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PubMed1996

Nuk controls pathfinding of commissural axons in the mammalian central nervous system.

Eph family receptor tyrosine kinases have been proposed to control axon guidance and fasciculation. To address the biological functions of the Eph family member Nuk, two mutations in the mouse germline have been generated: a protein null allele (Nuk1) and an allele that encodes a Nuk-beta gal fusion receptor lacking the tyrosine kinase and C-terminal domains (Nuk(lacZ)). In Nuk1 homozygous brains, the majority of axons forming the posterior tract of the anterior commissure migrate aberrantly to the floor of the brain, resulting in a failure of cortical neurons to link the two temporal lobes. These results indicate that Nuk, a receptor that binds transmembrane ligands, plays a critical and unique role in the pathfinding of specific axons in the mammalian central nervous system.

Alleles↗
PubMed1996

Dose-ranging study of riluzole in amyotrophic lateral sclerosis. Amyotrophic Lateral Sclerosis/Riluzole Study Group II.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a progressive disease with no effective treatment. In an initial study, riluzole decreased mortality and slowed muscle-strength deterioration in ALS patients. We have carried out a double-blind, placebo-controlled, multicentre study to confirm those findings and to assess drug efficacy at different doses. METHODS: 959 patients with clinically probable or definite ALS of less than 5 years' duration were randomly assigned treatment with placebo or 50 mg, 100 mg, or 200 mg riluzole daily; randomisation was stratified by centre and site of disease onset (bulbar or limb). The primary outcome was survival without a tracheostomy. Secondary outcomes were rates of change in functional measures (muscle strength, functional status, respiratory function, patient's assessments of fasciculation, cramps, stiffness, and tiredness). The primary analysis was the comparison of the 100 mg dose with placebo by intention-to-treat. Drug-effect on survival was assessed before (log-rank test) and after adjustment for known prognostic factors (Cox's model). FINDINGS: At the end of the study, after median follow-up of 18 months, 122 (50.4%) placebo-treated patients and 134 (56.8%) of those who received 100 mg/day riluzole were alive without tracheostomy (unadjusted risk 0.79, p = 0.076; adjusted risk 0.65, p = 0.002). In the groups receiving 50 mg and 200 mg riluzole daily, 131 (55.3%) and 141 (57.8%) patients were alive without tracheostomy (relative to placebo 50 mg adjusted risk 0.76, p = 0.04; 200 mg 0.61, p = 0.0004). There was a significant inverse dose response in risk of death. No functional scale discriminated between the treatment groups. The most common adverse reactions were asthenia, dizziness, gastrointestinal disorders, and rises in liver enzyme activities; they were commonest with the 200 mg dose. INTERPRETATION: Overall, efficacy and safety results suggest that the 100 mg dose of riluzole has the best benefit-to-risk ratio. This study confirms that riluzole is well tolerated and lengthens survival of patients with ALS.

Amyotrophic Lateral Sclerosis↗
PubMed2001

L1 cell adhesion molecule signal cascades: targets for ethanol developmental neurotoxicity.

A major mechanism guiding neural development is through cell-cell and cell-matrix adhesions and signaling mediated by cell adhesion molecules (CAMs). The majority of CAMs have been grouped into three families: the cadherins, the integrins and the members of the immunoglobulin superfamily including L1. While the elucidation of new receptors and matrix components has become a frequent occurrence, the elucidation of the mechanisms by which they operate, and the function of those mechanisms in complex developmental events remains rudimentary. Members of all three families participate in differential adhesion, signal transduction and physical/mechanical effects. Each of these modes of action is a potential target for developmental neurotoxicants. In this brief review, the role of L1 in normal and abnormal neurodevelopment will be summarized. L1 is a cell surface transmembrane glycoprotein with a single copy gene on the X chromosome. There are two alternatively spliced exons, with the RSLE containing form found only on axons and growth cones of post-mitotic neurons. L1 mediates the following functions: adhesion, neurite extension, neuronal migration, and axon fasciculation. L1 is critical for normal neural development; humans with genetic defects in L1, termed corpus callosum hypoplasia, mental retardation, adducted thumbs, spasticity and hydrocephalus (CRASH) syndrome, and mice lacking expression of L1 have extensive neuropathologic and aberrant behaviors. The observation that patients with fetal alcohol syndrome share similar features to patients with CRASH has lead to the investigation of the effects of ethanol on L1. Physiologic concentrations of ethanol have been shown to inhibit L1 mediated neurite outgrowth in cerebellar granule neurons. Such inhibition may result from decreased expression, altered cell surface distribution, impaired signal transduction, or impaired interaction with the cytoskeleton. These data indicate that L1 and its associated signaling pathways are potentially targets for developmental neurotoxicants.

