controlled by neurotactin and the other three genes.

Alleles↗
PubMed2000

Neuropilin-2 is required in vivo for selective axon guidance responses to secreted semaphorins.

Neuropilins are receptors for class 3 secreted semaphorins, most of which can function as potent repulsive axon guidance cues. We have generated mice with a targeted deletion in the neuropilin-2 (Npn-2) locus. Many Npn-2 mutant mice are viable into adulthood, allowing us to assess the role of Npn-2 in axon guidance events throughout neural development. Npn-2 is required for the organization and fasciculation of several cranial nerves and spinal nerves. In addition, several major fiber tracts in the brains of adult mutant mice are either severely disorganized or missing. Our results show that Npn-2 is a selective receptor for class 3 semaphorins in vivo and that Npn-1 and Npn-2 are required for development of an overlapping but distinct set of CNS and PNS projections.

Age Factors↗
PubMed1999

Ataxia and abnormal cerebellar microorganization in mice with ablated contactin gene expression.

Axon guidance and target recognition depend on neuronal cell surface receptors that recognize and elicit selective growth cone responses to guidance cues in the environment. Contactin, a cell adhesion/recognition molecule of the immunoglobulin gene superfamily, regulates axon growth and fasciculation in vitro, but its role in vivo is unknown. To assess its function in the developing nervous system, we have ablated contactin gene expression in mice. Contactin-/- mutants displayed a severe ataxic phenotype consistent with defects in the cerebellum and survived only until postnatal day 18. Analysis of the contactin-/- mutant cerebellum revealed defects in granule cell axon guidance and in dendritic projections from granule and Golgi cells. These results demonstrate that contactin controls axonal and dendritic interactions of cerebellar interneurons and contributes to cerebellar microorganization.

Animals↗
PubMed2002

Migration and function of a glial subtype in the vertebrate peripheral nervous system.

Glia-axon interactions are essential for the development and function of the nervous system. We combine in vivo imaging and genetics to address the mechanism by which the migration of these cells is coordinated during embryonic development. Using stable transgenic lines, we have followed the migration of one subset of glial cells and their target axons in living zebrafish embryos. These cells coalesce at an early stage and remain coupled throughout migration, with axons apparently pathfinding for glia. Mutant analysis demonstrates that axons provide instructive cues that are sufficient to control glial guidance. Furthermore, mutations in the transcription factor Sox10/cls uncouple the migration of axons and glia. Finally, genetic ablation of this glial subtype reveals an essential role in nerve fasciculation.

Animals↗
PubMed2001

Netrin-3 protein is localized to the axons of motor, sensory, and sympathetic neurons.

The netrin family of axon guidance cues has been shown to play a pivotal role in the guidance of a variety of axon projections during embryonic development, both in the vertebrate and invertebrate. While the guidance potential of netrin-1 has been examined in depth in many regions of the developing mouse brain very little information is available on the expression and activity of netrin-3. Here we show that the netrin-3 protein is present on motor neurons and subpopulations of neurons within sensory and sympathetic ganglia. Moreover, significant levels of netrin-3 protein were found to be associated with the axons projecting from these neurons suggesting a role for netrin-3 in axon pathfinding and fasciculation within the peripheral nervous system.

Animals↗
PubMed1995

Immunocytochemical identification of serotonergic supraependymal nerve fibers in the third ventricle of the house musk shrew, Suncus murinus.

Supraependymal fibers of the house musk shrew (Suncus murinus) were examined by conventional scanning electron microscopy (SEM), backscattered electron (BSE) imaging of enzyme immunohistochemistry and by immunotransmission electron microscopy in the dorsal part of the third ventricular wall. In this region, ependymal cells were not so heavily ciliated and conventional SEM studies showed two main categories of supraependymal fibers. The first type consisted of long fibers fasciculated which were distributed over the ventricular surface between the anterior commissure and the subfornical organ. The second category was a thin fiber which was observed on the ependymal luminal surface. Some of these fibers had varicoses or terminal-like swellings. This type of supraependymal fiber seemed to originate in the first type of fiber bundles. To confirm the nature and the distribution of serotonin-immunoreactive supraependymal fibers, BSE imaging using immunohistochemical reactions was used. Serotonin-immunoreactive structures were shown as highlighted structures by means of a backscattered electron mode. These investigations revealed that the majority of both types of supraependymal fibers observed by conventional SEM contained serotonin. A moderate number of serotonergic supraependymal fibers was observed on the ventricular surface of the subfornical organ. Immunohistochemical studies using Vibratome sections of identical ventricular regions revealed the presence of serotonin-immunoreactive processes, with the use of light- and electron-microscopy. They were distributed in in the third ventricle just adjacent to the ependymal luminal surfaces. These fibers contained immunoreactive large cored vesicles and immunonegative small clear vesicles.

