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PubMed2003

The upstream regulatory region of the gene for the human homologue of the adhesion molecule TAG-1 contains elements driving neural specific expression in vivo.

Cell adhesion molecules (CAMs) of the immunoglobulin superfamily (IgSF) exhibit restricted spatial and temporal expression profiles requiring a tight regulatory program during development. The rodent glycoprotein TAG-1 and its orthologs TAX-1 in the human and axonin-1 in chick are cell adhesion molecules belonging to the contactin/F3 subgroup of the IgSF. TAG-1 is expressed in restricted subsets of central and peripheral neurons, not only during development but also in adulthood, and is implicated in neurite outgrowth, axon guidance and fasciculation, as well as neuronal migration. In an attempt to identify the regulatory elements that guide the neuronal expression of TAG-1, we have isolated genomic clones containing 4 kb of the TAX-1 upstream sequence and used them to drive the expression of the LacZ reporter gene in transgenic mice. We demonstrate that this sequence includes elements not only sufficient to restrict expression to the nervous system, but also to recapitulate to a great extent the endogenous pattern of the TAG-1 expression in the developing CNS.

Aging↗
PubMed2005

Distribution of OL-protocadherin in axon fibers in the developing chick nervous system.

OL-protocadherin (OL-pc) is a homophilic cell adhesion molecule that belongs to the cadherin gene superfamily. We cloned and characterized the chicken homologue of OL-pc and examined its expression pattern in chick embryos mainly from embryonic day (E) 3.5 to E6.5. The structure of chick OL-pc was found to be essentially the same as that of mammalian OL-pc's except for some small deletions and insertions in the amino acid sequence. OL-pc protein was detected prominently along developing axonal fibers in the brain and also in the peripheral nervous system. In addition, it was detected in some mesenchymal cells and in the embryonic ectoderm of the mandible and limb bud. In the spinal cord, OL-pc was specifically expressed in motor neurons, and the protein was distributed along motor nerves. Motor nerves merged gradually with sensory nerves showing negative/faint OL-pc expression, but their fibers remained separated as small bundles in the nerves. Interestingly, OL-pc-positive motor nerves such as those to the sternocoracoideus became segregated from OL-pc-faint/weak motor nerves at the plexus region. Moreover, OL-pc was distributed along the path of the branchial nerves. These results suggest that OL-pc might play some roles in axon navigation such as in axon elongation, selective fasciculation, and pathfinding in the early stage of neural development.

Amino Acid Sequence↗
PubMed2005

Amyotrophic lateral sclerosis with predominant pyramidal signs -- early diagnosis by magnetic resonance imaging.

OBJECTIVE: To evaluate the role of magnetic resonance imaging (MRI) in the early diagnosis of amyotrophic lateral sclerosis (ALS) with predominant upper motor neuron (UMN) signs in the initial stage of the disease. PATIENTS AND METHOD: Two patients with ALS were found to have spastic quadriparesis with no wasting or fasciculation in the limbs in the early stage of the disease. Both were subjected to MRI of the head and cervical spine to look for any specific diagnostic feature. Both of them were followed with clinical evaluation and electroneuromyography (ENMG) for the definitive diagnosis of ALS. RESULTS: Magnetic resonance imaging showed selective degeneration of the pyramidal tracts in the contiguous axial cuts from subcortical white matter to cerebral peduncles. The finding was more visible in the coronal section. In addition, there was T1 hyperintensity visible along the anterior aspect of the spinal cord in the cervical region. These findings were suggestive of ALS, the diagnosis that was subsequently confirmed by serial clinical follow-up and ENMG. CONCLUSION: It is difficult to diagnose ALS in the early stage of the disease especially if the pyramidal signs predominate over the lower motor neuron (LMN) signs; MRI might be useful in such cases.

Adult↗
PubMed2004

Neuromuscular ultrasound.

High-resolution ultrasound now is capable of imaging muscle and nerve in fine detail. It is sensitive in detecting chronic myopathies and neurogenic atrophy and may be able to detect subtle changes associated with acute denervation. It is particularly well suited to the study of fasciculations and kinesiology. Recent studies show that ultrasound also is capable of imaging most peripheral nerves,including small branches, and of sensitively measuring the swelling that follows chronic compression. This noninvasive technology holds considerable promise for providing anatomic information to complement other tests of nerve and muscle function.

Humans↗
PubMed2004

Generation of recognition diversity in the nervous system.

