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PubMed2005

The C. elegans histone deacetylase HDA-1 is required for cell migration and axon pathfinding.

Histone proteins play integral roles in chromatin structure and function. Histones are subject to several types of posttranslational modifications, including acetylation, which can produce transcriptional activation. The converse, histone deacetylation, is mediated by histone deacetylases (HDACs) and often is associated with transcriptional silencing. We identified a new mutation, cw2, in the Caenorhabditis elegans hda-1 gene, which encodes a histone deacetylase. Previous studies showed that a mutation in hda-1, e1795, or reduction of hda-1 RNA by RNAi causes defective vulval and gonadal development leading to sterility. The hda-1(cw2) mutation causes defective vulval development and reduced fertility, like hda-1(e1795), albeit with reduced severity. Unlike the previously reported hda-1 mutation, hda-1(cw2) mutants are viable as homozygotes, although many die as embryos or larvae, and are severely uncoordinated. Strikingly, in hda-1(cw2) mutants, axon pathfinding is defective; specific axons often appear to wander randomly or migrate in the wrong direction. In addition, the long range migrations of three neuron types and fasciculation of the ventral nerve cord are defective. Together, our studies define a new role for HDA-1 in nervous system development, and provide the first evidence for HDAC function in regulating neuronal axon guidance.

Amino Acid Sequence↗
PubMed2006

Epithelial overexpression of BDNF and NT4 produces distinct gustatory axon morphologies that disrupt initial targeting.

Most fungiform taste buds fail to become innervated when BDNF or NT4 is overexpressed in the basal layer of tongue epithelium. Here, we examined when and how overexpression of BDNF and NT4 disrupt innervation to fungiform papillae. Overexpression of either factor disrupted chorda tympani innervation patterns either before or during the initial innervation of fungiform papillae. NT4 and BDNF overexpression each disrupted initial innervation by producing different gustatory axon morphologies that emerge at distinct times (E12.5 and E14.5, respectively). Chorda tympani nerve branching was reduced in NT4 overexpressing mice, and neuronal fibers in these mice were fasciculated and remained below the epithelial surface, as if repelled by NT4 overexpression. In contrast, many chorda tympani nerve branches were observed near the epithelial surface in mice overexpressing BDNF, and most were attracted to and invaded non-taste filiform papillae instead of gustatory papillae. These results suggest that BDNF, but not NT4, normally functions as a chemoattractant that allows chorda tympani fibers to distinguish their fungiform papillae targets from non-gustatory epithelium. Since BDNF and NT4 both signal through the p75 and TrkB receptors, trophin-specific activation of different internal signaling pathways must regulate the development of the distinct gustatory axon morphologies in neurotrophin-overexpressing mice.

Animals↗
PubMed1989

Neuromuscular involvement in mild, asymptomatic primary hyperparathyroidism.

PURPOSE: The classic neuromuscular abnormalities of primary hyperparathyroidism are based on observations from an earlier time when the disease presented commonly with signs and symptoms. The purpose of the present study was to test for neuromuscular abnormalities among patients currently seen with primary hyperparathyroidism, in whom the vast majority are asymptomatic. PATIENTS, METHODS, AND RESULTS: Forty-two patients (30 women, 12 men) were studied. Serum calcium level was 11.1 +/- 0.1 mg/dL (normal, 8.7 to 10.7 mg/dL); phosphorus level was 2.8 +/- 0.1 mg/dL (normal, 2.5 to 4.5 mg/dL). Parathyroid hormone levels by radioimmunoassay for N-terminal and for mid-molecule regions were 32.6 +/- 2.4 pg/mL (normal, 8 to 24 pg/mL) and 831 +/- 127 pg/mL (normal, 50 to 330 pg/mL), respectively. Although generalized weakness and easy fatigability were common complaints, they were not seen on neurologic examination. No patient showed typical neuromuscular findings such as muscle weakness or atrophy, hyperreflexia, abnormal gait, tongue fasciculations, or objective changes in mental status. On the other hand, paresthesias and muscle cramps were reported by 22 patients (52%). Neurologic examination in 12 patients (29%) demonstrated findings consisting of either stocking-glove loss of pain sensation or loss of vibratory sensation with diminished reflexes. Creatine phosphokinase levels were normal in all patients. Electromyography and nerve conduction studies were performed in nine patients. None showed myopathy or signs of motor unit denervation. Isolated nerve abnormalities (n = 6) and nonspecific sensory neuropathy (n = 2) were observed. CONCLUSION: We conclude that the classic neuromuscular syndrome of primary hyperparathyroidism is rarely seen among a typical modern-day group of patients with primary hyperparathyroidism. The results suggest that the neurologic component of primary hyperparathyroidism should be included among those features of the disease that have changed along with other aspects of the clinical profile of primary hyperparathyroidism.

