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At least 433 records · Page 24Linked to original sources
PubMed2001

Inclusion body myositis mimicking motor neuron disease.

OBJECTIVE: To describe the clinical and electrophysiologic features of patients with inclusion body myositis that was misinterpreted as motor neuron disease. PATIENTS AND METHODS: We retrospectively retrieved the medical records of 70 patients with a pathologic diagnosis of inclusion body myositis. From this group, we selected those who had been first diagnosed as having motor neuron disease or amyotrophic lateral sclerosis. We reviewed the clinical, electrophysiologic, laboratory, and morphologic studies. RESULTS: Nine (13%) of 70 patients with inclusion body myositis had been diagnosed as having motor neuron disease. Six of the 9 patients had asymmetric weakness; in 4 the distal arm muscles were affected. Eight patients had finger flexor weakness. Tendon reflexes were preserved in weak limbs in 6, hyperactive in 2, and absent in 1. Four patients had dysphagia. Fasciculation was seen in 2 patients. None had definite upper motor neuron signs or muscle cramps. Routine electromyographic studies showed fibrillation potentials and positive sharp waves in all 9. Fasciculation potentials were seen in 7 and long-duration polyphasic motor unit potentials were seen in 8. There was no evidence of a myogenic disorder in these 9 patients. Muscle biopsy was done because of slow progression or prominent weakness of the finger flexors and was diagnostic of inclusion body myositis. A quantitative electromyogram was myopathic in 4 of the 5 patients studied. CONCLUSIONS: Inclusion body myositis may mimic motor neuron disease. Muscle biopsy and quantitative electromyographic analysis are indicated in patients with atypical motor neuron disease, especially those with slow progression or early and disproportionate weakness of the finger flexors.

Aged↗
PubMed1996

Sprouting adult CNS cholinergic axons express NILE and associate with astrocytic surfaces expressing neural cell adhesion molecule.

To assess the cellular and molecular substrates for cholinergic axon growth in the adult central nervous system (CNS), we implanted grafts of control and nerve growth factor (NGF)-producing genetically modified fibroblasts within the striatum of rats. Sprouting cholinergic axonal processes that grew into grafts of NGF-producing fibroblasts were fasciculated and followed the surface of astrocytic processes for long distances within the grafts. The close and long distance anatomical relationship between the sprouted axons and the astrocytes supported previous ultrastructural evidence that astrocytes may serve as a cellular substrate for sprouting cholinergic axons in vivo. The sprouted axon processes were associated with the expression of nerve growth factor-inducible large external (NILE) glycoprotein on their surfaces. NILE expression was not seen in control grafts where there was an absence of cholinergic ingrowth. NILE has been demonstrated to play a role in axon fasciculation in a number of other neural systems. The astrocytic processes in both control and NGF-producing fibroblast grafts expressed neural cell adhesion molecule (NCAM), suggesting that NCAM-mediated adhesion may be responsible for the close relationship between the axons and astrocytes within the grafts. NGF-induced heterotypic interactions between neuronal NILE and astroglial NCAM may also be required for adult cholinergic axonal sprouting.

Acetylcholine↗
PubMed1996

Differential adhesion and the initial assembly of the mammalian olfactory nerve.

During the initial assembly of the olfactory pathway, the behavior of olfactory axons changes as they grow from the olfactory epithelium toward the telencephalic vesicle. The axons exit the epithelium singly or in small fascicles, and their growth cones are simple and bullet-shaped. Outside the epithelium, they make a sharp dorsal turn and fasciculate into a single nerve; the growth cones remain simple. Upon entering the ventromedial telencephalon, the axons defasciculate, branch extensively, and end in complex, lamellate growth cones which extend toward the ventrolateral aspect of the telencephalic vesicle. The distribution of laminin, collagen-IV, and fibronectin varies in register with these changes in olfactory axon and growth cone behavior. Each of these extracellular matrix molecules influences olfactory neurite outgrowth and growth cone morphology in vitro consistent with its distribution in vivo. The distribution of E-cadherin, L1, neural cell adhesion molecule (NCAM) and the polysialated form of NCAM also varies in register with changes in olfactory axon behavior. In vitro, L1 modulates embryonic olfactory neurite outgrowth and growth cone morphology consistent with its distribution in vivo. Thus, olfactory axon trajectory, fasciculation, and growth cone morphology change within distinct adhesive environments in the nascent olfactory pathway, and some of the molecules that characterize these environments have differential effects upon olfactory neurite growth and growth cone morphology. Consequently, the patterned expression and activity of extracellular matrix and cell surface adhesion molecules may contribute to the initial assembly of the olfactory pathway.

