bluuebunny/crossref_metadata_2025_split huggingface dataset:
Physiological and developmental implications of motor unit anatomy
Authors: Ounjian M. , Roy R. R. , Eldred E. , Garfinkel A. , Payne J. R. , Armstrong A. , Toga A. W. , Edgerton V. R. 
Published: January 2005

AbstractThere is increasing evidence that the architectural design and arrangement of the fibers within a motor unit have important physiological and developmental ramifications. Limited data, however, are available to directly address this issue. In the present study the physiological properties of one motor unit in each of seven cat tibialis anterior (TA) muscles were determined. Each of these units then was repetitively stimulated to deplete the glycogen in all muscle fibers within the unit. Subsequently, the length, type of ending, and spatial distribution of fibers sampled from these physiologically and histochemically typed motor units were determined. Four fast fatigable (FF), one fast, fatigue resistant (FR), and two slow (S) motor units (MU) were studied. The samples consisted of all those glycogen‐depleted fibers (9–27) contained within a single fascicle or a circumscribed area of each of the motor unit territories. The mean fiber lengths for the two slow motor units were 35.9 and 45.5 mm. The mean fiber lengths for the fast motor unit samples ranged from 8.8 to 48.5 mm. Some fibers of both the fast and slow units reached lengths of 58 mm. Most of the fibers in the slow units extended the entire distance between the proximal and distal musculotendinous planes, had relatively constant cross‐sectional areas, and terminated at the tendon as blunt endings. In contrast, the majority of the fibers in the fast units terminated intrafascicularly at one end, and the cross‐sectional area decreased progressively along their lengths, that is, showed a tapering pattern for a significant proportion of their lengths. Therefore, the force generated by units that end midfascicularly would appear to be transmitted to connective tissue elements and/or adjacent fibers. All fibers of a fast unit within a fascicle were located at approximately the same proximo‐distal location. Thus, developmentally the selection of muscle fibers by a motoneuron would seem to be influenced by their spatial distribution. The architectural complexities of motor units also have clear implications for the mechanical interactions of active and inactive motor units. For example, the tension capabilities of a motor unit may be influenced not only by the spatial arrangement of its own fibers, but also by the level of activation of neighboring motor units.
Directional control of neurite outgrowth from cultured hippocampal neurons is modulated by the lectin concanavalin A
Authors: Farmer Lynne M. , Hagmann Jörg , Dagan Daniel , Matus Andrew I. , Levitan Irwin B. 
Published: January 2005

AbstractCell surface carbohydrates play an important role in the regulation of neurite outgrowth during neuronal development. We have investigated the actions of the plant lectin concanavalin A (Con A), a carbohydrate‐binding protein, on neurite outgrowth from hippocampal pyramidal neurons in primary cell culture. Neurons plated in culture medium containing nanomolar concentrations of Con A have a larger number of primary neurites arising directly from the cell soma than do neurons plated in culture medium alone. Furthermore, Con A causes counterclock‐wise turning of neurites in over 70% of the cultured neurons. Both of these effects of Con A are blocked by the hapten sugar α‐methyl‐d‐mannopyranoside, suggesting that they result from the interaction of Con A with a cell surface carbohydrate. Another lectin with a different sugar specificity, wheat germ agglutinin, does not modulate neurite outgrowth. Analysis of neurite outgrowth using video‐enhanced microscopy reveals that the counter‐clockwise turning is accompanied by directionally biased extension of filopodia from the growth cones of growing neurites. Treatment of the neurons with cytochalasin, which disrupts actin polymerization, eliminates the neurite turning induced by Con A, suggesting that actin microfilaments are involved in directional control of neurite outgrowth. © 1992 John Wiley & Sons, Inc.
Transient neonatal denervation alters the proliferative capacity of myosatellite cells in dystrophic (129ReJdy/dy) muscle
Authors: Ontell M. P. , Hughes D. , Hauschka S. D. , Ontell M. 
Published: January 2005

