bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modulation of growth of Aplysia neurons by an endogenous lectin
Authors: Wilson Monita P. , Carrow Grant M. , Levitan Irwin B. 
Published: January 2005

AbstractWe have purified and characterized a galactose‐binding lectin from the gonads of the mollusk Aplysia californica that modulates neurite outgrowth from cultured Aplysia neurons. Agglutination of sheep red blood cells (RBC) by this lectin, termed Aplysia gonad lectin (AGL), is inhibited strongly by galactose and to a lesser extent by fucose. On SDS‐PAGE, AGL appears as a single species with a molecular weight of 34 kD under reducing conditions, and 65 kD under nonreducing conditions. This suggests that AGL is a disulfide‐linked dimer in its native state. Amino terminal sequence analysis of purified AGL indicates a similarity to another galactose‐binding lectin, phytohemagglutinin‐E (E‐PHA), found in red kidney beans. By using polyclonal antibodies prepared against AGL, we have found that the lectin is present in the gonads and eggs but not in other tissues of adult Aplysia californica. We have examined biological actions of AGL on Aplysia neurons growing in primary cell culture. AGL affects several properties of these neurons. The addition of 100 nM AGL to cultured neurons enhances neurite outgrowth from the cell soma, resulting in a greater number of primary processes. In addition, AGL acts as a neurotrophic agent, increasing neurite viability in vitro. This trophic effect is not seen with concanavalin A (con A), another lectin known to affect several properties of cultured Aplysia neurons. The results are consistent with the suggestion that AGL may play a role in neuronal differentiation and/or maintenance of viability. © 1992 John Wiley & Sons, Inc.
Modification of the dystrophic phenotype after transient neonatal denervation: Role of MHC isoforms
Authors: Ontell Martin P. , Moschella Maria C. , Schiaffino Stefano , Butler‐Browne Gillian , Whalen Robert , Ontell Marcia 
Published: January 2005

AbstractWhile it recently has been demonstrated that it is possible to modify the phenotypic expression of murine dystrophy (dy/dy) (i.e., prevent myofiber loss) by subjecting the extensor digitorum longus (EDL) muscle of 14‐day‐old dy/dy mice to transient neonatal denervation (Moschella and Ontell, 1987), the mechanism responsible for this phenomenon has not been determined. Since it has been suggested that the effects of dystrophy vary according to fiber type, the fiber type frequency in 100‐day‐old normal (+/+) and dy/dy EDL muscles subjected to transient neonatal denervation has been determined by immunohistochemical analysis of their myosin heavy chain (MHC) composition. This frequency has been compared with that found in the EDL muscles of 14 ‐and 100‐day‐old unoperated +/+ and dy/dy mice, in order to determine whether the reinnervation of transiently denervated neonatal muscle results in a preponderance of fibers of the type that might be spared dystrophic deterioration. In unoperated dy/dy muscle there is a progressive decrease in the frequency and in the absolute number of fibers that express MHC2B, with 100‐day‐old dy/dy muscles having ∼32% of the number of myofibers fibers containing MHC2B as is found in age‐matched +/+ muscles. The number of fibers containing the other fast isoforms (MHC2A and MHC2X) is similar in +/+ and dy/dy muscles at this age, indicating that fibers with MHC2B are most affected by the dystrophic process. Reinnervation following transient neonatal denervation of both the +/+ and the dy/dy EDL muscles results in a similar decrease (∼62%) in the number of myofibers containing MHC2B and an increase in myofibers containing the other fast MHC isoforms (MHC2A and MHC2X). The selective effect of dy/dy on fibers containing MHC2B and the sparing of myofibers in transiently denervated dy/dy muscle (which contains a reduced frequency of fibers containing MHC2B) are consistent with, although not direct proof of, the hypothesis that alterations in the fiber type may play a role in the failure of myofibers in transiently denervated dy/dy muscles to undergo dystrophic deterioration. Evidence is presented suggesting that neurons that supply myofibers containing MHC2B may be at a selective disadvantage in their ability to reinnervate neonatally denervated muscles. © 1992 John Wiley & Sons, Inc.
Formation and preservation of cortical layers in slice cultures
Authors: Götz Magdalena , Bolz Jürgen 
Published: January 2005