Animals↗
PubMed1997

Outgrowth patterns and directed growth of identified neurons induced by native substrates in culture.

In this study, we have tested how various identified leech neurons in culture grow on surfaces that they normally contact in situ. Neurons were cultured either on ganglion capsules from which neurons had been removed or on skin. On these substrates, outgrowth patterns were characteristic for each cell type. Retzius cells plated on capsules extended bundles of thick, fasciculated processes with few branching points and in the opposite direction a tangle of fine neurites. Anterior pagoda (AP) neurons plated on capsules extended two single processes in opposite directions but failed to grow on skin. Sensory P and N neurons on capsules extended multiple processes. On skin, P neurons extended only two long branches in opposite directions over the superficial body wall. N neurons on skin extended multiple processes. Varicosities were common in the processes of P and N neurons on capsules or skin. The branching patterns described here bore closer resemblance to those in the developing or adult nervous system than to those on Concanavalin A or laminin-enriched extract. Pairs of Retzius or AP neurons plated at a distance on the same capsule extended neurites from one neuron toward the other and formed contacts. Such directed growth failed in hybrid pairs of Retzius and AP neurons or in pairs plated on laminin-enriched extract or Concanavalin A. Our results suggest that multiple growth-promoting molecules anchored to the extracellular matrix may cooperate in regulating the branching pattern of neurons, fasciculation, and direction of growth.

Animals↗
PubMed1999

Callosal axon guidance defects in p35(-/-) mice.

Mice lacking p35, an activator of cdk5 in the central nervous system (CNS), exhibit defects in a variety of CNS structures, most prominently characterized by a disruption in the laminar structure of the neocortex (Chae et al., 1997). In addition, alterations of certain axonal fiber tracts are found in the cortex of p35 mutant mice. Notably, the corpus callosum appears bundled at the midline, but dispersed lateral to the midline. Tracer injection experiments in adult p35 mutant mice reveal that projecting cortical axons fail to assimilate into the corpus callosum, and take oblique paths to the midline. After crossing the midline, cortical axons defasciculate prematurely from the corpus callosum and take similarly oblique paths through the cortex. This callosal phenotype is not detected in reeler mice, which also exhibit defects in cortical lamination, suggesting that the lack of fasciculation of callosal axons is not an inherent manifestation of a disruption of cortical lamination. The embryonic callosal axon tract is defasciculated before crossing the midline, suggesting that axon guidance may be affected during embryonic development of the corpus callosum. In addition, embryonic thalamocortical afferents also exhibit a defasciculated phenotype. These results suggest that defective axonal fasciculation and guidance may be primary responses to the loss of p35 in the cortex. Furthermore, this study postulates a role for the p35/cdk5 kinase in molecular signaling pathways necessary for proper guidance of selective axons during embryonic development.

Agenesis of Corpus Callosum↗
PubMed1996

Role of GABAA receptors in the GABA attenuation of ethanol neurotoxicity.

We have previously reported that GABA reverses the neuronotoxic effects of ethanol in neuroblast-enriched cultures derived from 3-day-old whole chick embryo (E3WE). In the present study, we examined the effects of GABA agonists and antagonists on morphological growth patterns and on cholinergic neuronal phenotypic expression, using choline acetyltransferase (ChAT) activity as a marker. E3WE neuroblast-enriched cultures showed positive immunoreactivity for neurofilament and as previously reported, control cultures exhibited the characteristic pattern of outgrowth of neurites of varying thickness radiating from the aggregates. In contrast, cultures grown in ethanol consisted of neuronal aggregates lacking fasciculation but having a complex network of individual thin neurites. Both GABA and GABAA agonist muscimol enhanced neuritic fasciculation and arborization in control and ethanol-treated cultures, and this growth enhancement was inhibited by GABAA antagonist bicuculline. No effects were noted with GABAB agonist baclofen. GABA increased ChAT activity in E3WE control cultures, as previously reported. A similar effect was seen with GABAA agonist muscimol, but not with GABAB agonist baclofen. However, the GABA effect was not apparent in the presence of GABAB antagonist phaclofen. Thus, it appears that the cholinotrophic effects of GABA are mediated by both GABAA and GABAB receptors. In ethanol-treated cultures the already-reported ChAT decline was reversed by GABA and muscimol, but not by baclofen. Moreover, the GABA effect in ethanol-treated cultures was not antagonized by GABAB antagonist phaclofen, suggesting that the GABA effect was mediated by a GABAA receptor. We conclude from these findings that the cholinotrophic effects of GABA are mediated by GABAA and GABAB receptors, while the rescuing effects of GABA in the ethanol-treated cultures are mediated via GABAA receptors.