AbstractIt has been previously shown that transiently denervated, neonatal dystrophic muscle fails to undergo the degeneration–regeneration cycle characteristic of murine dystrophy (Moschella and Ontell, 1987). Thus, the myosatellite cells (myogenic stem cells) in these muscles have been spared the mitotic challenge to which dystrophic myosatellite cells are normally subjected early in the time course of the disease. By in vitro evaluation of the proliferative capacity of myosatellite cells derived from extensor digitorum longus (EDL) muscles of 100‐day‐old genetically normal (+/+) and genetically dystrophic [dy/dy (129ReJdy/dy)] mice and from muscles of age‐matched mice that had been neonatally denervated (by sciaticotomy) and allowed to reinnervate, it has been possible to directly determine whether the cessation of spontaneous regeneration in older dy/dy muscles in vivo, is due to an innate defect in the proliferative capacity of the myosatellite cells or exhaustion of the myosatellite cells' mitotic activity during the regenerative phase of the disease. This study demonstrates that transient neonatal denervation of dystrophic muscle (Den.dy/dy) increases the number of muscle colony‐forming cells (MCFs) permilligram of wet weight muscle tissue, increases the plating efficiency, and significantly increases the in vitro mitotic activity of dystrophic myosatellite cells toward normal values. The increased mitotic capability of myosatellite cells derived from Den.dy/dy muscle as compared to unoperated dy/dy muscle suggests that there is no innate defect in the proliferative capacity of the myosatellite cells of dy/dy muscles and that the cessation of spontaneous regeneration in the dy/dy muscles is related to the exhaustion of their myosatellite cells' mitotic capability. © 1992 John Wiley & Sons, Inc.
Preparation and biological properties of native and recombinant ciliary neurotrophic factor
Authors: Gupta S. K. , Altares M. , Benoit R. , Riopelle R. J. , Dunn R. J. , Richardson P. M. 
Published: January 2005

AbstractCNTF (ciliary neurotrophic factor), purified from rabbit sciatic nerves by a relatively simple procedure, is bioactive in tissue culture at low picomolar concentration and appears as a doublet on polyacrylamide gel electrophoresis (PAGE). In these nerves, CNTF accounts for more than one‐half of the survival‐promoting activity on ciliary neurons. The concentration of CNTF in rabbit sciatic nerves is estimated to be 5 nmol/kg, more than 1000 times higher than would seem to be required to support neurons if the neurotrophic factor were homogeneously distributed. With recombinant DNA technology, rat CNTF has been synthesized in Escherichia coli, purified without denaturating agents, and found to be bioactive at a slightly lower concentration than CNTF extracted from rabbit sciatic nerves. After radioiodination, CNTF retains biological activity but is not specifically internalized and retrogradely transported in motor and sensory axons. In peripheral nerves, ciliary neurotrophic factor differs biologically from nerve growth factor (NGF) by its much higher tissue concentration and apparent lack of internalization by peripheral nerve axons. © 1992 John Wiley & Sons, Inc.
GAP‐43 as a plasticity protein in neuronal form and repair
Authors: Strittmatter Stephen M. , Vartanian Timothy , Fishman Mark C. 
Published: January 2005

AbstractNeurons exhibit a remarkable plasticity of form, both during neural development and during the subsequent remodelling of synaptic connectivity. Here we review work on GAP‐43 and G0, and focus upon the thesis that their interaction may endow neurons with such plasticity. We also present new data on the role of G proteins in neurite growth, and on the interaction of GAP‐43 and actin. GAP‐43 is a protein induced during periods of axonal extension and highly enriched on the inner surface of the growth cone membrane. Its membrane localization is primarily due to a short amino terminal sequence which is subject to palmitoylation. Binding to actin filaments may also assist in restricting the protein to specific cellular domains. Consistent with its role as a „plasticity protein,”︁ there is evidence that GAP‐43 can directly alter cell shape and neurite extension, and several theses have been advanced for how it might do so. Two other prominent components of the growth cone membrane are the α and β subunits of G0. GAP‐43 regulates their guanine nucleotide exchange, which is an unusual role for an intracellular protein. We speculate that GAP‐43 may adjust the „set point”︁ of responsiveness for G0 stimulation by receptors, thereby altering the neuronal propensity to growth, without actually causing growth. To begin to address how G protein activity affects axon growth, we have developed a means to introduce guanine nucleotide analogs into sympathetic neurons. Stimulation of G proteins with GTP‐γ‐S retards axon growth, whereas GDP‐β‐S enhances it. This is compatible with G protein registration of inhibitory signals. © 1992 John Wiley & Sons, Inc.
Patterns of serotonin and SCP immunoreactivity during metamorphosis of the nervous system of the red abalone, Haliotis rufescens
Authors: Barlow Linda A. , Truman James W. 
Published: January 2005