For decades, it has been suggested that complex neural wiring might be specified by extensive diversity in receptor isoforms. Dscam is a cell surface protein with 38,016 potential alternatively spliced isoforms in the fly nervous system. Remarkable binding studies now show that Dscam isoform diversity indeed results in an unprecedented level of recognition diversity, showing isoform-specific homophilic binding. In vivo studies have begun to suggest models for use of Dscam diversity in neuron-target recognition, axon fasciculation, and neuron self-recognition.

Animals↗
PubMed2005

Distinct roles for secreted semaphorin signaling in spinal motor axon guidance.

Neuropilins, secreted semaphorin coreceptors, are expressed in discrete populations of spinal motor neurons, suggesting they provide critical guidance information for the establishment of functional motor circuitry. We show here that motor axon growth and guidance are impaired in the absence of Sema3A-Npn-1 signaling. Motor axons enter the limb precociously, showing that Sema3A controls the timing of motor axon in-growth to the limb. Lateral motor column (LMC) motor axons within spinal nerves are defasciculated as they grow toward the limb and converge in the plexus region. Medial and lateral LMC motor axons show dorso-ventral guidance defects in the forelimb. In contrast, Sema3F-Npn-2 signaling guides the axons of a medial subset of LMC neurons to the ventral limb, but plays no major role in regulating their fasciculation. Thus, Sema3A-Npn-1 and Sema3F-Npn-2 signaling control distinct steps of motor axon growth and guidance during the formation of spinal motor connections.

Animals↗
PubMed2004

Mice deficient for the extracellular matrix glycoprotein tenascin-r show physiological and structural hallmarks of increased hippocampal excitability, but no increased susceptibility to seizures in the pilocarpine model of epilepsy.

Recognition molecules provide important cues for neuronal survival, axonal fasciculation, axonal pathfinding, synaptogenesis, synaptic plasticity, and regeneration. Our previous studies revealed a link between perisomatic inhibition and the extracellular matrix glycoprotein tenascin-R (TN-R). Therefore, we here studied neuronal excitability and epileptic susceptibility in mice constitutively deficient in TN-R. In vitro analysis of populational spikes in hippocampal slices of TN-R-deficient mice revealed a significant increase in multiple spikes in the CA1 region, as compared with wild-type mice. This difference between genotypes was only partially reduced after blockade of GABA(A) receptors with picrotoxin, indicating a deficit in GABAergic inhibition and an increase in intrinsic excitability of CA1 pyramidal cells in TN-R-deficient mice. Using a battery of immunohistochemical markers and histological stainings, we were able to identify two abnormalities in the hippocampus of TN-R-deficient mice possibly related to increased excitability: the high number of glial fibrillary acidic protein-positive astrocytes and low number of calretinin-positive interneurons in the CA1 and CA3 regions. In order to test whether the revealed abnormalities give rise to increased susceptibility to seizures in TN-R-deficient mice, we used the pilocarpine model of epilepsy. No genotype-specific differences were found with regard to the time-course of pilocarpine-induced and spontaneous seizures, neuronal cell loss, aberrant sprouting and distribution of synaptic and inhibitory interneuron markers. However, pilocarpine-induced astrogliosis and reduction in calretinin-positive interneurons were less pronounced in TN-R mutants, thereby resulting in an occlusion of effects induced by TN-R deficiency and pilocarpine. Thus, TN-R-deficient mutants show several electrophysiological and morphological hallmarks of increased neuronal excitability, which, however, do not give rise to more accelerated or severe epileptogenesis in the pilocarpine model of epilepsy.

Animals↗
PubMed2006

Regulation of neurite growth in immortalized mouse hypothalamic neurons and rat hippocampal primary cultures by teneurin C-terminal-associated peptide-1.

Teneurins are a highly conserved family of four type II transmembrane proteins that are expressed in the CNS. The protein possesses several functional domains including a unique bioactive 40-41 amino acid sequence at the extracellular terminus. Synthetic versions of this teneurin C-terminal-associated peptide (TCAP) can modulate cyclic AMP accumulation, cell proliferation and teneurin mRNA levels in vitro. Furthermore, i.c.v. injections of TCAP-1 into rat brain induce major changes in acoustic startle response behavior 3 weeks after administration, suggesting that the peptide may act to alter interneuron communication via changes in neurite and axon outgrowth. Synthetic mouse/rat TCAP-1 was used to treat cultured immortalized mouse hypothalamic cells, to determine if TCAP-1 could directly regulate neurite and axon growth. TCAP-1-treated cells showed a significant increase in the length of neurites accompanied by a marked increase in beta-tubulin transcription and translation as determined by real-time PCR and Western blot analysis, respectively. Changes in alpha-actinin-4 transcription and beta-actin protein expression were also noted. Immunofluorescence confocal microscopy using beta-tubulin antiserum showed enhanced resolution of beta-tubulin cytoskeletal elements throughout the cell. In order to determine if the effects of TCAP-1 could be reproduced in primary neuronal cultures, primary cultures of E18 rat hippocampal cells were treated with 100 nM TCAP-1. The TCAP-1-treated hippocampal cultures showed a significant increase in both the number of cells, dendritic branching and the presence of large and fasciculated beta-tubulin immunoreactive axons. These data suggest that TCAP acts, in part, as a functional region of the teneurins to regulate neurite and axonal growth of neurons.