Animals↗
PubMed1996

Novel gene families involved in neural pathfinding.

Recent studies have uncovered a bifunctional role of the diffusible axon guidance molecules netrin-1 and UNC-6 in that they attract some axons and steer others away simultaneously. Homology screens have extended the semaphorin and collapsin family to include at least 20 members, in both secreted and membrane-bound forms. Eph-related receptors and their membrane-bound ligands, the function of which have only been characterized poorly to date, have been added to the growing number of molecules involved in axon guidance and fasciculation.

Animals↗
PubMed2000

Regulation of N-cadherin-mediated adhesion by the p35-Cdk5 kinase.

BACKGROUND: The p35-Cdk5 kinase has been implicated in a variety of functions in the central nervous system (CNS), including axon outgrowth, axon guidance, fasciculation, and neuronal migration during cortical development. In p35(-/-) mice, embryonic cortical neurons are unable to migrate past their predecessors, leading to an inversion of cortical layers in the adult cortex. RESULTS: In order to identify molecules important for p35-Cdk5-dependent function in the cortex, we screened for p35-interacting proteins using the two-hybrid system. In this study, we report the identification of a novel interaction between p35 and the versatile cell adhesion signaling molecule beta-catenin. The p35 and beta-catenin proteins interacted in vitro and colocalized in transfected COS cells. In addition, the p35-Cdk5 kinase was associated with a beta-catenin-N-cadherin complex in the cortex. In N-cadherin-mediated aggregation assays, inhibition of Cdk5 kinase activity using the Cdk5 inhibitor roscovitine led to the formation of larger aggregates of embryonic cortical neurons. This finding was recapitulated in p35(-/-) cortical neurons, which aggregated to a greater degree than wild-type neurons. In addition, introduction of active p35-Cdk5 kinase into COS cells led to a decreased beta-catenin-N-cadherin interaction and loss of cell adhesion. CONCLUSIONS: The association between p35-Cdk5 and an N-cadherin adhesion complex in cortical neurons and the modulation of N-cadherin-mediated aggregation by p35-Cdk5 suggests that the p35-Cdk5 kinase is involved in the regulation of N-cadherin-mediated adhesion in cortical neurons.

Cadherins↗
PubMed1999

Developmental and cell biological functions of the Drosophila DEAD-box protein abstrakt.

BACKGROUND: DEAD-box proteins are a large family of proteins found in bacteria, plants and animals, but only few have been analysed functionally. They are involved in the regulation of various aspects of RNA processing and metabolism, including splicing, transport and translation. The study of their function in multicellular organisms has been restricted to a few special cases, such as the Vasa protein in the fruit fly Drosophila. RESULTS: We show that abstrakt, a gene originally identified genetically by its effect on axon outgrowth and fasciculation of the Bolwig nerve, encodes a new Drosophila DEAD-box protein of which the closest homologue is a human gene of unknown function. Using temperature-sensitive alleles to assay its function, we found that abstrakt is essential for survival at all stages throughout the life cycle of the fly. Mutants show specific defects in many developmental processes, including cell-shape changes, localisation of RNA and apoptosis. CONCLUSIONS: Abstrakt is not globally required for RNA splicing, transport, subcellular localisation or translation. Nevertheless, there is a widespread requirement for Abstrakt during post-transcriptional gene expression. Abstrakt must affect processing of specific subsets of RNAs, suggesting that differential post-translational control during development is more common than previously suspected.

Amino Acid Sequence↗
PubMed1998

Errors in corticospinal axon guidance in mice lacking the neural cell adhesion molecule L1.

