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PubMed1994

The molecular cloning and characterization of potential chick DM-GRASP homologs in zebrafish and mouse.

A full-length zebrafish cDNA clone and a partial mouse cDNA clone similar to chick DM-GRASP were isolated and analyzed. The nucleotide sequence of the full-length zebrafish clone shares 54% identity, and predicts 39% amino acid identity, with chick DM-GRASP. The partial mouse clone shares 76% nucleotide identity, and predicts 76% amino acid identity, with chick DM-GRASP. The predicted proteins encoded by both of these clones exhibit conserved structural domains that are characteristic of the chick protein. These features may identify them as a distinct subfamily within the immunoglobulin superfamily of cell adhesion molecules. Expression of the zebrafish DM-GRASP protein is similar to chick DM-GRASP and is principally restricted to a small subset of developing sensory and motor neurons during axonogenesis. Zebrafish DM-GRASP expression was temporally regulated and limited to specific axon domains. This regional expression correlated with fasciculated axon domains. These results suggest that the zebrafish and mouse cDNA clones represent the respective fish and mammalian homologs of chick DM-GRASP. The highly selective expression of zebrafish DM-GRASP suggests that it is involved in the selective fasciculation and guidance of axons along their normal pathways.

Activated-Leukocyte Cell Adhesion Molecule↗
PubMed1995

Two chondroitin sulfate proteoglycans differentially expressed in the developing chick visual system.

Two monoclonal antibodies, 2B9 and 9BA12, were used to identify and characterize two different chondroitin sulfate proteoglycans (CSPGs) associated with the embryonic chick visual system. Monoclonal antibody 2B9 recognizes a carbohydrate epitope of collagen type IX proteoglycan. Immunohistochemistry showed that collagen type IX proteoglycan was abundant in the vitreous body and meninges, but absent in brain and retina. In developing trunk regions, collagen type IX proteoglycan is segmentally distributed in the somites, appearing only in the posterior sclerotome. Monoclonal antibody 9BA12 recognizes collagen type IX proteoglycan from vitreous body and an unidentified chondroitin sulfate proteoglycan in retina and brain, herein referred to as 9BA12 CSPG. Immunohistochemistry showed that 9BA12 CSPG is present in the optic fiber layer of the retina, coinciding temporally and spatially with the onset and cessation of ganglion cell axon growth. In the trunk region, 9BA12 immunostaining appears in the developing spinal cord and throughout the sclerotome. In culture, neither the collagen type IX proteoglycan nor the brain-derived 9BA12 CSPG were able to support neurite outgrowth from retinal ganglion cell explants. In combination with basal lamina proteins, collagen type IX proteoglycan slightly inhibited neurite outgrowth and led to a stronger fasciculation of retinal axons. In contrast, 9BA12 CSPG had no inhibitory effect on the outgrowth of retinal axons and had no effect on their fasciculation. Our study demonstrates the existence of two chondroitin sulfate proteoglycans in the developing visual system of the chick. Based on the developmental expression and the results from neurite outgrowth experiments, it was concluded that the 9BA12 CSPG does not operate as a neurite outgrowth inhibitor for retinal axons.

Animals↗
PubMed2000

Altered ionic conductances in axons of transgenic mouse expressing the human neurofilament heavy gene: A mouse model of amyotrophic lateral sclerosis.