Animals↗
PubMed2006

A case of neuromuscular mimicry.

Recognizing an ALS-mimic can be challenging. Here, we describe a patient with a slowly progressive dysarthria and dysphagia, with fasciculations of the tongue and general hyperreflexia, fulfilling the diagnostic criteria of 'clinical probable ALS'. Because of a non-conclusive EMG, a muscle biopsy was performed that surprisingly showed widespread nemaline rods. The clinical features and the histological findings were compatible with a sporadic late onset nemaline myopathy. Three years after initial presentation the patient died and post-mortem examination not only showed nemaline bodies in every muscle examined, but also revealed an unsuspected final diagnosis: sarcoid brainstem encephalitis. Nemaline rods can be found in various disorders, and neurosarcoidosis should be added to this list.

Amyotrophic Lateral Sclerosis↗
PubMed2005

Otolaryngologic presentations of amyotrophic lateralsclerosis.

OBJECTIVES/HYPOTHESIS: To determine the incidence of voice disturbance as a presenting symptom of amyotrophic lateral sclerosis (ALS) and describe laryngologic features of ALS. STUDY DESIGN: Retrospective review. METHODS: Records of patients with voice disturbance at a voice center and ALS patients at a neurology clinic were reviewed from January 1998 to March 2003. RESULTS: 15 of 1759 patients with voice disturbance were later diagnosed with ALS. Of 220 ALS patients presenting to neurology clinic, 44 had bulbar symptoms and 19 had initially presented to an otolaryngologist. Dysarthria, dysphagia, tongue fasciculation, and incomplete vocal fold closure were common findings. Neuromuscular disease was missed in 8 of 19 ALS patients seen by an otolaryngologist. CONCLUSIONS: Although otolaryngologists rarely encounter undiagnosed ALS patients, a significant portion of bulbar ALS patients are initially evaluated by otolaryngologists. SIGNIFICANCE: Vigilance for neuromuscular abnormalities on otolaryngologic exam is important in patients who present with dysarthria, dysphonia, or dysphagia. EBM RATING: C.

Adult↗
PubMed2006

PSA-NCAM in mammalian structural plasticity and neurogenesis.

Polysialic acid (PSA) is a linear homopolymer of alpha2-8-N acetylneuraminic acid whose major carrier in vertebrates is the neural cell adhesion molecule (NCAM). PSA serves as a potent negative regulator of cell interactions via its unusual biophysical properties. PSA on NCAM is developmentally regulated thus playing a prominent role in different forms of neural plasticity spanning from embryonic to adult nervous system, including axonal growth, outgrowth and fasciculation, cell migration, synaptic plasticity, activity-induced plasticity, neuronal-glial plasticity, embryonic and adult neurogenesis. The cellular distribution, developmental changes and possible function(s) of PSA-NCAM in the central nervous system of mammals here are reviewed, along with recent findings and theories about the relationships between NCAM protein and PSA as well as the role of different polysialyltransferases. Particular attention is focused on postnatal/adult neurogenesis, an issue which has been deeply investigated in the last decade as an example of persisting structural plasticity with potential implications for brain repair strategies. Adult neurogenic sites, although harbouring all subsequent steps of cell differentiation, from stem cell division to cell replacement, do not faithfully recapitulate development. After birth, they undergo morphological and molecular modifications allowing structural plasticity to adapt to the non-permissive environment of the mature nervous tissue, that are paralled by changes in the expression of PSA-NCAM. The use of PSA-NCAM as a marker for exploring differences in structural plasticity and neurogenesis among mammalian species is also discussed.

Aging↗
PubMed2004

Histopathological changes and inflammatory response induced by Tityus discrepans scorpion venom in rams.