Aged↗
PubMed2005

Developmental abnormalities of neuronal structure and function in prenatal mice lacking the prader-willi syndrome gene necdin.

Necdin (Ndn) is one of a cluster of genes deleted in the neurodevelopmental disorder Prader-Willi syndrome (PWS). Ndntm2Stw mutant mice die shortly after birth because of abnormal respiratory rhythmogenesis generated by a key medullary nucleus, the pre-Bötzinger complex (preBötC). Here, we address two fundamental issues relevant to its pathogenesis. First, we performed a detailed anatomical study of the developing medulla to determine whether there were defects within the preBötC or synaptic inputs that regulate respiratory rhythmogenesis. Second, in vitro studies determined if the unstable respiratory rhythm in Ndntm2Stw mice could be normalized by neuromodulators. Anatomical defects in Ndntm2Stw mice included defasciculation and irregular projections of axonal tracts, aberrant neuronal migration, and a major defect in the cytoarchitecture of the cuneate/gracile nuclei, including dystrophic axons. Exogenous application of neuromodulators alleviated the long periods of slow respiratory rhythms and apnea, but some instability of rhythmogenesis persisted. We conclude that deficiencies in the neuromodulatory drive necessary for preBötC function contribute to respiratory dysfunction of Ndntm2Stw mice. These abnormalities are part of a more widespread deficit in neuronal migration and the extension, arborization, and fasciculation of axons during early stages of central nervous system development that may account for respiratory, sensory, motor, and behavioral problems associated with PWS.

Animals↗
PubMed2003

Induction of neuropilins-1 and -2 and their ligands, Sema3A, Sema3F, and VEGF, during Wallerian degeneration in the peripheral nervous system.

The neuropilins, NP-1 and NP-2, are coreceptors for Sema3A and Sema3F, respectively, both of which are repulsive axonal guidance molecules. NP-1 and NP-2 are also coreceptors for vascular endothelial growth factor (VEGF). The neuropilins and their ligands are known to play prominent roles in axonal pathfinding, fasciculation, and blood vessel formation during peripheral nervous system (PNS) development. We confirmed a prior report (Exp. Neurol. 172 (2001) 398) that VEGF mRNA levels rise during Wallerian degeneration in the PNS and herein demonstrate that NP-1, NP-2, Sema3A, and Sema3F mRNA levels increase in peripheral nerves distal to a transection or crush injury. In a sciatic nerve crush model, in which axonal regeneration is robust, the highest levels of Sema3F mRNA below the injury site are in the epi- and perineurium. Our results suggest the possibility that the neuropilins and their semaphorin ligands serve to guide, rather than to impede, regenerating axons in the adult PNS.

Animals↗
PubMed2003

Isolation of delta-missulenatoxin-Mb1a, the major vertebrate-active spider delta-toxin from the venom of Missulena bradleyi (Actinopodidae).

The present study describes the isolation and pharmacological characterisation of the neurotoxin delta-missulenatoxin-Mb1a (delta-MSTX-Mb1a) from the venom of the male Australian eastern mouse spider, Missulena bradleyi. This toxin was isolated using reverse-phase high-performance liquid chromatography and was subsequently shown to cause an increase in resting tension, muscle fasciculation and a decrease in indirect twitch tension in a chick biventer cervicis nerve-muscle bioassay. Interestingly, these effects were neutralised by antivenom raised against the venom of the Sydney funnel-web spider Atrax robustus. Subsequent whole-cell patch-clamp electrophysiology on rat dorsal root ganglion neurones revealed that delta-MSTX-Mb1a caused a reduction in peak tetrodotoxin (TTX)-sensitive sodium current, a slowing of sodium current inactivation and a hyperpolarising shift in the voltage at half-maximal activation. In addition, delta-MSTX-Mb1a failed to affect TTX-resistant sodium currents. Subsequent Edman degradation revealed a 42-residue peptide with unusual N- and C-terminal cysteines and a cysteine triplet (Cys(14-16)). This toxin was highly homologous to a family of delta-atracotoxins (delta-ACTX) from Australian funnel-web spiders including conservation of all eight cysteine residues. In addition to actions on sodium channel gating and kinetics to delta-ACTX, delta-MSTX-Mb1a caused significant insect toxicity at doses up to 2000 pmol/g. Delta-MSTX-Mb1a therefore provides evidence of a highly conserved spider delta-toxin from a phylogenetically distinct spider family that has not undergone significant modification.