AbstractDuring cortical development, neurons generated at the same time in the ventricular zone migrate out into the cortical plate and form a cortical layer (Berry and Eayrs, 1963, Nature 197:984–985; Berry and Rogers, 1965, J. Anat. 99:691–709). We have been studying both the formation and maintenance of cortical layers in slice cultures from rat cortex. The bromodexyuridine (BrdU) method was used to label cortical neurons on their birthday in vivo. When slice cultures were prepared from animals at different embryonic and postnatal ages, all cortical layers that have already been established in vivo remained preserved for several weeks in vitro. In slice cultures prepared during migration in the cortex, cells contiuned to migrate towards the pial side of the cortical slice, however, migration ceased after about 1 week in culture. Thus, cortical cells reached their final laminar position only in slice cultures from postnatal animals, whereas in embryonic slices, migrating cells became scattered throughout the cortex. Previous studies demonstrated that radial glia fibers are the major substrate for migrating neurons (Rakic, 1972, J. Comp. Neurol. 145:61–84; Hatten and Mason, 1990, Experientia 46:907–916). Using antibodies directed against the intermediate filament Vimentin, radial glial cells were detected in all slice cutures where cell migration did occur. Comparable to the glia development in vivo, radial glial fibers disappeared and astrocytes containing the glia fibrillary‐associated protein (GFAP) differentiated in slice cultures from postnatal cortex, after the neurons have completed their migration. In contrast, radial glial cells were detected over the whole culture period, and very few astrocytes differentiated in embryonic slices, where cortical neurons failed to finish their migration. The results of this study indicate that the local environment is sufficient to sustain the layered organization of the cortex and support the migration of cortical neurons. In addition, our results reveal a close relationship between cell migration and the developmental status of glial cells. © 1992 John Wiley & Sons, Inc.
A specific brain tract guides follower growth cones in two regions of the zebrafish brain
Authors: Chitnis Ajay B. , Patel Chetan K. , Kim Stennis , Kuwada John Y. 
Published: January 2005

AbstractNeurons of the nucleus of the posterior commissure (nuc PC), an identifiable cluster of neurons in the embryonic zebrafish brain, project growth cones ventrally along the posterior commissure to the anterior tegmentum where the PC intersects two longitudinal tracts, the tract of the postoptic commissure (TPOC) and the medial longitudinal fasciculus (MLF). Once at the intersection, nuc PC growth cones turn posteriorly onto the TPOC in the dorsal tegmentum and follow it to the hindbrain. Previously we showed that in the absence of the TPOC, nuc PC growth cones often extended along aberrant path ways suggesting that fasciculation, that is, contact with TPOC axons is an important factor in guiding growth cones along their normal pathway. However, a significant number of nuc PC growth cones also followed their normal pathway suggesting that cues associated with the dorsolateral tegmentum, independent of the TPOC, can also guide nuc PC growth cones. We have now confirmed using electron microscopy that nuc PC growth cones fasciculate with axons in the TPOC. In the absence of the TPOC, the nuc PC growth cones that extend along their normal pathway do so in contact with dorsolateral neuroepithelial cells. This suggests that cues associated with these cells can also guide the nuc PC growth cones. Furthermore, in the absence of the TPOC axons, these growth cones now inappropriately turn onto axons that normally intersect the TPOC near the border of the midbrain and hindbrain, that is, at a second intersection of tracts. This suggests that fasciculation with TPOC axons may also guide nuc PC growth cones in this second region of the brain. © 1992 John Wiley & Sons, Inc.
Distribution and developmental change in [3H]MK‐801 binding within zebra finch song nuclei
Authors: Aamodt Sandra M. , Kozlowski Michael R. , Nordeen Ernest J. , Nordeen Kathy W. 
Published: January 2005