Animals↗
PubMed1997

Muscle hypertrophy in multifocal motor neuropathy is associated with continuous motor unit activity.

Multifocal motor neuropathy (MMN) is typically associated with distal upper limb weakness and wasting. However, proximal muscle bulk, particularly of biceps brachii, may be well preserved even in the presence of severe proximal weakness. Here we report 3 patients with MMN who had true muscle hypertrophy of severely weakened biceps muscles and positive motor symptoms including cramp and fasciculations in these muscles. Electromyographic studies demonstrated markedly impaired recruitment in the affected muscles and continuous motor unit activity comprising multiple fasciculation potentials at a frequency of up to 30 per minute. We propose that this continuous motor unit activity may have contributed to the hypertrophy in these muscles.

Adult↗
PubMed1997

The central pathway of primary olfactory axons is abnormal in mice lacking the N-CAM-180 isoform.

Although N-CAM has previously been implicated in the growth and fasciculation of axons, the development of axon tracts in transgenic mice with a targeted deletion of the 180-kD isoform of the neural cell adhesion molecule (N-CAM-180) appears grossly normal in comparison to wild-type mice. We examined the organization of the olfactory nerve projection from the olfactory neuroepithelium to glomeruli in the olfactory bulb of postnatal N-CAM-180 null mutant mice. Immunostaining for olfactory marker protein revealed the normal presence of fully mature primary olfactory neurons within the olfactory neuroepithelium of mutant mice. The axons of these neurons form an olfactory nerve, enter the nerve fiber layer of the olfactory bulb, and terminate in olfactory glomeruli as in wild-type control animals. The olfactory bulb is smaller and the nerve fiber layer is relatively thicker in mutants than in wild-type mice. Previous studies have revealed that the plant lectin Dolichos biflorus agglutinin (DBA) clearly stains the perikarya and axons of a subpopulation of primary olfactory neurons. Thus, DBA staining enabled the morphology of the olfactory nerve pathway to be examined at higher resolution in both control and mutant animals. Despite a normal spatial pattern of DBA-stained neurons within the nasal cavity, there was a distorted axonal projection of these neurons onto the surface of the olfactory bulb in N-CAM-180 null mutants. In particular, DBA-stained axons formed fewer and smaller glomeruli in the olfactory bulbs of mutants in comparison to wild-type mice. Many primary olfactory axons failed to exit the nerve fiber layer and contribute to glomerular formation. These results indicate that N-CAM-180 plays an important role in the growth and fasciculation of primary olfactory axons and is essential for normal development of olfactory glomeruli.

Animals↗
PubMed1997

Retarded formation of the hippocampal commissure in embryos from mouse strains lacking a corpus callosum.