Amino Acid Sequence↗
PubMed1997

Role of Csk in neural differentiation of the embryonic carcinoma cell line P19.

To examine the neural function of Csk (C-terminal Src kinase), a membrane-targeted form of Csk (Src/Csk) and its kinase-defective variant (DK-Src/Csk) were expressed in the embryonic carcinoma cell line P19. Expression of Src/Csk, but not DK-Src/Csk, caused reduction of the specific activities of Src and Fyn in the differentiated P19 cells. During neural differentiation, the specific activity of Src was elevated in the control P19 cells, whereas the activation was completely eliminated in the Src/Csk transfectant. In normally differentiated P19 cells, cross-linking of a cell adhesion molecule, L1, induced a short-term activation of Src and Fyn. In the Src/Csk transfectant, L1 stimulation induced delayed activation of Src and Fyn peaking at much lower levels than in the control cells. Src/Csk transfectants developed normally in the initial stages of neural differentiation, but exhibited an apparent defect in cell-to-cell interaction, i.e. neurite fasciculation and aggregation of cell bodies, in the latter stages. These findings imply that Csk is involved in the regulation of Src family kinases that play roles in cell-to-cell interaction mediated by cell adhesion molecules.

Animals↗
PubMed2001

The motor unit and electromyography--the legacy of Derek Denny-Brown.

With the development of the concept of the motor unit and new recording instruments, single motor unit action potentials (MUAPs) were recorded in 1929 in man by Adrian and Bronk and in the experimental animal by Denny-Brown. Studies of MUAPs in patients with neuromuscular disease followed, and in 1938, Denny-Brown and Pennybacker laid the foundation for clinical electromyography (EMG). Action potentials of single contracting or spontaneously firing motor units, termed fasciculations, were recorded and separated from the action potentials of single denervated muscle fibers, termed fibrillations. Thus, it was possible to interpret muscle twitching and cramping by EMG and separate neurogenic from myopathic diseases. Since then, EMG and neuromuscular disease have expanded greatly providing greater diagnostic capability and therapeutic success.

Boston↗
PubMed1998

Supplemental therapy in isolated vitamin E deficiency improves the peripheral neuropathy and prevents the progression of ataxia.

A 24-year-old male, who suffered since childhood from a progressive form of ataxia associated with peripheral neuropathy, was found severely deficient in serum vitamin E. He walked with bilateral aid and presented severe dysmetria of the limbs and dysarthric speech; muscular strength and trophism were slightly diminished in the distal muscles of four limbs and there was hypotonia of the arms; he presented absent deep tendon reflexes, bilateral Babinski's sign, reduced proprioception at four limbs, pes cavus and fasciculations of the tongue. Intestinal fat malabsorption and other gastrointestinal or haematological conditions associated with deficiency of this vitamin were ruled out. In this patient, after 2 years of a daily supplement of high doses of vitamin E, a further progression of the disease was not observed and, moreover, the neurophysiological characteristics of his neuropathy appeared clearly improved. A longitudinal evaluation of serum vitamin E levels showed values in the normal range after 13 months of therapy. The patient had molecular genetic analysis of chromosome 8 and was found homozygous for the unusual mutation 513insTT in the alpha-tocopherol transfer protein gene.

Administration, Oral↗
PubMed1999

Sporadic amyotrophic lateral sclerosis of long duration mimicking spinal progressive muscular atrophy: a clinicopathological study.