Neurofilaments (NFs; made by copolymerization of three intermediate filament proteins NF-L, NF-M, and NF-H, for light, medium, and heavy) constitute the most abundant cytoskeletal structure in large myelinated axons. The presence of aberrant NF accumulation has been associated with neurodegenerative diseases (such as ALS). The possible causal role of NF in neurodegeneration has been supported by studies on recently available transgenic mice in which expression of human NF-H (hNF-H +/+) leads to overt neuropathy. We have examined electrophysiological properties of myelinated axons in hNF-H +/+ mice using intraaxonal microelectrode recording from isolated sciatic and tibial nerves. Transgenic mice showed several deficits in physiological properties of low threshold myelinated fibers: conduction velocity and resting membrane potential were significantly decreased (20 +/- 1.6 vs 40 +/- 2 m/s; -71.3 +/- 0.9 vs -75.5 +/- 0.5 m/s; mean +/- SE; n = 25; 22 degrees C). While the amplitude of action potentials was of comparable size (82 +/- 5 vs 86 +/- 3 mV) duration of action potential (at half-amplitude, AP/2) in hNF-H +/+ was significantly prolonged (0.82 +/- 0.02 vs 0.65 +/- 0.02 ms). Voltage-current properties of axonal membrane indicate a significant decrease in inward and outward rectification. Occasionally, impaled axons of hNF-H +/+ showed membrane oscillations and repetitive activity (reminiscent of fasciculations) never observed in normal animals. These results are compatible with an imbalance between ion conductances in axons from transgenic animals (an increase in Na(+) and a decrease in K(+) conductances), in agreement with recent suggestion based on clinical studies on ALS patients (H. Bostock et al., 1995, Brain 118, 217-225). One may hypothesize that these changes could contribute to neurodegenerative processes (i.e., via an increase in [Na(+)](i)), as well as clinical symptoms (fasciculations) observed in patients with degenerative motor neuron diseases.

Action Potentials↗
PubMed1991

Microtubule bundles in fish cerebellar Purkinje cells.

The initial axon segments and the cell bodies of Purkinje cells were examined in electron microscopic serial sections and toluidine blue semithin sections of goldfish cerebellum. We observed two characteristic cytoplasmic features different from those of other vertebrate neurons, 1. The areas of Nissl substance and Golgi apparatus are sharply divided in the periphery and center of the cytoplasm, 2. Microtubules fasciculated by cross-bridges in the axon hillock and initial axon segment remain bundled in the perikaryon, pass near the eccentric nucleus, and enter into the Golgi area of the central cytoplasm, where they are surrounded by mitochondria. We suggest that the intracellular fasciculated microtubules may establish a prepared pathway for fast anterograde and retrograde transport to and from the Golgi area of the cell body.

Animals↗
PubMed1995

The human optic nerve: fascicular organisation and connective tissue types along the extra-fascicular matrix.

Fibres in the mammalian optic nerve are arranged into fascicles between which there is an extra-fascicular matrix containing connective tissue, a feature similar to that found in association with fibres in peripheral nerves, but not otherwise found in the CNS. The relationship between these major features of the nerve architecture are not known. We have addressed this question by examining the fascicular organisation of the optic nerve and the distribution of connective tissue and specific collagen types in the human. We have also examined the spatial development of connective tissue in the human nerve to determine when and from where it originates. Fibres are grouped into fascicles at all locations along the nerve, except intracranially, close to the chiasm where this pattern is lost. Relatively large fascicular numbers are found directly behind the eye and in the region of the optic canal, but decline in the mid-orbital segment of the nerve. Connective tissue is present in the extra-fascicular matrix throughout the fasciculated segment, but in many cases it does not fully encircle fascicles. The proportion of matrix occupied by connective tissue is similar along the length of the nerve (approximately 60%). Within the matrix, collagen types I, III, IV, V and VI are present throughout fasciculated regions. Staining for types V and VI appeared relatively weak compared with that for the other types. Although the collagen types in the nerve are similar to those at the lamina cribrosa and in peripheral nerves, they did not appear to be differentially distributed as in regions of the PNS. Connective tissue enters the nerve at a number of wide-spread locations early in development, consistent with the notion that it enters the nerve with the blood supply. It is present within the matrix before it is established at the lamina cribrosa.

Aged↗
PubMed1989

Immunocytological characterization of the expression of cell adhesion molecule L1 during early innervation of mouse otocysts.