A precise description of the timing and route traveled by axons traversing the telencephalic midline through the ventral hippocampal commissure (HC) is essential for understanding the role it plays in the formation of the corpus callosum (CC). A normal baseline of HC development was described in B6D2F2 hybrid mice and then compared with two inbred strains of mice displaying callosal agenesis, BALB/cWah1 (50% CC defect) and 129/J (70% CC defect), their F2 hybrid (C129F2-33% CC defect), and a recombinant inbred strain (RI-1-100% CC defect) derived from pairs of C129F2 mice. Embryos weighing from 0.25 g to 0.70 g (E14.5-E17) were collected and fixed by perfusion. Axon tracts were labeled using crystals of the lipophilic dyes DiI and DiA inserted into the hippocampal fimbria and cerebral cortex. HC axons in B6D2F2 mice first cross the midline at about 0.350 g body weight (E14.8) by traveling over the dorsal septum and along the pia membrane lining the longitudinal fissure. Earlier crossing was prevented by the presence of a deep cleft formed by the longitudinal fissure extending down into the septal region. Subsequent axons fasciculated along existing axons, gradually building the dorsoventral height of the HC to about 200 microns by 0.600 g. The earliest callosal axons from frontal cortex crossed the midline at 0.620 g and were clearly seen fasciculating along and between existing hippocampal axons at the dorsal surface of the HC as they crossed. In the acallosal strains, HC formation was delayed by the continued presence of the cleft deep in the septal region. This delay in time of crossing was correlated with later CC defect expression. Initial HC crossing occurred at about 0.470 g (E16.25) in BALB mice and about 0.520 g (E16.5) in 129 mice. In the RI-1 embryos, first HC crossing was estimated at about 0.750 g (E17.5), although several older embryos showed no crossing. These results show the importance of the HC for successful CC formation and suggest that absent CC arises as a consequence of a developmental defect which affects the formation of the hippocampal commissure prior to arrival of CC axons at midplane.

Agenesis of Corpus Callosum↗
PubMed2000

Chondroitin sulfate proteoglycan expression pattern in hippocampal development: potential regulation of axon tract formation.

A variety of molecular influences in the extracellular matrix (ECM) interact with developing axons to guide the formation of hippocampal axon pathways. One of these influences may be chondroitin sulfate proteoglycans (CSPGs), which are known to inhibit axonal extension during development and following central nervous system injury. In this study, we examined the role of CSPGs and cell adhesion molecules in the regulation of axon tract formation during hippocampal development. We used indirect immunofluorescence to examine the developmental pattern of CSPG expression relative to axon tracts that express the cell adhesion molecule L1. Additionally, we used dissociated and explant cell cultures to examine the effects of CSPGs on hippocampal axon development in vitro. In vivo, we found that the CSPG neurocan is expressed throughout the alveus, neuropil layers, and parts of the dentate gyrus from E16 to P2. The CSPG phosphacan is expressed primarily in the neuropil layers at postnatal stages. After E18, intense labeling of neurocan was observed in regions of the alveus surrounding L1-expressing axon fascicles. In vitro, axons from brain regions that project through the alveus during development would not grow across CSPG substrata, in a concentration-dependent manner. In addition, hippocampal axons from dissociated neuron cultures only traveled across CSPG substrata as fasciculated axon bundles. These findings implicate CSPG in the regulation of axon trajectory and fasciculation during hippocampal axon tract formation.

Animals↗
PubMed1977

Glucocorticoid effects on the edrophonium responsiveness of normal and degenerating mammalian motor nerve terminals.

An intensive short-term triamcinolone regimen in cats preserves the prejunctional actions of edrophonium in degenerating motor nerves. These edrophonium actions include the induction of a stimulus-dependent afterdischarge and the initiation of fasciculations. The relationship between fasciculations and stimulus-dependent afterdischarge is discussed. The glucocorticoid preservation of these edrophonium effects is like that previously reported for the preservation of posttetanic facilitation in motor nerves equally compromised. The results therefore show that glucocorticoid and facilitatory drug actions synergize to increase facilitation in degenerating but still functional motor nerves. This drug synergy is comparable to that which occurs in normal motor nerves. This interaction may provide a basis for effectively combining glucocorticoid and facilitatory drugs in the treatment of myasthenia gravis.

Animals↗
PubMed1984

Severe neurological disease associated with hyperparathyroidism.

Two patients, one with ataxia, internuclear ophthalmoplegia, muscle weakness, atrophy, fasciculations, and bilateral Babinski's signs, the other with dysarthria, dysphagia, muscle weakness, atrophy, fasciculations, and hyperreflexia, had elevated serum calcium and parathyroid hormone levels, establishing the diagnosis of primary hyperparathyroidism (HPT). Removal of a parathyroid adenoma in one patient and three hyperplastic parathyroid glands in the other resulted in remission of the hyperparathyroidism but left both patients with residual neurological damage. Postmortem examination of the second patient showed typical features of amyotrophic lateral sclerosis. The findings in these patients show that hyperparathyroidism may be associated with signs of severe central nervous system disease and that patients with unexplained neurological signs or symptoms should be checked for hyperparathyroidism.

