bluuebunny/crossref_metadata_2025_split huggingface dataset:
C‐kinase manipulations disrupt activity‐driven retinotopic sharpening in regenerating goldfish retinotectal projection
Authors: Schmidt John T. 
Published: January 2005

AbstractRegenerating optic axons initially branch over a wide area in tectum to form a crude retinotopic map. The map is sharpened, and retinotopically appropriate synapses are stabilized via NMDA receptors that detect, via summation of EPSPs, the coincident activity of neighboring ganglion cells that make synapses onto common tectal cells. Sharpening shares a number of properties with long‐term potentiation (LTP) in hippocampus. This study tested whether protein kinase C (PKC) activation is necessary for sharpening as it is for LTP. Intracular (IO) or intracranial (IC) injections of kinase inhibitors or activators were made every other day from 19 to 37 days postcrush (sensitive period), and the projections formed were later recorded. Retinotopic sharpening was prevented by IC injection of the following agents: (1) general kinase inhibitors sphingosine and H7 (100‐200 μM in fluid above brain), (2) active but not inactive phorbols (TPA, 1 μM), and (3) calphostin C (1 μM), a specific and irreversible PKC inhibitor. The mature projection on the opposite tectum, however, when examined was not unsharpened. Lack of sharpening was reflected in multiunit fields at each tectal point that averaged 27°–30° versus 11° in Ringers and inactive phorbol control regenerates. Intraocular injections of either TPA (1 μM), or calphostin C (1 μM) also prevented sharpening (26° and 32° multiunit fields), suggesting action on PKC axonally transported to the presynaptic terminals. Calphostin C had no noticeable effect on the firing patterns of retinal ganglion cells. The endogenous activator of PKC, arachidonic acid (AA), disrupted sharpening at 20 μM or higher (IC injection, 32° multiunit fields), while a control fatty acid, elaidic acid, had no effect. Although AA at 5 μM showed no effect, and diacylglycerol at 5 μM exhibited only small effects, together they produced a large synergistic effect (32° multiunit fields). Such synergy mirrors the synergy in the activation of several isoforms of PKC. Actual concentrations in the extradural fluid around the brain were assayed via injections of 3H‐AA. Levels fell about sixfold after a day and by an additional fivefold the second day before the next injection. The results confirm that activity‐driven retinotopic sharpening is very sensitive to manipulations of kinases, especially PKC. © 1994 John Wiley & Sons, Inc.
Origin and clonal relationship of common inhibitory motoneurons CI1 and CI3 in the locust CNS
Authors: Wolf Harald , Lang Dirk M. 
Published: January 2005

AbstractIn the primordial thoracic ganglia of locust embryos, the bromodeoxiuridine (BrdU) technique for labelling proliferating cells and their progeny was combined with intracellular dye injection to investigate the origin and the clonal relationship of common inhibitory motoneurons. Common inhibitors 1 (CI1) and 3 (CI3) were found to be siblings, that is, they are produced by the division of one ganglion mother cell. This ganglion mother cell results from the first division of neuroblast 5–5, at about 30% of embryonic development. A large portion, at least, of the ganglion mother cells produced by subsequent divisions of neuroblast 5–5 give rise to interneurons with contralaterally ascending or descending axons and GABA‐like immunoreactivity. Thus, CI1 and CI3 are more closely related to putative inhibitory interneurons than they are to other, that is, excitatory, motoneurons. Consistent with this, the CI somata are associated with cell bodies of putative inhibitory interneurons rather than with clusters of excitatory motoneuron somata. These results elicit speculations regarding the evolutionary origin of inhibitory motoneurons. 1994 John Wiley & Sons, Inc.
In vitro analysis of neurite outgrowth indicate a potential role for tenascin‐like molecules in the development of insect olfactory glomeruli
Authors: Krull Catherine E. , Oland Lynne A. , Faissner Andreas , Schachner Melitta , Tolbert Leslie P. 
Published: January 2005