Doubts exist as to whether afferent nerve fibers exert a neurotrophic effect on the differentiation of sensory cells in the developing vestibular neuroepithelium. To determine whether innervation of hair cells precedes their differentiation, we have used the L1 adhesion molecule as a marker for axons. The detection of L1 on afferent axons in the otic vesicle of mouse embryos on gestation day 11 shows that nerve fibers penetrate the neuroepithelium before the sensory cells differentiate. L1-immunoreactivity of nerve endings also reveals the considerable fiber ramification on gestation days 14 and 15, i.e., corresponding to the first stages of sensory cell differentiation. The expression of L1 at successive stages of nerve fiber growth in the neuroepithelium, such as fasciculation and ramification, is not consistent with the previous role proposed for L1 as a fascicule-promoting factor and raises the possibility that other mechanisms are involved in L1 mediated adhesion.

Animals↗
PubMed1982

Peripheral neuropathy with a syndrome of continuous motor unit activity.

A chronic alcoholic who had also been submitted to partial gastrectomy developed a syndrome of continuous motor unit activity responsive to phenytoin therapy. There were signs of minimal distal sensorimotor polyneuropathy. Symptoms of the syndrome of continuous motor unit activity were fasciculation, muscle stiffness, myokymia, impaired muscular relaxation and percussion myotonia. Electromyography at rest showed fasciculation, doublets, triplets, multiplets, trains of repetitive discharges and myotonic discharges. Trousseau's and Chvostek's signs were absent. No abnormality of serum potassium, calcium, magnesium, creatine kinase, alkaline phosphatase, arterial blood gases and pH were demonstrated, but the serum Vitamin B12 level was reduced. The electrophysiological findings and muscle biopsy were compatible with a mixed sensorimotor polyneuropathy. Tests of neuromuscular transmission showed a significant decrement in the amplitude of the evoked muscle action potential in the abductor digiti minimi on repetitive nerve stimulation. These findings suggest that hyperexcitability and hyperactivity of the peripheral motor axons underlie the syndrome of continuous motor unit activity in the present case.

Alcoholism↗
PubMed1984

The ultrastructure and synaptic architecture of phrenic motor neurons in the spinal cord of the adult rat.

Although light microscopic studies have analysed phrenic motor neurons in several different species, there has never been an ultrastructural investigation of identified phrenic motor neurons. In addition, electrophysiological studies have raised questions relating to the function of phrenic motor neurons which may be answered only by direct electron microscopic investigation. Thus, the present study was carried out to provide a detailed ultrastructural analysis of identified phrenic motor neurons. Phrenic motor neurons in the spinal cord of the rat were labelled by retrogradely transported horseradish peroxidase (HRP) after transecting the phrenic nerve in the neck and applying the enzyme directly to the central stump of the transected nerve. The results showed that the general ultrastructural characteristics of phrenic motor neurons were similar to those previously reported for other spinal motor neurons. However, phrenic primary dendrites appeared to be isolated from all other dendritic profiles in the neuropil. Primary dendrites were not fasciculated. Fasciculation occurred only among the more distal secondary and tertiary phrenic dendritic branches. Direct dendrodendritic or dendrosomatic apposition was rarely seen; gap junctions between directly apposing phrenic neuronal membranes were not observed. The membranes of adjacent phrenic neuronal profiles were most frequently separated by intervening sheaths of astroglial processes. Myelinated phrenic axons and a phrenic axon collateral were identified. The initial portion of the phrenic axon collateral was cone-shaped, lacked myelin, and thus resembled a miniature axon hillock. In one instance, a large accumulation of polyribosomes was observed within the hillock-like structure of a phrenic axon collateral. Eight morphological types of synaptic boutons, M, P, NFs, S, NFf, F, G and C were classified according to criteria used by previous investigators. Most of these endings (M, NFs, NFf, S and F) made synaptic contact with profiles of labelled phrenic somata and dendrites. F, NFf, and S boutons also terminated on phrenic axon hillocks. C and G boutons contacted exclusively phrenic somata and small calibre dendrites, respectively. P boutons established axo-axonic synaptic contacts with the M and NFs bouton. The morphological findings of the present study provide new data that may be related to phrenic synchronized output and presynaptic inhibition of primary afferents terminating on phrenic motor neurons.