Adenoma↗
PubMed1997

Botulinum toxin treatment of muscle cramps: a clinical and neurophysiological study.

Botulinum toxin is now widely used in the treatment of several hyperkinetic movement disorders. To evaluate its efficacy in treating muscle cramping syndromes, we studied clinical and neurophysiological variables before and after botulinum toxin injections into calf muscles and small flexor muscles of the foot in patients with an inherited benign cramp-fasciculation syndrome. At each assessment the clinical severity of cramp was scored and the cramp threshold frequency was measured with repetitive electrical peripheral nerve stimulation. Botulinum toxin injection significantly lowered our patients' clinical cramp severity scores (mean +/- SD: before, 3.80 +/- 0.44; after, 1.40 +/- 0.54), left muscle strength unchanged and significantly increased their cramp threshold frequencies (before, 4.22 +/- 2.26 Hz; after, 10.0 +/- 3.74 Hz). The clinical benefit induced by botulinum toxin lasted about 3 months. Botulinum toxin injections also significantly reduced fasciculation potentials in relaxed muscles (before, 0.86 +/- 0.19 fasciculations/sec; after, 0.45 +/- 0.11 fasciculations/sec). These findings show that local intramuscular injections of botulinum toxin provide effective, safe, and long-lasting relief of cramps possibly by reducing presynaptic cholinergic stimulation of motor nerve terminals and by impairing the input/output function of intrafusal and extrafusal motor end plates.

Adult↗
PubMed2001

Chemically and morphologically identifiable glomeruli in the rat olfactory bulb.

Primary olfactory neurons that express the same odorant receptor are distributed mosaically throughout the olfactory neuroepithelium lining the nasal cavity, yet their axons converge and form discrete glomeruli in the olfactory bulb. We previously proposed that cell surface carbohydrates mediate the sorting out and selective fasciculation of primary olfactory axons en route to glomeruli. If this were the case, then axons that terminate in the same glomerulus would express the same complement of cell surface carbohydrates. In this study, we examined the expression of a novel carbohydrate (NOC-3) on neural cell adhesion molecule in the adult rat olfactory system. NOC-3 was expressed by a subset of neurons distributed throughout the olfactory neuroepithelium. The axons of these neurons entered the nerve fiber layer and terminated in a subset of glomeruli. It is interesting to note that we identified three unusually large glomeruli in the lateral, ventrolateral, and ventromedial olfactory bulb that were innervated by axons expressing NOC-3. NOC-3-expressing axons sorted out and fasciculated into discrete fascicles prior to entering these glomeruli. Each of these glomeruli was in a topographically fixed position in the olfactory bulbs of the same animal as well as in different animals, and their lengths were approximately 10% of the total length of the bulb. They could be identified reliably by both their topographical position and their unique morphology. These results reveal that axons expressing the same cell surface carbohydrates consistently target the same topographically fixed glomeruli, which supports a role for these molecules in axon navigation in the primary olfactory nerve pathway.

Animals↗
PubMed2004

Radial glia defines boundaries and subdivisions in the embryonic midbrain of the lizard Gallotia galloti.

We have studied the organization of the midbrain radial glia in embryos of Gallotia galloti using the fluorescent lipophilic dye 1,1'-dioctadecyl-3,3,3',3'-tetramethyl-indocarbocyanine perchlorate (DiI) and the antibodies H5 and RC2. Our goal was to verify if the radial glia takes part in the midbrain boundaries formation and if it defines different zones. Our exam reveals two clear limits, anterior or mesencephalic-diencephalic (m/d) and posterior or mesencephalic-rhombencephalic (m/r), that can be defined as the borders where the midbrain radial glia processes end. Moreover, fasciculate radial glia processes characterize these limits totally or partially. They coincide with gene expression limits and with cytoarchitectonic limits defined by other criteria. Six different subdivisions, five alar and one basal, can be defined according to radial glia distribution, fasciculation, and immunohistochemical features. The ventral part of the alar region is defined by an RC2-positive bundle of radial glial cells. This bundle supposes a trustworthy landmark to point out the tectal/tegmental boundary. We hypothesize that this pattern of midbrain radial glia represents a basic model in amniota.

Animals↗
PubMed2004

Differential expression of the mammalian homologue of fasciclin II during olfactory development in vivo and in vitro.