AbstractTenascin‐like material is associated with glial cells that form borders around developing glomerular units in the olfactory (antennal) lobe of the moth Manduca sexta and is present at critical stages of glomerulus formation (Krull et al., 1994, J. Neurobiol. 25:515–534). Tenascinlike immunoreactivity declines in the mature lobe, coincident with a wave of synapse formation within the glomeruli and glomerulus stabilization. Tenascin‐like molecules associated with neuropilar glia are in the correct position to influence the branching patterns of growing neurites by constraining them to glomeruli. In this study, we examine the growth of cultured moth antennal‐lobe neurons in response to mouse CNS tenascin. Uniform tenascin provides a poor substrate for cell‐body attachment and neurite outgrowth. Neuronal cell bodies provided with a striped substratum consisting of tenascin and concanavalin‐A (con‐A)/laminin attach preferentially to con‐A/laminin lanes. Most neurons restrict their branching to con‐A/laminin lanes both at early and later times in culture but others send processes across multiple tenascin and con‐/laminin lanes in an apparently indiscriminate manner. Tenascin can inhibit the neuritic outgrowth of most antennal‐lobe neurons, and this raises the possibility that the tenascin‐like molecules associated with neuropilar glia in vivo act to constrain growing neurites to glomeruli. Thus, glial cells, acting in concert with olfactory axons, might act to promote glomerular patterns of branching by antennal‐lobe neurons. 1994 John Wiley & Sons, Inc.
Neural organization of the ventilatory activity in the frog, Rana catesbeiana. II
Authors: Kago Naoki , Remmers John E. 
Published: January 2005

AbstractThe paralyzed, decerebrate frog, Rana catesbeiana, displays “fictive” oropharyngeal and pulmonary ventilations. In order to evaluate the neuronal correlates of these two centrally programmed ventilatory bursting patterns, we have performed intra‐and extracellular recordings of bulbar respiratory neurons in this fictively breathing preparation. A total of 123 respiratory neurons were recorded from the caudal medulla. Of 51 antidromically activated neurons, 20 were vagal motoneurons and 31 were hypoglossal motoneurons. Respiratory neurons that depolarized during the lung (L) or non‐lung (N) ventilatory phases were classified as L or N neurons, respectively. Phase spanning neurons (S) were active during both L and N phases. Some neurons showed oscillations of membrane potential synchronous with oropharyngeal ventilation. Those active during the buccal elevation phase were exclusively L neurons whereas those having buccal depressor activity were exclusively N neurons.Synaptic drive potentials were observed in all neurons recorded intracellularly. In some neurons, hyperpolarization was caused by inhibitory postsynaptic potentials, as demonstrated by reversal of membrane potential trajectory after intracellular chloride iontophoresis. Some individual motoneurons and interneurons exhibited both pulmonary and buccal ventilatory activity, indicating that both pattern generators project to a common motor control system. 1994 John Wiley & Sons, Inc.
Anti‐β1 integrin antibody inhibits schwann cell meylination
Authors: Fernandez‐Valle Cristina , Gwynn Lisa , Wood Patrick M. , Carbonetto Salvatore , Bunge Mary Bartlett 
Published: January 2005

AbstractSchwann cells (SCs) co‐cultured with sensory neurons require ascorbate supplementation for basal lamina assembly and differentiation into myelinating cells. The ascorbate requirement can be bypased by adding a purifed basal lamina component, laminin, to SC/neuron cocultures. We have examined the role of laminin receptors, Namely, the β1 subfamily of integrins, in the process of myelination. We demonstrate by immunostaining or immunoprecipitation that undifferentiated SCs in contact with axons express large amounts of the β1 subunit in association with the α1 or α6 subunit. In co‐cultures of myelinating SCs, α1β1 is no longer present, α6β1 is still present but at reduced levels, and α6β4 is expressed at much higher levels than in co‐cultures of undifferentiated SCs. Immunogold labelling at the electron microscope level suggested that β1 integrins are randomly distributed on undifferentiated SCs, become localized to the SC surface contacting basal lamina in differentiating SCs before the onset of myelination, and are not detected on myelinating SCs. Fab fragments of β1 function‐blocking antibody block both attachment of isolated SCs to laminin and formation of myelin sheaths by SCs co‐cultured with neurons in ascorbate‐supplemented medium. SCs unable to myelinate in the presence of the anti‐β1 antibody assemble patchy basal lamina that is only loosely attached to the cell surface and in some cases appears to be detaching from the membrane. In contrast, an α1β1 function‐blocking antibody only partially blocks attachment of isolated SCs to laminin but has no inhibitory effect on SC myelination. These results are consistent with the hypothesis that a member of the β1 subfamily of integrins other than α1β1 binds laminin present in basal lamina to the SC surface and transduces signals that are critical for initiation of SC differentiation into a myelinating cell. 1994 John Wiley & Sons, Inc.
Fibrolast growth factors in the nervous system
Authors: Exkenstien Felix P. 
Published: January 2005