AbstractIn many songbirds, vocal learning depends upon appropriate auditory experience during a sensitive period that coincides with the formation and reorganization of song‐related neural pathways. Because some effects of early sensory experience on neural organization and early learning have been linked to activation of N‐methyl‐d‐aspartate (NMDA) receptors, we measured binding to this receptor within the neural system controlling song behavior in zebra finches. Quantitative autoradiography was used to measure binding of the noncompetitive antagonist [3H]MK‐801 (dizocilpine) in the brains of both adult and juvenile male zebra finches, focusing on four telencephalic regions implicated in song learning and production. Overall, the pattern of MK‐801 binding in zebra finches was similar to the pattern found in rats (Monaghan and Cotman, 1985, J. Neurosci. 5:2909–2919; Sakurai, Cha, Penney, and Young, 1991, Neuroscience 40:533–543). That is, binding was highest in the telencephalon, intermediate in thalamic regions, and virtually absent from the brain stem and cerebellum. The telencephalic song areas exhibited intermediate levels of binding, and binding in the juveniles was not significantly different from adult levels in most song nuclei. However, in the lateral magnocellular nucleus of the anterior neostriatum (IMAN), binding at 30 days of age was significantly higher than binding in adults. Given the established role of NMDA receptors in other developing neural systems, both their presence in song control nuclei and their developmental regulation within a region implicated in song learning suggest that NMDA receptors play a role in mediating effects of auditory experience on the development of song behavior.
Hypertrophy of gonadotropin releasing hormone‐containing neurons after castration in the teleost, Haplochromis burtoni
Authors: Francis Richard C. , Jacobson Ben , Wingfield John C. , Fernald Russell D. 
Published: January 2005

AbstractIn the African cichlid fish, Haplochromis burtoni, males are either territorial or nonterritorial. Territorial males suppress reproductive function in the nonterritorial males, and have larger gonads and larger gonadotropin‐releasing hormone‐ (GnRH) containing neurons in the preoptic area (POA). We describe an experiment designed to establish the causal relationship between large GnRH neurons and large testes in these males by determining the feedback effects of gonadal sex steroids on the GnRH neurons. Territorial males were either castrated or sham‐operated, 4 weeks after which they were sacrificed. Circulating steroid levels were measured, and the GnRH‐containing neurons were visualized by staining sagittal sections of the brains with an antibody to salmon GnRH. The soma areas of antibody‐stained neurons were measured with a computer‐aided imaging system. Completely castrated males had markedly reduced levels of circulating sex steroids [11‐ketotestosterone (11 KT) and testosterone (T)], as well as 17β‐estradiol (E2). POA GnRH neurons in castrates showed a significant increase in mean soma size relative to the intact territorial males. Hence, in mature animals, gonadal steroids act as a brake on the growth of GnRH‐containing neurons, and gonadal products are not responsible for the large GnRH neurons characteristic of territorial males. © 1992 John Wiley & Sons, Inc.
Ipsilateral retinopetal projection of the nucleus olfactoretinalis (NOR) during development and regeneration: A dil study in a cichlid fish
Authors: Wilm Claudia , Fritzsch Bernd 
Published: January 2005

AbstractThe development and regeneration of the ipsilateral retinopetal projection of the nucleus olfactoretinalis (NOR) in the cichlid fish Haplochromis burtoni was studied with 1,1′‐dioctadecyl‐3,3,3′,3′‐tetramethyl indocarbocyanine perchlorate (DiI) in fixed tissue. Through out development most NOR cells projected to the contralateral retina. Only an insignificant, transient elevation of a projection to the ipsilateral retinawas found in a few animals; however, after severing the contralateral processes of NOR cells by either enucleation or nerve crush, many animals had significantly more NOR cells with a regenerated process to the ipsilateral retina. Nevertheless, within a few weeks of surgery, the number of animals with ipsilaterally projecting cells were reduced to control values. The transiently enhanced ipsilateral projections to the retina imply changes in the guiding mechanism after these operations and the existence of control mechanisms against unusual connections to the retina in this bony fish. © 1993 John Wiley & Sons, Inc.
Cell lineage analysis in neural crest ontogeny
Authors: Le Douarin Nicole M. , Dupin Elisabeth 
Published: January 2005

AbstractThe neural crest is a transitory and pluripotent structure of the vertebrate embryo composed of cells endowed with developmentally regulated migratory properties. We review here a series of studies carried out both in vivo and in vitro on the ontogeny of the neural crest in the avian embryo. Through in vivo studies we established the fate map of the neural crest along the neuraxis prior to the onset of the migration and we demonstrated the crucial role played by the tissue environment in which the crest cells migrate in determining their fate. Moreover, the pathways of neural crest cell migration could also be traced by the quail‐chick marker system and the use of the HNK1/NC1 monoclonal antibody (Mab).A large series of clonal cultures of isolated neural crest cells showed that, at migration time, most crest cells are pluripotent. Some, however, are already committed to a particular pathway of differentiation. The differentiation capacities of the pluripotent progenitors are highly variable from one to the other cell. Rare totipotent progenitors able to give rise to representatives of all the phenotypes (neuronal, glial, melanocytic, and mesectodermal) encountered in neural crest derivatives were also found. As a whole we propose a model according to which totipotent neural crest cells become progressively restricted (according to a stochastic rather than a sequentially ordered mechanism) in their potentialities, while they actively divide during the migration process. At the sites of gangliogenesis, selective forces allow only certain crest cells potentialities to be expressed in each type of peripheral nervous system (PNS) ganglia. © 1993 John Wiley & Sons, Inc.
Cell fate determination in the peripheral nervous system: The sympathoadrenal progenitor
Authors: Anderson David J. 
Published: January 2005