BACKGROUND: Neural cell adhesion molecules of the immunoglobulin superfamily (IgCAMs) have been implicated in both the fasciculation and guidance of axons, but direct genetic evidence of a role for neural IgCAMs in axon guidance in vertebrates is lacking. The L1 subfamily of vertebrate neural IgCAMs function as both homophilic and heterophilic receptors for a variety of cell-surface and extracellular ligands and may signal through intracellular kinases or by recruitment of the fibroblast growth factor receptor. L1 itself has been implicated in many neural processes and is expressed widely in the embryonic and adult nervous systems. In humans, mutations in the L1 gene are linked with a spectrum of brain disorders, including loss of the corticospinal tract, but the mechanistic basis for these disorders is unknown. RESULTS: We show that mice that do not express L1 have defects in the guidance of axons of the corticospinal tract, a major motor control pathway projecting from the cortex to the spinal cord. Although the pathway to the caudal medulla appears normal, a substantial proportion of axons fail to cross the midline to the opposite dorsal column as normal. In adults, this results in a reduced decussation and in large numbers of axons projecting ipsilaterally. There is also a varying, but reduced, number of corticospinal axons in the dorsal columns of the spinal cord. These do not project beyond cervical levels. We show that these are defects in axon guidance, because they arise during the early stages of the development of the decussation. The presence of a ligand for L1, CD24, specifically at the point of decussation suggests a mechanism in which L1 functions to guide corticospinal axons across the midline. CONCLUSIONS: L1 function is necessary for the guidance of corticospinal axons across the pyramidal decussation in mice. Some of the defects in the corticospinal tract of humans with mutations in L1 could be due to errors in axon guidance at the pyramidal decussation.

Animals↗
PubMed1998

Essential role of alpha 6 integrins in cortical and retinal lamination.

Extracellular matrix (ECM) is believed to play important roles in many aspects of nervous system development [1]. The laminins are ECM glycoproteins expressed in neural tissues and are potent stimulators of neurite outgrowth in vitro [1-3]. Genetic approaches using Drosophila and Caenorhabditis elegans have demonstrated a role for laminin and a laminin receptor in vivo in axon pathfinding and fasciculation, respectively [4,5]. In higher organisms, however, the role of laminins in the development of the nervous system is poorly understood. Integrins alpha 6 beta 1 and alpha 6 beta 4 are major laminin receptors. A role for the alpha 6 integrin in neurulation has been reported in amphibians [6]. We previously described mice lacking integrin alpha 6; these mice died at birth with severe skin blistering [7]. Detailed analyses of integrin alpha 6-/- mice reported here revealed abnormalities in the laminar organization of the developing cerebral cortex and retina. Ectopic neuroblastic outgrowths were found on the brain surface and in the vitreous body in the eye. Alterations of laminin deposition were found in mutant brains. Thus, this study provides evidence for an essential role of integrin-laminin interactions in the proper development of the nervous system. These observations are particularly significant given the recent report that human patients suffering from epidermolysis bullosa can carry mutations in ITGA6, the gene encoding the alpha 6 integrin chain [8,9].

Animals↗
PubMed2002

[Dorsal and lumbar paraspinal electromyographic study. Multi-MUP analysis and drawing up normal values in a reference population].

OBJECTIVE: The aim of this study was to contribute to draw up reference values relating to electromyographic (EMG) parameters in dorsal and lumbar paraspinal muscles. MATERIALS AND METHODS: 75 healthy subjects without back pain underwent electromyography of multifidus bundles, which are innervated uni-segmentally by the dorsal ram of the spinal nerve. T8, L3, L4, L5 and S1 myotomes were systematically explored. Output variables were spontaneous denervation activity and quantitative EMG data obtained by multi-MUP (Motor Unit action Potential) analysis. RESULTS: No abnormal insertional or spontaneous activity (such as fibrillation, positive sharp waves or fasciculation) was recorded at rest. Neither sex nor age influenced motor unit action potential features in our series. Reference values were drawn up for T8 and L5 segmental levels using the mean values of 20 motor unit potentials in each patient studied, the reference interval being defined by the lower and the upper outlier limits on individual values. CONCLUSION: This study offers reference data to electromyographers to help better identifying possible myogenic or neurogenic pathological changes, especially in lumbosacral radiculopathies.

Adult↗
PubMed2003

Single chain Fv antibodies against neural cell adhesion molecule L1 trigger L1 functions in cultured neurons.