AbstractFibroblast growth factors (FGFs) exhibit widespread mitogenic and neurotrophic activities. Nine members of the family are currently known, and FGF‐1 and FGF‐2 are present in relatively high levels in CNS. FGF‐1 is expressed by a subset of neuronal populations, while FGF‐2 is expressed by astrocytes. FGF‐1 and FGF‐2 lack signal peptides and appear to be present mainly in inracellular compartmens. This suggests that the factors may act as initiators of a repair response after injury. Support for this notion comes from observations that FGF‐1 and FGF‐2 levels are low during critical phases of development, but high in the adult CNS. A family of transmembrane tyrosine kinase receptors (FGFRs) mediates the effects of FGFs. Four different genes coding for FGF receptors are currently known, three of which are expressed in cell type‐specific patterns in the CNS The main receptor variants present in this tissue, however, can by themselves not distinguish between FGF‐1 and FGF‐2. Additional selectivity may be established by interaction of the FGFs and their receptors with select heparan proteoglycans (HSPGs). Therefore, the precise physiological role of FGFs is determined by the combination of cell type‐specific patterns of expression of FGFs, FGFRs and HSPGs together with the mechanisms that regulate the extracellular availability of FGFs. 1994 John Wiley & Sons, Inc.
Neurons in culture maintain acetylcholine receptor levels with far fewer transcripts than in vivo
Authors: Corriveau Roderick A. , Berg Darwin K. 
Published: January 2005

AbstractOf the 10 neuronal nicotinic acetylcholine receptor (AChR) genes identified in chick, five are expressed by ciliary ganglion neurons in vivo (α3, α5, α7, β2, and β4), and the mRNA levels produced increase during development approximately in parallel with the two major classes of AChRs present. Here we report that when chick ciliary ganglion neurons from 8‐day embryos are transferred to dissociated cell culture, they express the same five genes but at much lower levels. The α3 and α7 transcripts, chosen for detailed analysis because they encode subunits segregated between the two AChR species, decrease rapidly in abundance on transfer to culture and, after 1 week, are at levels less than a 20th of those found in vivo for neurons of the same age. Co‐culturing the neurons with skeletal myotubes did not increase the levels of AChR transcripts in the neurons. Despite low amounts of mRNA from all five genes, neither class of AChRs was much reduced in culture compared to in vivo. The numbers of AChRs on the cell surface actually increased with time in culture. Several culture conditions known to down‐regulate the receptors in culture did not reduce the abundance of the α3 and α7 mRNAs. The results suggest that post‐transcriptional controls can play an important role in determining AChR abundance on the neurons. © 1994 John Wiley & Sons, Inc. 1994 John Wiley & Sons, Inc.
Segmental independence and age dependence of neurite outgrowth from embryonic chick sensory neurons
Authors: Parson Simon H. , Ribchester Richard R. 
Published: January 2005