AbstractLarvae of the red abalone, Haliotis rufescens, rely on external chemical cues to trigger metamorphosis; thus, the timing of metamorphosis is depedent upon the larva's chance encounter with the appropriate substrate. We examined the effect of the timing of metamorphosis on the development of the central nervous system (CNS), concentrating on the pattern of serotonin and small cardioactive peptide‐ (SCP) immunopositive neurons in the cerebral ganglia. By 4 days postfertilization the cerebral ganglion has five pairs of serotonin‐immunoreactive (IR) neurons, one pair of which (the V cells) innervate the velum. This complement of cells remains stable for as long as the larval stage persists but metamorphosis causes the rapid loss of the V cells. In the case of SCP‐IR neurons, one pair is present prior to metamorphic competency, but as larvae continue to age in the absence of inducing cues, additional pairs are gradually added. Metamorphosis causes an acceleration in SCP‐IR neuron addition. This separation of developmental patterns is well adapted for the inherent uncertainty of the timing of metamorphosis in abalone larvae. © 1992 John Wiley & Sons, Inc.
The paired domain‐containing nuclear factor Pax[b] is expressed in specific commissural interneurons in zebrafish embryos
Authors: Mikkola Ingvild , Fjose Anders , Kuwada John Y. , Wilson Stephen , Guddal Per Henrik , Krauss Stefan 
Published: January 2005

AbstractThe zebrafish paired box (Pax) genes are expressed in the early neural tube and are thought to be transcription factors that regulate the differentiation of cells in the central nervous system (CNS). The protein product of one of these Pax genes, pax[b], is detectable as a nuclear antigen in all the regions of the embryo that transcribe the gene including the posterior midbrain, the nephritic primordium, the Wolffian duct, the optic stalk, and, in specific neurons, in the hindbrain and spinal cord. The timing and pattern of axonal outgrowth by the early pax[b]‐positive neurons suggest that they are the commissural secondary ascending (CoSA) interneurons in the spinal cord; the primary commissural interneurons (MiD2c and MiD3c) in hindbrain rhombomeres mi2 and mi3; and a previously unclassified set of commissural interneurons that we termed the commissural caudalrhombomere ascending (CoCaA) interneurons in the caudal hindbrain. In contrast, the Mauthner interneurons do not express pax[b] early in development. Shortly after the appearance of the first pax[b]‐positive interneurons, additional nuclei adjacent to the first pax[b]‐positive interneurons become pax[b] positive. This pattern of expression suggests that the pax[b] protein may be involved in determining the identity of specific commissural interneurons. © 1992 John Wiley & Sons, Inc.
The distribution of tyrosine hydroxylase immunoreactivity in the brains of male and female zebra finches
Authors: Bottjer Sarah W. 
Published: January 2005