AbstractStudies of postnatal chromaffin cells, sympathetic neurons and Small Intensely Fluorescent (SIF) cells have suggested that these cells develop from a common progenitor, the sympathoadrenal (SA) progenitor, whose fate is determined by the relative levels of nerve growth factor (NGF) and glucocorticoid (GC) in its environment (Unsicker et al., 1978, Proc. Natl. Acad. Sci. USA 75:3498–3502; Doupe et al., 1985a, J. Neurosci. 5:2119–2142). Recent studies have identified such a bipotential SA progenitor in the rat embryo. Surprisingly, this progenitor is initially unresponsive to NGF; neuronal differentiation is instead promoted by fibroblast growth factor (FGF). However, FGF appears to promote NGF responsiveness, suggesting that neuronal differentiation involves a relay or cascade of growth factor action. Furthermore, chromaffin cell differentiation appears to involve two sequential, GC‐dependent events: the inhibition of neuronal differentiation and the induction of epinephrine synthesis. The former event is a prerequisite to the latter. Thus both the chromaffin and neuronal pathways of differentiation follow a series of dependent events, involving changes in the responsiveness of SA progenitors to environmental factors. Such changes correlate with changes in antigenic marker expression that can be observed in vivo. In addition to choosing between neuronal and endocrine fates, SA progenitors must also express an appropriate neurotransmitter phenotype. For example, sympathetic neurons can become either noradrenergic or cholinergic. This cholinergic potential is already present in uncommitted SA progenitors, as evidenced by their ability to synthesize acetylcholine. Recent studies suggest that these cells may have yet other developmental capacities, including the ability to synthesize serotonin. This capacity is consistent with the hypothesis that SA progenitors are closely related to progenitors of enteric neurons, an idea supported by recent observations using novel antigenic markers. The SA progenitor may be, therefore, a “master” neuroendocrine progenitor for the peripheral nervous system. © 1993 John Wiley & Sons, Inc.
Regulation of substance P is similar to that of vasoactive intestinal peptide after axotomy or explantation of the rat superior cervical ganglion
Authors: Rao M. S. , Sun Y. , Vaidyanathan U. , Landis S. C. , Zigmond R. E. 
Published: January 2005

AbstractThe regulation of the expression of substance P (SP) in the rat superior cervical ganglion was compared to that of vasoactive intestinal peptide (VIP) in vivo after axotomy and in vitro after explantation. Previous studies have demonstrated that both neuropeptides increase after explantation, depolarization, and decentralization; however, whereas VIP expression increases after postganglionic axotomy, SP expression reportedly does not. To compare the effect of axotomy on these two peptides directly, the content of both was determined in individual ganglia at various times after surgery. The level of VIP‐like immunoreactivity (IR) is increased at 2 days, reaches a peak at 6 days, and then declines by 14 days to approximately half its peak value. The level of SP‐IR also increases 2 days after axotomy, but returns to control values by day 6. The increase in SP‐IR is accompanied by an increase in β‐preprotachykinin mRNA, suggesting that the elevation in SP content is due, at least in part, toenhanced peptide synthesis. Immunocytochemical localization of SP‐IR revealed the presence of immunoreactive principal neurons in axotomized, but not in sham‐operated ganglia. Similarities in the regulation of these two neuropeptides were also investigated in organ culture by examining the effects of dexamethasone and interleukin‐1β on VIP content, since the former has been shown to prevent the increase in SP in culture, while the latter has been found to enhance this increase (Kessler, Adler, Bell, et al., 1983, Neuroscience 9:309–321; Freidin and Kessler, 1991, Proc. Natl. Acad. Sci. USA 88:3200–3203; Hart, Shadiack, and Jonakait, 1991, J. Neurosci. Res. 29:282–291). As with SP expression, dexamethasone reduces the increases in VIP expression, while interleukin‐1β increases it. Thus, both in vivo and in vitro, similar changes in VIP and SP expression are observed following a number of experimental manipulations, suggesting that expression of the two peptides is regulated by qualitatively similar mechanisms in sympathetic neurons. © 1993 John Wiley & Sons, Inc.
Accommodation of mouse DRG growth cones to electrically induced collapse: Kinetic analysis of calcium transients and set‐point theory
Authors: Fields R. Douglas , Guthrie Peter B. , Russell James T. , Kater Stanley B. , Malhotra Bithika S. , Nelson Phillip G. 
Published: January 2005