AbstractTargets in limb regions of the chick embryo are further removed from the dorsal root ganglia that innervate them compared with thoracic ganglion‐to‐target distances. It has been inferred that axons grow into the limb regions two to three times faster than into nonlimb regions. We tested whether the differences were due to intrinsic properties of the neurons located at different segmental levels. Dorsal root ganglia (DRG) were isolated from the forelimb, trunk, and hind limb regions of stage 25–30 embryos. Neurite outgrowth was measured in dissociated cell culture and in cultures of DRG explants. Although there was considerable variability in the amount of neurite outgrowth, there were no substantive differences in the amount or the rate of outgrowth comparing brachial, thoracic, or lumbosacral neurons. The amount of neurite outgrowth in dissociated cell cultures increased with the stage of development. Overall, our data suggest that DRG neurons express a basal amount of outgrowth, which is initially independent of target‐derived neurotrophic influences; the magnitude of this intrinsic growth potential increases with stage of development; and the neurons of the DRG are not intrinsically specified to grow neurites at rates that are matched to the distance they are required to grow to make contact with their peripheral targets in vivo. We present a speculative model based on Poisson statistics, which attempts to account for the variability in the amount of neurite outgrowth from dissociated neurons. © 1995 John Wiley & Sons, Inc.
Axotomy of developing rat spinal motoneurons: Cell survival, soma size, muscle recovery, and the influence of testosterone
Authors: Lubischer Jane L. , Arnold Arthur P. 
Published: January 2005

AbstractDuring the period of synapse elimination, motoneurons are impaired in their ability to generate or regenerate axonal branches: following partial denervation of their target muscle, young motoneurons do not sprout to nearby denervated fibers and after axonal injury, they fail to reinnervate the muscle. In the rat levator ani (LA) muscle, which is innervated by motoneurons in the spinal nucleus of the bulbocavernosus (SNB), synapse elemination ends relatively late in development and can be regulated by testosterone. We took advantage of this system to determine if the end of synapse elimination and the development of regenerative capabilities by motoneurons share a common mechanism, or, alternatively, if these two events can be dissociated in time. Axotomy on or before postnatal day 14 (P14) caused the death of SNB motoneurons. By P21, toward the end of synapse elimination in the LA muscle, SNB motoneurons had developed the ability to survive axonal injury. Altering testosterone levels by castration on P7 followed by 4 weeks of either testosterone propionate or control injections did not change the ability of SNB motoneurons to survive axonal injury during development, although these same treatments alter the time course of synapse elimination in the LA muscle. Thus, we dissociated the inability of SNB motoneurons to recover from axonal injury from their developmental elimination of synaptic terminals. We also measured the effect of early axotomy on motoneuronal soma size and on target muscle weight. Axotomy on P14 caused a long‐lasting decrease in the soma size of surviving SNB motoneurons, whereas motoneurons axotomized on P28 recovered their normal soma size. Axotomy on or before P7 caused severe atrophy of the target muscles, matching the extensive loss of motoneurons. However, target muscle recovery after axotomy on P14 was as good as recovery after axotomy at later ages, despite greater motoneuronal death after axotomy on P14. This result may reflect an increase in motor unit size, a decrease in polyneuronal innervation by SNB motoneurons that survive axotomy on P14, or a combination of the two. © 1995 John Wiley & Sons, Inc.
The role of receptor/channel activity in neuronal cell migration
Authors: Rakic Pasko , Komuro Hitoshi 
Published: January 2005

AbstractConfocal laser microscopy, in conjunction with carbocyanine dyes and calcium‐sensitive fluorescent indicators, was used in slices and explant cultures of developing cerebellum to study cellular mechanisms underlying a motility of neuronal cell migration. The results indicate that a combination of voltage‐ and ligand‐activated ion channels cooperatively regulates Ca2+ influx into the migrating cells. We suggest that molecules, present in the local cellular milieu, affect cell motility by activating specific ion channels and second messengers that influence polymerization of stiff and contractile cytoskeletal proteins. This early interaction between postmitotic neurons and surrounding cells controls the rate of their movements, sculpts their shapes, establishes their positions, and, therefore, indirectly determines their identities to prior formation of synaptic connections. © 1995 John Wiley Sons, Inc.
Fast and slow excitation of inhibitory cells in the CA3 region of the hippocampus
Authors: Poncer Jean‐Christophe , Miles Richard 
Published: January 2005