Anesthetized rams envenomed s.c. with 40 microg/kg Tityus discrepans scorpion venom developed fasciculation, hypothermia, polyuria, pulmonary wet rales, tachypnea, respiratory distress and arrhythmia. Rams developed a cascade of inflammation reactions, characterized by activation of macrophages, fibroblasts and neutrophils, neutrophil infiltration and aggregation, vasculitis, arteritis and abundant fibrin deposition. At the inoculation site, venom was detected by immunohistochemistry in the extra cellular matrix, lymphatic vessels' and venules' lumen, inside macrophages and surrounding nerves. Extra cellular matrix was degraded at the inoculation site perhaps by activated neutrophils. Envenoming produced hepatocytes with Mallory body-like vacuoles which may be due to the increased plasmatic levels of TNF-alpha and IL6. Venom produced degranulation and vacuolization of acinary cells as well as interstitial swelling and necrosis. Necrosis of the Langerhan's islets occurred occasionally. Lungs showed the most deleterious effects developing wall collapse and necrosis, diffuse injury of the alveolar capillary barrier, interstitial and alveolar fibrin deposits with strong neutrophil infiltration. Massive infiltration of lymphocytes and macrophage occurred in the intestinal submucose, to the point that it modified villi and intestinal folding morphology. Envenomation developed a marked leukocyte aggregation surrounding nerves at the inoculation site. This study reveals that beyond its neurotoxicity, Tityus venom produces a severe and widespread inflammatory syndrome, expressed as histopathological changes at the site of inoculation, as well as in remote organs such as pancreas, lungs, intestine and liver. Our results suggest that not all remote targets are directly affected by the venom but that, as proposed earlier, are modified by inflammation by products produced elsewhere.

Animals↗
PubMed2006

Toxic effects seen in a herd of beef cattle following exposure to ash residues contaminated by lead and mercury.

Lead poisoning was diagnosed in three cattle along with increased mercury levels in the liver and kidney tissues of two of these animals. The clinical signs were different in each case and included salivation, anorexia, delayed menace response, delayed withdrawal reflex, head pressing, localized muscle fasciculation, reduced tongue tone, ataxia, rumen atony and seizures. Blood lead concentration was increased in all three cases to 0.76, 0.37 and 0.454ppm. Post mortem changes characteristic of lead poisoning were only recognized in one case and included cerebro-cortical oedema, cortical neuronal necrosis and endothelial proliferation, especially at the tips of the cerebral gyri. The animals were poisoned by ingestion of lead-contaminated ash residues from a bonfire. The abnormal levels of mercury in the liver and kidney tissues of two animals may also be at least partly attributable to the intake of the metal in the ash residues. The levels of mercury in the three samples from the ash residue were relatively low (1.31, 0.7 and 2.1ppm).

Animals↗
PubMed2006

Characteristics of an outbreak of West Nile virus encephalomyelitis in a previously uninfected population of horses.

Equine West Nile virus (WNV) encephalomyelitis cases - based on clinical signs and ELISA serology test results - reported to Texas disease control authorities during 2002 were analyzed to provide insights into the epidemiology of the disease within a previously disease-free population. The epidemic occurred between June 27 and December 17 (peaking in early October) and 1,698 cases were reported. Three distinct epidemic phases were identified, occurring mostly in southeast, northwest and then central Texas. Significant (P<0.05) disease clusters were identified in northwest and northern Texas. Most (91.1%) cases had no recent travel history, and most (68.9%) cases had not been vaccinated within the previous 12 months. One-third of cases did not survive, 71.2% of which were euthanatized. The most commonly reported presenting signs included ataxia (69%), abnormal gait (52%), muscle fasciculations (49%), depression (32%) and recumbency (28%). Vaccination status, ataxia, falling down, recumbency and lip droop best explained the risk of not surviving WNV disease. Results suggest that the peak risk period for encephalomyelitis caused by WNV may vary substantially among regions within Texas. Recumbent horses have a poor prognosis for survival. Vaccines, even if not administered sufficiently in advance of WNV infection within a district, may reduce the risk of death by at least 44%.

Animals↗
PubMed2004

Developmental switch in axon guidance modes of hippocampal mossy fibers in vitro.