Animals↗
PubMed1994

Immunoelectron microscopic localization of E-cadherin in dorsal root ganglia, dorsal root and dorsal horn of postnatal mice.

Sensory neurons and associated glial cells are known to express the cell-cell adhesion molecule E-cadherin. The cellular and subcellular localization of this molecule in the dorsal root ganglion, dorsal root, and spinal cord of postnatal mice was studied by the pre-embedding immunoelectron microscopic labelling technique. In the dorsal root and the superficial layer of the dorsal horn, a subset of fasciculating unmyelinated axons expressed E-cadherin at their axon-axon contacts at all ages studied, and these axons were clustered together and segregated from E-cadherin-negative axons. In contrast, pre-myelinating large-diameter axons in P2 mice as well as myelinated axons in mice from P14 to adulthood were E-cadherin-negative. Glial cells also expressed E-cadherin: In the dorsal root ganglia, all of the satellite cells expressed E-cadherin at contact sites with neurons, other satellite cells, and basal lamina, at all ages studied. In dorsal roots from P14 to adulthood, myelin-forming Schwann cells expressed E-cadherin at the outer mesaxons and the contact sites with basal lamina. Non-myelin-forming Schwann cells occasionally stained for this molecule at contact sites with the plasma membrane of E-cadherin-positive axons and at other sites. These results strongly suggest that E-cadherin plays an important role in the selective fasciculation of a particular subset of unmyelinated sensory fibres, and also in glial cell contacts.

Animals↗
PubMed1990

Immunohistological localization of the neural adhesion molecules L1 and N-CAM in the developing hippocampus of the mouse.

The expression of the neural cell adhesion molecules L1 and N-CAM was investigated in developing postnatal mouse hippocampus by immunocytochemical techniques at the light and electron microscopic levels. In the 1, 8 and 21-day-old hippocampus, L1 was only observed on fasciculating axons. L1 was not detectable on dendrites and cell bodies of pyramidal cells, granule cells and interneurons in any of the hippocampal regions studied. Also, synapses were never found to be L1-immunoreactive either pre- or postsynaptically. L1 was not detectable at contacts between astrocytes and axons. Polyclonal N-CAM antibodies reacting with the three components of N-CAM (N-CAM total) stained all neuronal and glial cell types in the 1, 8 and 21-day-old hippocampus. In contrast, the 180 kDa component of N-CAM (N-CAM 180) was only detectable on neuronal cell bodies and dendrites of the 1 and 8-day-old hippocampus. In the 21-day-old hippocampus N-CAM 180 was not recognized on neuronal cell bodies. N-CAM 180 was strongly expressed in postsynaptic sites at all ages studies. We infer from these observations that L1 is predominantly involved in axon fasciculation, whereas N-CAM 180 appears to be more characteristic of stabilizing cell contacts, particularly at the synapse.

Animals↗
PubMed1978

Dermatomyositis, suxamethonium action and atypical plasmacholinesterase.

A 19-year-old girl suffering from active dermatomyositis was given suxamethonium 60 mg during anaesthesia for termination of pregnancy. A prolonged suxamethonium action occurred which was explained by the finding of homozygous atypical plasmacholinesterase in her blood. Although no fasciculations were seen immediately after injection of the drug, a period of fasciculations progressing from the extremities to the head and trunk occurred during recovery of muscle tone. No hyperpyrexia or elevation of serum creatine phosphokinase occurred. This was ascribed to the steroid therapy she received. Plasma from four other patients suffering from dermatomyositis was also investigated and one young woman, also pregnant, was found to be heterozygous for the atypical enzyme.

Adult↗
PubMed1983

Oral diazepam premedication reduces the incidence of post-succinylcholine muscle pains.