We report an autopsy case of amyotrophic lateral sclerosis (ALS) clinically diagnosed as spinal progressive muscular atrophy (SPMA). The patient was a Japanese woman without hereditary burden. She developed muscle weakness of the distal part of the left lower extremity at age 42, followed by muscle weakness and atrophy of the right lower extremity and upper extremities. At age 57, she needed transient ventilatory support. Slight weakness in the facial muscles and fasciculation of the tongue appeared at age 60. At age 61, she died of sudden respiratory arrest. During the clinical course, neurological examination revealed neither Babinski signs nor hyperreflexia. The neuropathological examination revealed not only neuronal loss with gliosis in the facial nucleus, hypoglossal nucleus, and anterior horns of the spinal cord, but also loss of Betz cells and degeneration of the pyramidal tracts. Based on these clinicopathological findings and review of literature, we conclude that sporadic ALS mimicking SPMA is present.

Amyotrophic Lateral Sclerosis↗
PubMed1999

Guamanian neurodegenerative disease: electrophysiologic findings.

Amyotrophic lateral sclerosis (ALS), parkinsonism and/or dementia are highly prevalent among the Chamorro population of Guam. The incidence of Guamanian ALS has markedly declined in recent years, but these incidence figures may reflect underascertainment of subclinical disease. Guamanian Chamorro patients have not been systematically studied using modern clinical neurophysiological techniques. Electromyography (EMG: needle exam and nerve conduction studies) was used to study 29 patients with the major subtypes of Guamanian neurodegenerative disease, as well as 11 neurologically normal Guamanian Chamorro subjects. Central conduction was assessed by somatosensory evoked potentials (SEP's) in 16 patients. EMG evidence of peripheral neuropathy, (often subclinical) was found in 45% of Guamanian patients but no Chamorro control subjects. Diabetes mellitus, which is highly prevalent in this population, was present in some, but not all of these cases. Clinically unsuspected motor neuron disease was identified by EMG in only one of the 23 Guamanian patients with parkinsonism and/or dementia and in none of the 11 Chamorro control subjects. Two of seven patients with the clinical phenotype of Guamanian ALS had a more benign EMG pattern on the needle electrode exam with absence of fibrillation and fasciculation potentials. Three of 16 patients (all with parkinsonism and dementia) had mildly abnormal tibial SEP's. No patient had EMG evidence of myopathy or a defect of neuromuscular transmission. We conclude: (1) peripheral neuropathy may be a manifestation of Guamanian neurodegenerative disease; (2) the declining prevalence of ALS on Guam is not associated with the development of a subclinical form of motor neuron disease; (3) the substantial overlap of Guamanian ALS with parkinsonism-dementia reported in prior decades is no longer apparent; (4) abnormal central conduction, as assessed by tibial SEP's, is present in some patients with Guamanian parkinsonism-dementia.

Adult↗
PubMed2006

[Finnish amyloid polyneuropathy in a French patient].

INTRODUCTION: Finnish amyloid variety is a rare familial amiloidosis polyneuropathy essentially observed in Finland. It concerns about six hundred people in the world in which five hundred reside in Finland. OBSERVATION: We report a case of a 58-year-old French woman with a 10-year history of lattice cornea dystrophy. She consulted in January 2004 for impaired swallowing, facial paralysis principally of the right superior territory and symptoms of arthritis which had developed a few months earlier. Observation revealed facial cutis laxa, tongue amyotrophy and some fasciculation. Electroneuromyography showed chronic neurogenic involvement of the facial muscles. Limbs and the sympathetic neuronal system were free of involvement. Pathological examination revealed areas of peri vascular amiloid deposits. Molecular biology confirmed the diagnosis of Finnish amiloidosis: substitution of aspartic acid by tyrosine in the 187 codon in the 9th chromosome (gelsoline gene). This mutation has been previously found in Denmark and the Czech Republic. CONCLUSION: Finnish amiloidosis is a familial polyneuropathy characterized by an association of cornea lattice dystrophy, cutis laxa and a chronic neurogenic involvement of the cranial nerves. Two mutations are known. Life expectancy is not affected, but quality of life is altered.

Amyloid Neuropathies, Familial↗
PubMed2002

Cross-reactivity of Sydney funnel-web spider antivenom: neutralization of the in vitro toxicity of other Australian funnel-web (Atrax and Hadronyche) spider venoms.