Developing olfactory sensory neurons are guided to the glomeruli of the olfactory bulb by an increasingly stringent process that is influenced by expression of odorant receptors, cell adhesion molecules (CAMs), and other kinds of signaling cascades. A fundamental feature of the projection is the connecting of broad zones in the epithelium to broad zones in the bulb, also termed rhinotopy. One molecule that parallels and may aid neurons in establishing rhinotopy is the mammalian homologue of fasciclin II (OCAM/mamFas II; also known as RNCAM and NCAM-2), an immunoglobulin superfamily CAM that is differentially expressed in the developing and mature olfactory epithelium (OE): Axons elaborated by ventral and lateral epithelium express the protein at high levels, whereas dorsomedial axons express little or no OCAM/mamFas II. Our investigation has demonstrated that OCAM/mamFas II is detectable early in the development of the rat OE. mRNA is evident on RT-PCR and in situ hybridization by E12.5, and protein is apparent by immunohistochemistry by E13.5. By using a tissue culture system that separates ventral septal epithelium (OCAM/mamFas II-positive) from dorsal (OCAM/mamFas II-negative), we find that explants maintain protein expression levels in vitro that are characteristic of the phenotype at the original location in vivo. At least some neurons are born in culture, suggesting that any cues that direct differential expression are also maintained in vitro. Finally, high OCAM/mamFas II expression correlates with increased growth and fasciculation of olfactory axons in vitro. These data and the similarity between OCAM/mamFas II, on the one hand, and fasciclin II and NCAM, on the other, suggest that OCAM/mamFas II might play a role in growth and fasciculation of primary olfactory axons during development of the projection.

Animals↗
PubMed2004

Expression and putative role of lactoseries carbohydrates present on NCAM in the rat primary olfactory pathway.

Primary olfactory neurons project axons from the olfactory neuroepithelium lining the nasal cavity to the olfactory bulb in the brain. These axons grow within large mixed bundles in the olfactory nerve and then sort out into homotypic fascicles in the nerve fiber layer of the olfactory bulb before terminating in topographically fixed glomeruli. Carbohydrates expressed on the cell surface have been implicated in axon sorting within the nerve fiber layer. We have identified two novel subpopulations of primary olfactory neurons that express distinct alpha-extended lactoseries carbohydrates recognised by monoclonal antibodies LA4 and KH10. Both carbohydrate epitopes are present on novel glycoforms of the neural cell adhesion molecule, which we have named NOC-7 and NOC-8. Primary axon fasciculation is disrupted in vitro when interactions between these cell surface lactoseries carbohydrates and their endogenous binding molecules are inhibited by the LA4 and KH10 antibodies or lactosamine sugars. We report the expression of multiple members of the lactoseries binding galectin family in the primary olfactory system. In particular, galectin-3 is expressed by ensheathing cells surrounding nerve fascicles in the submucosa and nerve fiber layer, where it may mediate cross-linking of axons. Galectin-4, -7, and -8 are expressed by the primary olfactory axons as they grow from the nasal cavity to the olfactory bulb. A putative role for NOC-7 and NOC-8 in axon fasciculation and the expression of multiple galectins in the developing olfactory nerve suggest that these molecules may be involved in the formation of this pathway, particularly in the sorting of axons as they converge towards their target.

Amino Sugars↗
PubMed2005

Connexin45 mediates gap junctional coupling of bistratified ganglion cells in the mouse retina.

Direction selectivity, a key feature of visual perception, originates in the retina and is transmitted by bistratified ganglion cells that, in the rabbit retina, exhibit a particular coupling pattern. We intracellularly labeled ganglion cells in different transgenic mouse lines, allowing a morphological classification of bistratified ganglion cells, an analysis of their coupling pattern, and the molecular identification of the connexins responsible for the coupling. Based on dendritic characteristics including co-fasciculation with the dendrites of cholinergic starburst amacrine cells, we were able to distinguish three types of bistratified ganglion cells. Two of these co-fasciculate with starburst amacrine cells and exhibit a specific homologous coupling pattern. Connexin45 (Cx45) appears to be the major component of the gap junctional channels because tracer coupling is absent in Cx45-deficient animals whereas it persists in Cx36-deficient animals. It is speculated that the transjunctional voltage dependence of Cx45 channels could support the transmission of direction selectivity.

Animals↗