Animals↗
PubMed2003

Muscle injury in organophosphorous poisoning and its role in the development of intermediate syndrome.

Muscle injury and its role in the development of Type II paralysis was studied in 25 patients with acute organophosphate poisoning. All patients were assessed for severity of poisoning at admission and through the course of poisoning for the development and duration of intermediate syndrome (IS) (Type II paralysis). Blood levels of acetylcholinesterase, creatine kinase, creatine kinase MM, LDH and LDH5 were estimated through the course of the poisoning. Of the 25 patients, 22 were severely poisoned and 3 had mild to moderate poisoning. Severely poisoned patients had a significantly greater rate of developing intermediate syndrome (17/22) (P = 0.026). Type I paralysis and fasciculations occurred in 76 and 70.5% of patients who developed intermediate syndrome, in comparison to 38 and 50%, respectively, of those who did not develop intermediate syndrome. Weakness developed in the same groups of muscles in both Types I and II paralysis but was of longer duration in patients who developed Type II paralysis. Acetylcholinesterase was inhibited > 90% throughout the course of poisoning with greater inhibition in patients with longer duration intermediate syndrome. Muscle injury was seen in all patients beginning at admission, peaking over the first 5 days and then declining over the next 5 days. Temporal profiles of blood muscle isoenzymes showed significantly greater muscle injury in those patients with greater severity of poisoning at admission, those who developed intermediate syndrome and in patients with longer duration intermediate syndrome. The findings of this study suggest that Types I and II paralysis in organophosphate poisoning are not separate syndromes but a clinical continuum determined by the severity of poisoning. The magnitude of organophosphate exposure and of muscle injury during the cholinergic crises appears to determine the occurrence and severity of intermediate syndrome.

Acetylcholinesterase↗
PubMed2000

L1 and GAD65 are expressed on dorsal commissural axons in embryonic rat spinal cord.

Using immunocytochemical methods, the cell adhesion molecule L1 was detected on axons crossing in the dorsal commissure of developing rat spinal cord. Immunoreactive axons were found in locations similar to fiber bundles illustrated by Ramón y Cajal and designated the anterior, middle and posterior bundles of the dorsal commissure. L1-immunoreactive dorsal commissural axons were first observed on embryonic day 17 (E17), appeared more numerous by E19, and remained detectable in early postnatal ages. The massive middle axon bundles extended bilaterally from the dorsolateral funiculi towards the midline and crossed in the central part of the commissure. In horizontal sections, bundles of L1-labeled middle axons were observed to traverse the dorsal commissure in a periodic pattern along the entire rostrocaudal extent of the spinal cord. Bundles of glutamic acid decarboxylase (GAD65)-positive axons were detected crossing in the middle and posterior regions of the dorsal commissure between E17 and E20. Results from double-labeling experiments demonstrated that GAD65-positive fibers were embedded in larger bundles of L1-labeled axons and that some dorsal commissural axons were double-labeled. To determine if there were axons crossing in the dorsal commissure that did not express L1, double-labeling experiments were conducted using neurofilament and L1 antibodies. Results indicated that bundles of axons identified with anti-neurofilament antibodies were also L1-positive, whereas individually coursing axons within the commissure were L1-negative. The predominance of L1 on fiber bundles traversing the dorsal commissure adds to the growing evidence that this molecule may play a role in axon outgrowth and fasciculation.

Animals↗
PubMed2002

Distribution of alpha-amino-3-hydroxy-5-methyl-4 isoazolepropionic acid and N-methyl-D-aspartate receptor subunits in the vestibular and spiral ganglia of the mouse during early development.

We investigated the distribution of the glutamate receptor subunits, alpha-amino-3-hydroxy-5-methyl-4 isoazolepropionic acid (AMPA) GluR2 and GluR2/R3, and N-methyl-D-aspartate (NMDA) NR1, and the timing of their appearance during early development of the mouse vestibular and spiral ganglia. NMDA NR1 was the first to be expressed, in the statoacoustic ganglion neurons on E11. GluR2/R3 immunoreactivity was detected in these neurons on E12. This signal probably corresponded exclusively to GluR3, as no signal was obtained for GluR2 alone at this stage. The appearance of these proteins began much earlier than previously reported. GluR2 staining was observed later, on E14 in the vestibular neurons and on E17 in the spiral neurons. The sequence in which these three glutamate receptors appeared suggested possible differences in their roles in the establishment of neuronal circuitry in the inner ear sensory epithelia. The production of NR1 and GluR2/R3 began during the early period of neuron growth and fasciculation. GluR2 appeared later and its expression paralleled synaptogenesis in the vestibular sensory epithelia and in the organ of Corti.