Hippocampal mossy fibers (MFs), axons of dentate granule cells, run through a narrow strip, called the stratum lucidum, and make synaptic contacts with CA3 pyramidal cells. This stereotyped pathfinding is assumed to require a tightly controlled guidance system, but the responsible mechanisms have not been proven directly. To clarify the cellular basis for the MF pathfinding, microslices of the dentate gyrus (DG) and Ammon's horn (AH) were topographically arranged in an organotypic explant coculture system. When collagen gels were interposed between DG and AH slices prepared from postnatal day 6 (P6) rats, the MFs passed across this intervening gap and reached CA3 stratum lucidum. Even when the recipient AH was chemically pre-fixed with paraformaldehyde, the axons were still capable of accessing their normal target area only if the DG and AH slices were directly juxtaposed without a collagen bridge. The data imply that diffusible and contact cues are both involved in MF guidance. To determine how these different cues contribute to MF pathfinding during development, a P6 DG slice was apposed simultaneously to two AH slices prepared from P0 and P13 rats. MFs projected normally to both the host slices, whereas they rarely invaded P0 AH when the two hosts were fixed. Early in development, therefore, the MFs are guided mainly by a chemoattractant gradient, and thereafter, they can find their trajectories by a contact factor, probably via fasciculation with pre-established MFs. The present study proposes a dynamic paradigm in CNS axon pathfinding, that is, developmental changes in axon guidance cues.

Animals↗
PubMed2004

Contacts between the commissural axons and the floor plate cells are mediated by nectins.

During development of the central nervous system (CNS), commissural axons grow toward the ventral midline. After crossing the floor plate, they abruptly change their trajectory from the circumferential to the longitudinal axis. The contacts between the commissural axons and the floor plate cells are involved in this axonal guidance, but their mechanisms or structures have not fully been understood. In this study, we found that nectin-1 and -3, immunoglobulin-like cell-cell adhesion molecules, asymmetrically localized at the contact sites between the commissural axons and the floor plate cells, respectively. In vitro perturbation of the endogenous trans-interaction between nectin-1 and -3 caused abnormal fasciculation of the commissural axons and impairment of the contacts, and resulted in failure in longitudinal turns of the commissural axons at the contralateral sites of the rat hindbrain. These results indicate that the contacts between the commissural axons and the floor plate cells are mediated by the hetero-trans-interaction between nectin-1 and -3 and involved in regulation of the trajectory of the commissural axons.

Animals↗
PubMed2005

ten-1, an essential gene for germ cell development, epidermal morphogenesis, gonad migration, and neuronal pathfinding in Caenorhabditis elegans.

ten-m (odz) is the only pair-rule gene discovered in Drosophila that encodes a transmembrane protein and not a transcription factor. The vertebrate Ten-m orthologues have been implicated in pattern formation and neuronal development. To investigate the role of this protein in development, we characterize here the structure and function of the Caenorhabditis elegans orthologue ten-1. We found that two promoters control the expression of two different ten-1 transcripts. This results in the expression of type II transmembrane protein variants differing in their intracellular domains. Both ten-1 transcripts show complex, but distinct, expression patterns during development and in the adult. Interference with Ten-1 expression by RNAi experiments leads to multiple phenotypes resulting in defects in hypodermal cell migration, neuronal migration, pathfinding and fasciculation, distal tip cell migration, the establishment of the somatic gonad, and gametogenesis. The RNAi phenotypes were confirmed by the analysis of a deletion mutant which revealed that Ten-1 is essential for somatic gonad formation. The intracellular domain of the long form was detected at the cell membrane and in the nucleus. We propose that Ten-1 acts as a receptor for morphogenetic cue(s) and directly signals to the nucleus by translocation of its intracellular domain to the nucleus following its proteolytic release from the cell membrane.

Animals↗
PubMed2005

Novel genes controlling ventral cord asymmetry and navigation of pioneer axons in C. elegans.

The ventral cord in C. elegans is the major longitudinal axon tract containing essential components of the motor circuit. In genetic screens using transgenic animals expressing neuron specific GFP reporters, we identified twelve genes required for the correct outgrowth of interneuron axons of the motor circuit. In mutant animals, axons fail to navigate correctly towards the ventral cord or fail to fasciculate correctly within the ventral cord. Several of those mutants define previously uncharacterized genes. Two of the genes, ast-4 and ast-7, are involved in the generation of left-right asymmetry of the two ventral cord axon tracts. Three other genes specifically affect pioneer-follower relationships between early and late outgrowing axons, controlling either differentiation of a pioneer neuron (lin-11) or the ability of axons to follow a pioneer (ast-2, unc-130). Navigation of the ventral cord pioneer neuron AVG itself is defective in ast-4, ast-6 and unc-130 mutants. Correlation of these defects with navigation defects in different classes of follower axons revealed a true pioneer role for AVG in the guidance of interneurons in the ventral cord. Taken together, these genes provide a basis to address different aspects of axon navigation within the ventral cord of C. elegans.

Animals↗