AbstractA system of brain nuclei controls song learning and behavior in zebra finches (Poephila guttata). The size of song‐control nuclei are much larger in males, which sing, than in females, which do not sing. This study examined the distribution of fibers, terminals, and cell bodies that are immunoreactive for tyrosine hydroxylase (TH) (the rate‐limiting enzyme in the synthesis of catecholamines) in song‐control nuclei of adult males and females and juvenile males. In addition, the broad pattern of TH staining throughout the brain was described. There was a sex difference in TH immunoreactivity within song‐control nuclei: males had light to moderate staining in all three cortical nuclei examined, whereas females had little or no label in corresponding areas [lateral magnocellular nucleus of the anterior neostriatum (IMAN), higher vocal center (HVC), and robust nucleus of the archistriatum (RA)]. The song‐control nucleus area X (X), located in the striatum of avian basal ganglia, was more darkly stained than the surrounding striatum only in males; X was not defined by more intense immunoreactivity in females and hence could not be visualized. There were no apparent differences in TH staining in males ranging in age from 50 days to adulthood (>90 days). Outside of the song‐control system there were no substantive differences as a function of sex or age in the pattern or intensity of TH labeling. Major areas of telencephalic staining included the striatal region of basal ganglia, which was covered with dense, fine‐grained label, and the septum, where cell bodies were encircled by extremely well‐labeled thick processes. In the diencephalon, the preoptic area and hypothalamus included a complex pattern of darkly stained somata and fiber and terminal labeling. Darkly stained somata surrounded the pretectal nucleus, and labeled processes ramified throughout the superficial layers of the optic tectum. The midbrain and hindbrain contained a dense plexus of extremely dark cell bodies corresponding to mammalian substantia nigra, adjacent tegmental areas, and locus ceruleus. Labeled hindbrain cells were also seen in the pontine region, around nucleus solitarius, and in the ventrolateral medulla. © 1993 John Wiley & Sons, Inc.
From neural crest to bowel: Development of the enteric nervous system
Authors: Gershon Michael D. , Chalazonitis Alcmèe , Rothman Taube P. 
Published: January 2005

AbstractThe ENS resembles the brain and differs both physiologically and structurally from any other region of the PNS. Recent experiments in which crest cell migration has been studied with DiI, a replication‐deficient retrovirus, or antibodies that label cells of neural crest origin, have confirmed that both the avian and mammalian bowel are colonized by émigrés from the sacral as well as the vagal level of the neural crest. Components of the extracellular matrix, such as laminin, may play roles in enteric neural and glial development. The observation that an overabundance of laminin develops in the presumptive aganglionic region of the gut in Is/Is mutant mice and is associated with the inability of crest‐derived cells to colonize this region of the bowel has led to the hypothesis that laminin promotes the development of crest‐derived cells as enteric neurons. Premature expression of a neuronal phenotype would cause crest‐derived cells to cease migrating before they complete the colonization of the gut. The acquisition by crest‐derived cells of a nonintegrin, nervespecific, 110 kD laminin‐binding protein when they enter the bowel may enable these cells to respond to laminin differently from their pre‐enteric migrating predecessors. Crest‐derived cells migrating along the vagal pathway to the mammalian gut are transiently catecholaminergic (TC). This phenotype appears to be lost rapidly as the cells enter the bowel and begin to follow their program of terminal differentiation. The appearance and disappearance of TC cells may thus be an example of the effects of the enteric microenvironment on the differentiation of crest‐derived cells in situ. Crest‐derived cells can be isolated from the enteric microenvironment by immunoselection, a method that takes advantage of the selective expression on the surfaces of crest‐derived cells of certain antigens. One neurotrophin, NT‐3, promotes the development of enteric neurons and glia in vitro. Because trkC is expressed in the developing and mature gut, it seems likely that NT‐3 plays a critical role in the development of the ENS in situ. Although the factors that are responsible for the development of the unique properties of the ENS remain unknown, progress made in understanding enteric neuronal development has recently accelerated. The application of new techniques and recently developed probes suggest that the accelerated pace of discovery in this area can be expected to continue. © 1993 John Wiley & Sons, Inc.
Immunocytochemical localization of sodium channels in an insect central nervous system using a site‐directed antibody
Authors: French A. S. , Sanders E. J. , Duszyk E. , Prasad S. , Torkkeli P. H. , Haskins J. , Murphy R. A. 
Published: January 2005

AbstractAntibodies to channel proteins and specific peptide sequences have been previously used to localize voltage‐activated sodium channels in the rat brain. Here we describe the first localization of sodium channels in an insect nervous system using a site‐directed antibody. The mesothoracic ganglion of the cockroach was stained with an antibody to the highly conserved SP19 sequence. Antibody labelling was visualized by light microscopy using the avidin/biotin method on was sections, and transmission electron microscopy of immunogold‐labelled thin sections. Central ganglia of insects contain clearly separated regions of cell bodies, synaptic neuropil, axon tracts, and nerves. Antibody staining by light microscopy was limited to neurons, and was intense in axons throughout the ganglion and nerves. Staining was also strong in the cytoplasm, but not the nuclei, of many neuronal cell bodies. Neuropil regions were relatively lightly labelled. These findings can be correlated with the known electrophysiology of the ganglion. Electron microscopy detected sodium channels in areas surrounding axons, probably including axon membranes and enveloping glial cell membranes. Axonal mitochondria were also heavily labelled, suggesting a sodium channel transport function for these organelles. © 1993 John Wiley & Sons, Inc.
Injury‐associated induction of GAP‐43 expression displays axon branch specificity in rat dorsal root ganglion neurons
Authors: Schreyer David J. , Skene J. H. Pate 
Published: January 2005