Animals↗
PubMed2003

Developmental distribution of coxsackie virus and adenovirus receptor localized in the nervous system.

Mouse coxsackie virus and adenovirus receptor (mCAR), which was isolated from the nerve growth cone-enriched fraction of newborn mouse brains, is a member of immunoglobulin-super family, and functions as a homophilic adhesion molecule. We observed the expression of mCAR in embryos to adult tissues by means of immunohistochemical analysis with a peptide antibody. mCAR expression was first detected in the embryonic ectoderm in the uterus on embryonic day 6.5 (E6.5). Then it was strongly expressed in the neuroepithelium of the neural tube, the developing brain and the spinal cord from E8.5 to postnatal day 7 (P7), in the cranial motor nerves from E9.5 to E11.5, and in the optic nerve from E13.5 to P7, which agrees with periods of their respective morphogenetic peaks. This expression of mCAR decreased postnatally and was absent in adult tissues. We found that mCAR occurred in a few proliferating cells of the hippocampal dentate gyrus, the subventricular zone (SVZ) of the lateral ventricles, and the rostral migratory stream (RMS) over P21. These observations demonstrate that mCAR was expressed characteristically in the immature neuroepithelium including progenitor cells or radial cells derived from the neural tube and in immature cells in a selected germinal zone of the mature brain. Based on our findings, we propose that mCAR is involved in migration and fasciculation during a restricted period as an adhesion molecule.

Animals↗
PubMed1999

Expression of galectin-1 in the olfactory nerve pathway of rat.

The olfactory neuroepithelium is characterised by the mosaic distribution of primary olfactory neurons that express different odorant receptors and cell surface glycoconjugates. Carbohydrates are believed to form a glycocode that mediates sorting out and fasciculation of primary olfactory axons through interactions with carbohydrate-binding proteins such as galectin-1. In the present study, we describe in detail the expression pattern of galectin-1 in the developing and adult rat olfactory system. We demonstrate that galectin-1 is expressed by olfactory ensheathing cells both in olfactory nerve and within the nerve fibre layer of the olfactory bulb of the embryonic and adult rat. In the adult rat, galectin-1 was preferentially expressed by olfactory ensheathing cells in the nerve fibre layer of the ventromedial and lateral surfaces of the olfactory bulb. Galectin-1 was also expressed by subsets of periglomerular cells and granule cells, particularly in the ventromedial region of the olfactory bulb. In adult rat, the galectin-1 ligand, N-acetyl-lactosamine, was expressed by primary olfactory axons that terminated in glomeruli present in the ventromedial and lateral olfactory bulb. These results suggest that expression of galectin-1 may provide a mechanism for the sorting of subpopulations of axons in the nerve fibre layer of the olfactory bulb during development as well as play a role in the postnatal maintenance of specific glomerular connections.

Aging↗
PubMed2000

Axonal flip-flops and oscillators.

The strange and unpleasant sensations (paraesthesiae) or asynchronous motor-unit activation (fasciculation) that result from a period of limb ischaemia are examples of ectopic discharge in peripheral nerves. Ectopic activity also results from demyelination and is associated with serious neurological conditions, such as multiple sclerosis. A build-up of extracellular K(+) in the internode and persistent Na(+) currents are now implicated in generating the different forms of activity arising in normal and demyelinated axons.

Animals↗
PubMed2002

How the lateral line gets its glia.

During development, the numbers and positions of neurons and glial cells must become precisely matched. A recent study has addressed how the zebrafish lateral line nerve matches up with its glia. Using elegant two-color time-lapse imaging, the authors showed that migrating glia track along the axons precisely and very closely. Combined genetic and embryonic perturbations showed that glia require axons for migration, but not vice versa; however, glia are later required for proper maintenance of axonal fasciculation.

Animals↗
PubMed1998

Neural repair of the injured spinal cord by grafting: comparison between peripheral nerve segments and embryonic homologous structures as a conduit of CNS axons.