In a prospective, double-blind placebo controlled trial, the effect of oral diazepam premedication on post-succinylcholine fasciculations and myalgia was studied. Forty patients undergoing septoplasty procedures received orally identical capsules containing either 10 mg of diazepam or a placebo 90 minutes preoperatively. A standardized anaesthetic regimen included induction with 5 mg X kg-1 of thiopental and 1 mg X kg-1 of succinylcholine. The diazepam and control groups did not differ significantly in extent of fasciculations or ease of intubation. However, only 15 per cent of the diazepam premedicated patients had myalgias postoperatively compared to 50 per cent of the control patients, a statistically significant difference (p = 0.04).

Adult↗
PubMed2001

Expression and function of the LIM homeodomain protein Apterous during embryonic brain development of Drosophila.

We analyzed the expression and function of the LIM-homeodomain transcription factor Apterous (Ap ) in embryonic brain development of Drosophila. Expression of Ap in the embryonic brain begins at early stage 12 and is subsequently found in approximately 200 protocerebral neurons and in 4 deutocerebral neurons. Brain glia do not express Ap. Most of the Ap-expressing neurons are interneurons and project their axons across the midline to the contralateral hemisphere; a smaller subset projects their axons into the ventral nerve cord. A few Ap-expressing neurons project to the ring gland, suggesting that they are neurosecretory cells. In ap loss-of-function mutants, some of the protocerebral and deutocerebral interneurons that express Ap in the wild type show axon pathfinding errors and fasciculation defects in the brain, notably in the fascicles of the brain commissure. In contrast, the interneurons that project to the ring gland do not appear to be affected in ap mutants. Thus, in brain development, Ap is required for correct axon guidance and fasciculation of interneurons, and Ap-expressing cells may also be involved in the brain neuroendocrine system.

Animals↗
PubMed2005

Patched regulation of axon guidance is by specifying neural identity in the Drosophila nerve cord.

Within an axon bundle, one or two are pioneering axons and the rest are follower axons. Pioneering axons are projected first and the follower axons are projected later but follow a pioneering axon(s) pathway. It is not clear whether the pioneering axons have a guidance role for follower axons. In this paper, we have investigated the role of Patched (Ptc) in regulating the guidance of medial tract, one of the longitudinal tracts in the nerve cord. In patched mutants the medial longitudinal tract fails to fasciculate on its own side along the nerve cord, instead it abnormally crosses the midline and fasciculates with the contralateral tract. Interestingly, the medial tracts cross the midline ignoring the axon-repellant Slit on the midline and Roundabout on growth cones. The medial tract is pioneered by neurons pCC and vMP2. Our results show that guidance defects of this tract are due to loss and mis-specification of vMP2, which results in the projection from pCC to either stall or project outward near the location of vMP2. Thus, both pioneering neurons are necessary for the proper guidance of pioneering and follower axons. We also show that the loss of Ptc activity in the neuroectoderm prior to the formation of S1 and S2 neuroblasts causes the majority of axon guidance defects. These results provide insight into how mis-specification and loss of neurons can non-autonomously contribute to defects in axon pathfinding.

Animals↗
PubMed1991

Prevention of succinylcholine-induced myalgia with lidocaine pretreatment.

We studied the effects of 3 mg.kg(-1) lidocaine iv on the succinylcholine (SCh)-induced myalgia in 94 unpremedicated ambulant patients undergoing dilatation and curettage of the uterus. The post-SCh myalgia was confirmed through interview by telephone. The data were correlated with the degree of fasciculation and changes in the serum electrolytes and creatine kinase (CK) levels following SCh administration. Pretreatment with lidocaine, 3 mg.kg(-1) iv, significantly reduced the incidence of myalgia from 40.4% of control group to 12.8% lidocaine-treated group, but not the CK levels. The severity of myalgia was not related to the intensity of fasciculation assessed by visual observation. The pretreatment with lidocaine had no untoward effect on the circulation, although the peak arterial and peak venous lidocaine levels achieved were 29.6 +/- 23 micro g.ml(-1) and 10.1 +/- 3.3 micro g.ml(-1) respectively. These finding indicated that the pretreatment with lidocaine, 3 mg.kg(-1) iv, was effective in prevention of SCh-induced myalgia.