Australian funnel-web spiders are recognized as one of the most venomous spiders to humans world-wide. Funnel-web spider antivenom (FWS AV) reverses clinical effects of envenomation from the bite of Atrax robustus and a small number of related Hadronyche species. This study assessed the in vitro efficacy of FWS AV in neutralization of the effects of funnel-web spider venoms, collected from various locations along the eastern seaboard of Australia, in an isolated chick biventer cervicis nerve-muscle preparation. Venoms were separated by SDS-PAGE electrophoresis to compare protein composition and transblotted for Western blotting and incubation with FWS AV.SDS-PAGE of venoms revealed similar low and high molecular weight protein bands. Western blotting with FWS AV showed similar antivenom binding with protein bands in all the venoms tested. Male funnel-web spider venoms (7/7) and female venoms (5/10) produced muscle contracture and fasciculation when applied to the nerve-muscle preparation. Venom effects were reversed by subsequent application of FWS AV or prevented by pretreatment of the preparation with antivenom.FWS AV appears to reverse the in vitro toxicity of a number of funnel-web spider venoms from the eastern seaboard of Australia. FWS AV should be effective in the treatment of envenomation from most, if not all, species of Australian funnel-web spiders.

Antivenins↗
PubMed2000

Investigation of the haemodynamic effects of Phoneutria nigriventer venom in anaesthetised rabbits.

The haemodynamic alterations induced by the central and peripheral administration of the armed spider (Phoneutria nigriventer) venom (PNV) were investigated in anaesthetised rabbits. The intracerebroventricular injection of increasing doses of PNV (30 and 100 microg/kg) elicited a biphasic cardiovascular response characterised by a brief hypotension (1-3 min) followed by a marked and sustained (more than 30 min) increase in mean arterial pressure (61 +/- 5 and 61 +/- 10%, respectively) and in systemic vascular resistance (135 +/- 21 and 161 +/- 37%) accompanied by mild increases in cardiac contractility. Systemic alterations such as salivation and muscular fasciculation were also observed. At the opposite, the dose of 100 microg/kg of PNV injected intravenously produced only a hypotensive effect (29 +/- 4% decrease in mean arterial pressure) and a decrease in vascular resistance (38 +/- 5%). Nevertheless, a much higher dose of PNV (1 mg/kg) injected intravenously produced a hypertensive response analogous to the one observed upon central administration. The central hypertensive response induced by PNV was not affected by preteating the animals with selective antagonists of receptors of different neurotransmitters or endogenous mediators such as: acethylcoline muscarinic, bradykinin B2, angiotensin II AT1 receptors and also antagonists of the excitatory amino acid receptors of the central nervous system. Nevertheless, the intravenous pretreatment with the selective alpha1-adrenergic receptor antagonist prazosin significantly blunted the excitatory cardiovascular response evoked by the central injection of PNV. It is concluded that PNV can induce central as well as peripheral haemodynamic effects. The central component seems to be mediated by the activation of cardiovascular centres which in turn lead to an increase in the sympathetic outflow to the periphery, whereas the peripheral component can be accounted for either by direct activation of the vascular alpha1-adrenergic receptors or by catecholamine release from the sympathetic nerve endings.

Adrenergic alpha-Antagonists↗
PubMed1999

A case of infantile rhabdomyofibrosarcoma with immunohistochemical, electronmicroscopical, and genetic analyses.

A case of infantile rhabdomyofibrosarcoma arising on the buttocks of a 15-month-old boy is reported with histological, immunohistochemical, electronmicroscopical, and cytogenetic findings. Histological examination showed a proliferation of spindle-shaped cells in a fasciculated pattern, with occasional rounded rhabdomyoblastic cells with abundant eosinophilic cytoplasm. Immunohistochemically, the tumor cells expressed desmin and MyoD1 but were only weakly positive for myoglobin. No clear rhabdomyoblastic features were observed by electronmicroscopic examination. Chromosome analysis showed a clone of 46, XY, der(2)t(2;11)(q37;q13), different from any karyotypic abnormality in the original report of this neoplasm. Loss of heterozygosity at 11p15.5, the most frequent genetic alteration in embryonal rhabdomyosarcoma, was not detected. The low degree of striated muscle differentiation and tumor localization supported the diagnosis of infantile rhabdomyofibrosarcoma rather than spindle-cell rhabdomyosarcoma in this case. The present case has been uneventful as of 25 months after surgery. The rather long recurrence-free period, which has not been reported in previous cases, may be attributable to chemotherapy-induced rhabdoid differentiation of the tumor cells.