To study the differences between peripheral nerve (PN) and embryonic homologous CNS structures as a conduit for CNS axons, spinal cord segments in neonatal rats were removed at the mid-thoracic level and PN or embryonic spinal cord (ESC) segments were grafted into the vacancy. Neural connections across the graft were examined by the anterograde and retrograde tracing methods. Anterogradely labeled pyramidal tract fibers entered the PN segment meanderingly and were dispersed; most stopped at the caudal end of the graft. Although a small fraction of fibers re-entered the host spinal cord, they terminated near the graft-host interface without further extension. By contrast, similarly labeled fibers entering the ESC segments crossed the graft and extended further to reach the lumbar segments. The fibers were defasciculated in the graft but became fasciculated and oriented dorsally near the caudal end of the graft, and descended in the normal path. Consistent with these findings, the retrograde tracing study revealed that in animals with ESC segment grafts but not in those with PN segment grafts, many neurons in the upper brain structures were labeled with Fast Blue that was injected into the lumbar enlargement. The difference between the two kinds of graft as a conduit for CNS axons is likely to be due to differences in matching growing axons and their guidance cues through the graft-host interface.

Animals↗
PubMed1999

CEPU-1, an immunoglobulin superfamily molecule, has cell adhesion activity and shows dynamic expression patterns in chick embryonic spinal cord.

In an attempt to isolate novel molecules involved in motoneuron differentiation and target muscle innervation during embryogenesis, we performed mRNA differential display analysis by comparing cDNAs of motoneurons purified by immunopanning from different portions along the rostro-caudal axis of chick embryonic spinal cord, and cloned an immunoglobulin superfamily protein named C30. By sequence comparison, C30 was shown to be an alternatively spliced isoform of CEPU-1, which was formerly reported as a member of the immunoglobulin superfamily specifically expressed in cerebellar Purkinje cells (Spaltmann and Brummendorf, 1996, J. Neurosci. 16, 1770-1779). We analyzed the expression pattern of CEPU-1 both at the mRNA and protein levels in the spinal cord of the chick embryo. Until stage 23, CEPU-1 was expressed faintly in the ventral part of the neural tube but gradually it became localized to a specific group of cells. In the motor column, CEPU-1 was expressed transiently in many columnar layers. A C30-transfected cell line showed Ca(2+)-independent cell-cell binding activity. These results suggest a role for CEPU-1 in specific axon guidance and/or fasciculation of motoneurons during development.

Animals↗
PubMed1996

Expression of L1 in primary astrocytes via a defective herpes simplex virus vector promotes neurite outgrowth and neural cell migration.

The neural cell adhesion molecule L1 is a transmembrane glycoprotein of approximately 200 kDa molecular weight that is a member of the immunoglobulin super family. Multiple functions of L1 have been reported, including cell-cell interactions, neurite elongation, axonal fasciculation, cell migration, and myelination. L1 plays important roles in neural development and axonal regeneration in the peripheral nervous system (PNS), however, in the adult it is only present on neurons in the central nervous system (CNS). In the present study we have used defective herpes simplex virus (HSV) vectors to express full-length human or rat L1 in cultured primary rat cortical astrocytes. Rat cerebellar granule cells, a rather homogeneous population of neurons, co-cultured on a substrate layer of L1-expressing astrocytes demonstrated increased migration and neurite extension compared with neurons co-cultured on lacZ-expressing astrocytes of uninfected astrocytes. There was no detectable difference between human and rat L1. Because this vector system can be used to confer phenotypic changes in primary nervous system cells it will be useful for in vitro and in vivo studies of neural regenerative sprouting and plasticity in the CNS.

Animals↗
PubMed1997

Functional organization of the promoter region of the mouse F3 axonal glycoprotein gene.

F3 is a developmentally regulated adhesive glycoprotein expressed by subpopulations of central and peripheral neurons which mediates neurite growth and fasciculation via cis- and trans-interactions with cell-surface or matrix components. We previously reported on the characterization of the F3 gene 5' flanking region in which we identified promoter and enhancer elements. Here, we report on the functional organization of the F3 gene regulatory regions. We show that the F3 promoter is built of linearly arranged positive and negative elements scattered through the 5' flanking region of the F3 gene and the 1st exon (exon 0). Neural- and cell type-specific expression of F3 appears to be governed by elements located in the most proximal promoter region which includes a neural-specific enhancer. In retardation assays, all these cis-acting elements bind nuclear proteins, three of which interact with the identified enhancer element while a single species interacts with sequences located within exon 0. Some of these proteins are also specifically expressed within the brain, indicating that they could correspond to neural-specific trans-acting factors. Elements located immediately upstream of the cell type-specific enhancer and within exon 0 are responsible for regulation of F3 expression by cAMP and retinoic acid.