AbstractElectrical stimulation causes growth cones of mouse dorsal root ganglion neurons to collapse. During chronic stimulation, however, growth cones resume motility. In addition, these growth cones are now resistant to the collapsing effects of subsequent stimulation, a process we term accommodation. We compared the kinetics of electrically induced Ca2+ transients in naive and accommodated growth cones in order to determine whether the accommodation process results from a change in the Ca2+ transient, or a change in the Ca2+ sensitivity of the growth cones. Three kinetics were determined: (1) the initial increase to peak Ca2+ levels produced by 10 Hz stimulation; (2) recovery from peak Ca2+ levels during stimulus trains lasting 15 min; and (3) clearing of Ca2+ from growth cones after terminating the stimulus. These kinetics were analyzed using single exponential fits to changes in fura‐2 fluorescence ratios. The electrically evoked increase in Ca2+ was significantly slower in accommodated growth cones (τ = 6.0 s) compared to naive growth cones (τ = 1.4 s). Desptie the slower increase of [Ca2+]i in accommodated growth cones, peak [Ca2+]i was similar to that reached in naive growth cones, and the steady‐state Ca2+ level was significantly elevated after chronic stimulation. Thus, accommodated growth cones maintained outgrowth at [Ca2+]i that caused collapse initially. Time course experiments show that accommodation is a slow process (t1/2 = about 3 h). Accommodation did not induce measurable changes in the rates of Ca2+ homeostasis during or after stimulus trains. The kinetics of Ca2+ recovery during (τ = 90 s) and after 15 min of stimulation (τ = 8.5 s) was not significantly different in accommodated versus naive growth cones. Rates of 45Ca2+ efflux were also similar in both types of growth cones. These results suggest two regulatory processes contributing to growth cone motility during chronic stimulation: (1) recovery of [Ca2+]i to levels permissive to neurite outgrowth, and (2) an increase in the range of optimal [Ca2+]i for growth cone motility. These adaptive responses of mammalian growth cones to chronic stimulation could be involved in the modulation of CNS development by electrical activity of neurons. © 1993 John Wiley & Sons, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Differential sensitivity to androgens within a sexually dimorphic muscle of male frogs (Xenopus laevis)
Authors: Regnier Michael , Herrera Albert A. 
Published: January 2005

AbstractMale frogs use their forelimb flexor muscles to clasp females during the mating behavior known as amplexus. We investigated the effects of testosterone on a principal forelimb flexor, the flexor carpi radialis muscle (FCR), using morphological and histochemical techniques. Male Xenopus laevis were surgically manipulated to produce high or low levels of circulating testosterone for an 8‐week period. After this treatment, measurement of fibers in muscle cross‐sections revealed that average fiber size was positively correlated with testosterone level. This effect was not the same for all muscle fibers, however. Fibers in the shoulder region were more sensitive to testosterone than fibers in other regions of the muscle. Histochemical staining of cross‐sections showed that the patterns of staining for myosin ATPase or succinic dehydrogenase (SDH) were not influenced by testosterone levels, but total SDH activity was increased by testosterone treatment. When sensitivity to testosterone was correlated with ATPase activity, fibers with high ATPase activity were found to be more sensitive to testosterone than fibers with low activity, regardless of position within the muscle. Most fibers with high ATPase activity were located in the shoulder region of the muscle. These fibers are innervated by different motor axons than are fibers in the elbow region of the muscle, and contractions of shoulder (but not elbow) region fibers, elicited by stimulation of motor axons, are slowed by testosterone treatment (Regnier and Herrera, 1993, J. Physiol. 461:565–581). © 1993 John Wiley & Sons, Inc.