AbstractPeripheral nerve injury results in the increased synthesis and axonal trasnport of the growth‐associated protein GAP‐43 in dorsal root ganglion (DRG) neurons, coincident with regenerative growth of the injured peripheral axon branches. To determine wheter the injury‐associated signalling mechanism which leads to GAP‐43 induction also operates through the central branches of DRG axons, we used immunocytochemistry to compare the expression of GAP‐43 in adult rat DRG neurons 2 weeks after dorsal root crush lesions (central axotomy) or peripheral nerve crush lesions (peripheral axotomy). In uninjured ganglia, a subpopulation of smaller DRG neurons expresses moderate levels of GAP‐43, whereas larger neurons generally do not. At 2 weeks following peripheral axotomy, virtually all axotomized neurons, large and small, express high levels of GAP‐43. At 2 weeks following dorsal root lesions, no increase in GAP‐43 expression is detected. Thus, the injury‐associated up‐regulation of GAP‐43 expression in DRG neurons is triggered by a mechanism that is responsive to injury of only the peripheral, and not the central, axon branches. These findings support the hypothesis that GAP‐43 induction in DRG neurons is caused by disconnection from peripheral target tissue, not by axon injury per se. © 1993 John Wiley & Sons, Inc.
Induction and axial patterning of the neural plate: Planar and vertical signals
Authors: Altaba A. Rulz i 
Published: January 2005

AbstractIn this review I summarize recent findings on the contributions of different cell groups to the formation of the basic plan of the nervous system of vertebrate embryos. Midline cells of the mesoderm—the organizer, notochord, and prechordal plate—and midline cells of the neural ectoderm—the notoplate and floor plate—appear to have a fundamental role in the induction and patterning of the neural plate. Vertical signals acting across tissue layers and planar signals acting through the neural epithelium have distinct roles and cooperate in induction and pattern formation. Whereas the prechordal plate and notochord have distinct vertical signaling properties, the initial anteroposterior (A‐P) pattern of the neural plate may be induced by planar signals originating from the organizer region. Planar signals from the notoplate may also contribute to the mediolateral (M‐L) patterning of the neural plate. These and other findings suggest a general view of neural induction and axial patterning. © 1993 John Wiley & Sons, Inc.
Pax: Gene regulators in the developing nervous system
Authors: Chalepakis Georges , Stoykova Anastassia , Wijnholds Jan , Tremblay Patrick , Gruss Peter 
Published: January 2005

AbstractIn recent years, the discovery of Pax genes in mouse has played an invaluable role in furthering our understanding in mouse developmental processes and disorders. To date, eight murine paired box‐containing genes have been cloned. Seven of these exhibit a distinct spationtemporal expression pattern in the developing nervous system implying a role in the regional specification of the developing spinal cord and brain. The Pax genes encode for sequence‐specific DNA binding transcription factors that play a key role in embryonic development. Three of these developmental control genes are altered in mutant mice and two are associated with human diseases. Disruption of these Pax genes leads to abnormalities in neural crest derivatives, neuroectoderm, sclerotome or myotome‐derived tissues. Disruption of the Pax‐3 gene causes the Splotch phenotype in mice and Waardenburg syndrome in humans. Pax‐6 mutations result in Small eye mice and the human genetic disorder aniridia. The Pax‐1 gene is mutated in undulated mice. Pax proteins can transform cells in culture which then form tumours following injection in nude mice. Consistent with this activity, PAX3 has been recently implicated in the generation of the tumour alveolar rhabdomyosarcoma. © 1993 John Wiley & Sons, Inc.