Journal Article↗
PubMed2001

Expression of R-cadherin in the regenerating chick sciatic nerve.

The ultrastructural localization of R-cadherin in normal and regenerating chick sciatic nerves was investigated immunocytochemically, and was compared with that of N-cadherin. R-cadherin was found on the plasmalemmae of axons and Schwann cells where cell-cell contacts were made in the normal unmyelinated fibers. It was also noted that R-cadherin was expressed on the axolemmae where regenerating axons contacted with each other, and formed fasciculations. The normal myelinated fibers displayed no immunoreactivity except at the mesaxon. These findings of R-cadherin were almost the same as those of N-cadherin of our previous study. N- and R-cadherin seemed to be co-expressed at the cell-cell contact points as mentioned above in the double labeling study. It is probable that cadherins contribute to the pathfinding of regenerating axons by causing them to form fasciculation. However, it seemed that there was no selective sorting of axons by N- and R-cadherin during regeneration as far as the present study was concerned.

Animals↗
PubMed1987

Growth pattern of pioneering chick spinal cord axons.

The early growth pattern of axons in the embryonic chick spinal cord was studied by electron microscopy. Serial perisagittal thin sections were obtained from the lateral margins of spinal cords of stage 17 (S17) and S19 embryos. A simple stereotypic pattern of axonal growth was found. Axons originated from a dispersed population of presumptive interneurons located along the lateral spinal cord margin. They first grew ventrally in a nonfasciculative pattern and later turned at right angles and grew in a fasciculative manner longitudinally in the ventrolateral fasciculus. Growth along the circumferential pathway was analyzed in detail by reconstructing individual axons and growth cones from the S17 specimen. Most circumferential axons, regardless of their site of origin, grew in a parallel orientation, and each of their growth cones projected ventrally. This pattern suggested that circumferential growth cones were guided at many, if not all, points along their path. Study of the region in front of these seven growth cones, however, revealed no apparent structural basis for their guidance. Alternative guidance mechanisms are discussed. In conjunction with previous studies (e.g., Windle and Baxter, 1936; Lyser, 1966), these findings suggest that the circumferential-nonfasciculative and the longitudinal-fasciculative patterns of axonal growth are the two fundamental patterns followed by most early forming axons in the brain stem and spinal cord of all higher vertebrates.

Animals↗
PubMed1988

The regulation of intramuscular nerve branching during normal development and following activity blockade.

In vertebrates, approximately 50% of the lumbosacral motoneurons die during a short period of development that coincides with synaptogenesis in the limb. Although it has been postulated that these motoneurons die because they fail to obtain adequate trophic support from the muscles, it is not clear how this factor is supplied. The mechanism by which activity blockade prevents motoneurons cell death is also unknown. In order to begin to understand the nature of these proposed trophic interactions, we have examined the temporal sequence of axonal invasion and ramification within two muscles of the chick hindlimb, the predominantly slow iliofibularis and the fast posterior iliotibialis, during the cell death period. We found striking differences in intramuscular nerve ingrowth and branching between fast and slow muscle. We also observed differences in the molecular composition of fast and slow myotubes that may contribute to the nerve pattern differences. In addition, we observed a progressive increase in the degree of intramuscular nerve fasciculation as well as a precise temporal sequence of nerve branching. The earliest detectable response to chronic curarization was a dramatic decrease in the degree of intramuscular nerve fasciculation. Activity blockade also greatly enhanced nerve branching within the muscles from the time that nerve branches normally formed, and, additionally, interfered with the normal cessation of axon growth. Our results support the idea that nerve endings are the sites of trophic uptake. Furthermore, although our results do not allow us to exclude other activity-dependent influences on motoneuron survival, they suggest the following testable hypotheses: (1) the normal regulation of motoneuron survival may result from the precise control of intramuscular nerve branching, (2) activity blockade may increase motoneuron survival by enhancing intramuscular nerve branching, and (3) anything which affects this complex process of nerve branching may also alter motoneuron survival.

Age Factors↗