Cell Division↗
PubMed2003

Cell adhesion molecules during inner ear and hair cell development, including notch and its ligands.

Cellular adhesion plays a key role in a number of unique developmental events, including proliferation, cell fate, morphogenesis, neurite outgrowth, fasciculation, and synaptogensis. The number of families of molecules that can mediate cell adhesion and the number of members of each of those families has continued to increase over time. Moreover, the potential for the formation of different pairs of heterodimers with different binding specificities, and for both homo- and hetero-dimeric interactions suggest that a vast number of specific signaling events can be mediated through the expression of different combinations of adhesion factors at different developmental time points. By comparison with the number of known adhesion molecules and their potential effects, our understanding of the role of adhesion in ear development is extremely limited. The patterns of expression for some adhesion molecules have been determined for some aspects of inner ear development. Similarly, with a few exceptions, functional data to indicate the roles of these adhesion molecules are also lacking. However, a consideration of even the limited existing data must lead to the conclusion that adhesion molecules play key roles in all aspects of the development of the auditory system. Unique expression domains for different groups of adhesion molecules within the developing otocyst and ear strongly suggest a role in the determination of different cellular domains. Similarly, the specific expression of adhesion molecules on developing neurites and their target hair cells, suggests a key role for adhesion in the establishment of neuronal connections and possible the development of tonotopy. Finally, the recent demonstration that Cdh23 and Pcdh15 play specific roles in the formation of the hair cell stereociliary bundle provides compelling evidence for the importance of adhesion molecules in the development of stereocilia. With the imminent completion of the mouse genome, it seems likely that the number of adhesion molecules can soon be fixed and that it will then be possible to generate a more comprehensive map of expression of these molecules within the developing inner ear. At the same time, the generation of new transgenic and molecular technologies promises to provide researchers with new tools to examine the specific effects of different adhesion molecules during inner ear development.

Animals↗
PubMed2003

The thrombospondin type 1 repeat (TSR) and neuronal differentiation: roles of SCO-spondin oligopeptides on neuronal cell types and cell lines.

SCO-spondin is a large glycoprotein secreted by ependymal cells of the subcommissural organ. It shares functional domains called thrombospondin type 1 repeats (TSRs) with a number of developmental proteins expressed in the central nervous system, and involved in axonal pathfinding. Also, SCO-spondin is highly conserved in the chordate phylum and its multiple domain organization is probably a chordate innovation. The putative involvement of SCO-spondin in neuron/glia interaction in the course of development is assessed in various cell culture systems. SCO-spondin interferes with several developmental processes, including neuronal survival, neurite extension, neuronal aggregation, and fasciculation. The TSR motifs, and especially the WSGWSSCSVSCG sequence, are most important in these neuronal responses. Integrins and growth factor receptors may cooperate as integrative signals. We discuss the putative involvement of the subcommissural organ/Reissner's fiber complex in developmental events, as a particular extracellular signaling system.

Amino Acid Sequence↗
PubMed2002

Neuronal changes during forebrain evolution in amniotes: an evolutionary developmental perspective.

Embryology is the interface of genetic inheritance and phenotypic expression in adult forms, and as such is uniquely positioned to illuminate both. Embryonic cell migration pattern, transient connectivity, axonal growth kinetics and fasciculation patterns can clearly be substantially impacted at the striatocortical junction, which appears to be critical for telencephalic development. Similarly, the big questions concerning pallial evolution in amniotes all involve the pivotal region at the pallial-subpallial boundary, an area where complex developmental cross-currents may be involved in the specification of multiple structures that are thus related to each other. We review some of the positions based on recent genetic data and/or hodology, then suggest that comparative studies of intervening, embryological events may resolve some of the apparent conflicts and illuminate the evolutionary scenario. We propose a new hypothesis, the collopallial field hypothesis, which specifies that the anterior dorsal ventricular ridge of sauropsids and a set of structures in mammals--the lateral neocortex, basolateral amygdalar complex, and claustrum-endopiriform nucleus formation--are homologous to each other as derivatives of a common embryonic field. We propose that in mammals the laterally lying collopallium splits, or differentiates, into deep (claustroamygdalar) and superficial (neocortical) components, whereas in sauropsids, this split does not occur.

Animals↗