The neural cell adhesion molecule L1 plays important roles in cell adhesion, neuronal migration, neurite outgrowth, fasciculation and pathfinding, neuronal survival, and synaptic plasticity. Many of these functions have been identified and characterized by using antibodies. Because of the need for reproducible and functionally active antibodies, we have generated two single-chain variable fragment antibodies against mouse L1 from a human synthetic phage display library. The complementarity determining region 3 of the variable heavy chains of the two antibodies differed in length and sequence. Both antibodies recognized mouse, but not human L1, by enzyme-linked immunosorbent assay, Western blot, and immunofluorescence staining of cultured neurons. Epitope mapping showed reactivity with the fibronectin type III repeats 1-2 of mouse L1. The antibodies stimulated neurite outgrowth from cerebellar dorsal, root ganglion and motor neurons when offered in substrate-coated form in a dose-dependent manner with maximal effects at approximately 32 nM. Furthermore, substrate-coated antibodies enhanced survival of cerebellar neurons. Peptides comprising 8 and 11 amino acids derived from the complementarity determining region 3 of the variable heavy chains of the two single-chain variable fragment antibodies also promoted neurite outgrowth. The combined observations indicate that single-chain variable fragment antibodies against L1 and peptides derived from their binding domains can mimic some beneficial functions of homophilically binding L1 in vitro and may thus serve to trigger these functions in vivo.

Amino Acid Sequence↗
PubMed2003

Amyotrophic lateral sclerosis and other motor neuron diseases.

The anterior horn cell diseases, with the exception of polio, are progressive degenerative diseases of the motor neurons. These disorders include SMA types I to III in children and familial and sporadic ALS and its variants (PMA, PLS, and PBP), Kennedy's disease, and SMA type IV in adults. The electrodiagnostic study is a crucial step in the diagnostic process for all of these disorders. In general, motor NCS may be normal or reveal low CMAP amplitudes with relatively normal conduction velocities. Sensory NCS, except in the case of Kennedy's disease, are normal. The NEE is notable for the often abundant presence of abnormal spontaneous activity, including fibrillation potentials and positive sharp waves, fasciculation potentials, and complex repetitive discharges. Motor unit morphology is abnormal, with polyphasic motor units and large amplitude and duration MUAPs when the disease is slowly progressive. Recruitment in affected muscles is reduced with abnormally rapidly firing motor units. To diagnose a widespread disorder of the motor neurons, abnormalities must be present in multiple muscles with different nerve root and peripheral nerve innervation in multiple limbs. The Lambert Criteria and the El Escorial Criteria are the two most widely accepted sets of electrodiagnostic criteria for ALS. The electrodiagnostic diagnosis must be supported by appropriate history and physical examination findings and the exclusion, via neuroimaging and laboratory testing, of other diseases that may mimic a generalized disorder of the motor neurons.

Amyotrophic Lateral Sclerosis↗
PubMed1999

Nodular fasciitis and solitary fibrous tumor of the oral region: tumors of fibroblast heterogeneity.

OBJECTIVE: Fibroblastic proliferations of the oral cavity are extremely varied, yet they share certain features-spindle cell morphology, collagen synthesis, and fasciculation. Nodular fasciitis is a cellular fibroblastic lesion, uncommonly located in the oral submucosa, that shows smooth muscle actin (SMA) immunoreactivity. Solitary fibrous tumor expresses a CD34 fibroblast phenotype. The aim of this study is to report instances of nodular fasciitis and solitary fibrous tumor in the orofacial region and investigate immunohistochemical markers to compare and contrast fibroblastic phenotypic heterogeneity in these tumors. STUDY DESIGN: Seven benign cellular fibrogenic tumors initially diagnosed as nodular fasciitis over a 10-year period were examined. Immunohistochemical markers, including S-100 protein, SMA, CD68, CD34, and vimentin, were used to further characterize these lesions. RESULTS: All tumors occurred in adults, and the buccal mucosa was found to be the favored site. The spindle cells in these tumors showed phenotypic heterogeneity both within and between tumors. All were vimentin-reactive and harbored small populations of CD68-positive macrophage/dendrocytes. Five tumors were SMA-positive and CD34-negative; the tumor in one case was SMA-negative and CD34-positive, and that in another was SMA-positive and CD34-positive. CONCLUSION: Although rare, nodular fasciitis and solitary fibrous tumor arise in oral submucosa, usually in the cheek. The histopathologic features and immunomarkers indicative of myofibroblastic differentiation are seen in nodular fasciitis, whereas solitary fibrous tumor is CD34-positive; however, one instance was found to be positive for both markers. All of these cases harbored subpopulations of CD68-positive cells. Immunomarkers are a valuable adjunct in differentiating nodular fasciitis from solitary fibrous tumor, yet some tumors may harbor heterogeneous fibroblast phenotypes.

Actins↗