Animals↗
PubMed1999

Differential effects of GDNF and BDNF on cultured ventral mesencephalic neurons.

Previous studies have shown that brain derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) can enhance the survival of dopaminergic neurons in the ventral mesencephalon (VM). Here we compared several non-survival functions of the two factors in VM neurons in culture. We found that both BDNF and GDNF elicited an increase in the depolarization-induced release of dopamine, but had no effect on GABA release, in the VM cultures. BDNF, but not GDNF, significantly enhanced the expression of the calcium binding protein calbindin and synaptic protein SNAP25. In contrast, treatment of the cultures with GDNF, but not BDNF, elicited a marked fasciculation of the processes of the VM neurons. Thus, although both act on VM neurons, BDNF and GDNF have distinct functions.

Actins↗
PubMed1981

Acute temporomandibular joint pain-dysfunction syndrome: neuro-otologic and electromyographic study.

To test the hypothesis that the acute temporomandibular joint pain-dysfunction syndrome might represent a variant of acute benign cranial polyneuritis, a prospective study was designed using neuro-otologic examination and electromyography. Seven consecutive patients with cardinal symptoms of the temporomandibular joint pain-dysfunction syndrome (pain, tenderness, clicking, and limitation of jaw movement) were examined within one week after the onset of their acute symptoms. Another three with chronic symptoms were tested for comparison to the acute cases. All seven patients with the acute condition had asymptomatic hypesthesia of all three divisions of the trigeminal nerve and decreased volitional muscle action potentials in the masseter and temporalis muscles. At the end of three weeks the hypesthesia resolved in all seven patients, and the muscle action potentials returned to normal in six of the seven. Electromyographic testing of the single patient with persistent decreased muscle action potentials and three patients with chronic symptoms showed fibrillations, decreased polyphasic regeneration potentials, and spontaneous fasciculations with clinical atrophy and spasm of the affected masseter and temporalis muscles. Other acute cranial nerve findings included unilateral hypesthesia of the glossopharyngeal and second cervical nerves, motor paralysis of the superior laryngeal branch of the vagus nerve, and increased facial nerve latency. These findings suggest an organic neuromuscular, rather than a psychophysiologic, cause for the temporomandibular joint pain-dysfunction syndrome.

Acute Disease↗
PubMedDate not supplied

Integrin alphav and NCAM mediate the effects of GDNF on DA neuron survival, outgrowth, DA turnover and motor activity in rats.

Glial cell line-derived neurotrophic factor (GDNF) is a specific neurotrophic factor for midbrain dopamine (DA) neurons, but the mechanism underlying the neurotrophic action of GDNF is not well known. The cell adhesion molecules integrin and Neural cell adhesion molecule (NCAM) play important roles in neurite outgrowth and fasciculation. In the present study, we found that subchronic GDNF administration to the pars compacta of substantia nigra in rats increased the expression of integrin alphav and NCAM. Immunostaining results demonstrated the wide distribution of integrin alphav and NCAM in all mesencephalic neurons. The results also demonstrated the co-expression of TH with integrin alphav and NCAM in the same neurons of mesencephalic culture. Further, GDNF significantly increased integrin alphav expression in single TH-positive neurons. Function-blocking anti-integrin alphav and anti-NCAM antibodies antagonized the effects of GDNF on DA neuron survival, outgrowth, DA turnover, and locomotor activity in rats. These results demonstrate that integrin alphav and NCAM mediate the effects of GDNF on DA neuron survival and outgrowth during development and on DA turnover and motor function during adulthood.

Analysis of Variance↗
PubMed2004

[Sonography of peripheral nerves--first part: upper limb].

At sonography, peripheral nerves have a fibrillar appearance, that is tape-like on longitudinal scans and ovoid on transverse scans. Nerves are composed by hypoechoic fascicules within a hyperechoic environment. Less subject to anisotropy and soft to the pressure of the probe, nerves lie between muscles, often with vessels, or within channels. Recent advances in sonographic technology allow accurate imaging of peripheral nerves of the upper and lower limbs, but adequate anatomical and clinical knowledge, as well as rigorous technique are mandatory. The purpose of this general review is to present, as clearly as possible, in two parts, the sonographic features of normal and pathological nerves of upper and lower limbs. This first part will discuss nerves of the upper limb.

Arm↗