AbstractPyramidal cells form excitatory synaptic connections with local inhibitory neurons in the hippocampus. This recurrent synapse plays a crucial stabilizing role in the control of hippocampal activity, since it transforms pyramidal cell population. Using a combination of dual recording from presynaptic and postsynaptic cells and anatomical techniques, we show that these synaptic connections often comprise a single site for liberation of excitatory transmitter. The resulting excitatory postsynaptic potentials (EPSCs) have a fast time course and a similar amplitude to miniature EPSCs recorded in tetrodotoxin and cobalt. In contrast, activation of metabotropic glutamate receptors (mGluRs) by transmitter liberated during repetitive activation of these synapses produces an excitation with a much slower time course. In addition to somatodendritic mGluRs, which excite inhibitory cells, a different species of mGluR is present on inhibitory cell terminals. This mGluR is activated by higher concentrations of the agonist t‐1‐amino‐cyclopentyl–1,3‐decarboxylate and acts to reduce γ‐aminobutyric acid release. mGluRs, thus, have a dual action to enhance and to depress synaptic inhibition in the hippocampus. © 1995 John Wiley & Sons, Inc.
Possible strategies for finding the substrate for learning‐induced changes in the hippocampal cortex
Authors: Andersen Per , Trommald Mari 
Published: January 2005

AbstractFor long‐lasting memory traces, structural synaptic changes remain a probable mechanism. However, in higher animals it has proved difficult to provide positive evidence for this notion. The main reason may be that the changes are subtle and are to be found in a relatively small subset of synapses and in a distributed manner in the cellular network in question. Here, we discuss possible strategies for finding structural changes in the hippocampus associated with spatial learning, an activity for which this structure is important. Spatial learning may induce new excitatory synapses in a small subset of hippocampal CA1 neurons because we observe a higher spine density without alteration in dendritic length or branching. The dendritic synapses are regularly spaced, irrespective of spine density, suggesting the operation of an intersynaptic dispersing force. © 1995 John Wiley & Sons, Inc.
Role of the transforming growth factor‐β family in the expression of cranial neural crest‐specific phenotypes
Authors: Leblanc Gabrielle G. , Holbert Timothy E. , Darland Tristan 
Published: January 2005

AbstractCranial and trunk neural crest cells produce different derivatives in vitro. Cranial neural crest cultures produce large numbers of cells expressing fibronectin (FN) and procollagen I (PCol I) immunoreactivities, two markers expressed by mesenchymal derivatives in vivo. Trunk neural crest cultures produce relatively few FN or PCol I immunoreactive cells, but they produce greater numbers of melanocytes than do cranial cultures. Treatment of trunk neural crest cultures with transforming growth factor‐β1 (TGF‐β1) stimulates them to express both FN and PCol I immunoreactivities at levels comparable to those normally seen in cranial cultures and simultaneously decreases their expression of melanin. These observations raised the possibility that endogenous TGF‐β is involved in specifying differences in the phenotypes expressed by cranial and trunk neural crest cells in vitro. Consistent with this idea, we found that treatment of cranial cultures with a function‐blocking TGF‐β antiserum inhibits the development of FN immunoreactive cells and stimulates the development of melanocytes. Cranial and trunk neural crest cells express approximately equal levels of TGF‐β mRNA. However, trunk neural crest cells are significantly less sensitive to the FN‐inducing effect of TGF‐β1 than are cranial neural crest cells. These results suggest that: (1) endogenous TGF‐β is required for the expression of mesenchymal phenotypes by cranial neural crest cells, and (2) differences in the phenotypes expressed by cranial and trunk neural crest cells in vitro result in part from differences in the sensitivities of these two cell populations to TGF‐β. © 1995 John Wiley & Sons, Inc.
Purkinje cell dendritic arbors in chick embryos following chronic treatment with an N‐methyl‐D‐aspartate receptor antagonist
Authors: Vogel Michael W. , Prittie Jennifer 
Published: January 2005

AbstractThe normal development of Purkinje cell dendrites is dependent on afferent innervation. To investigate the role of neuronal activity in Purkinje cell dendritic development, chick embryos were chronically treated with a potent, selective, and systemically active competitive N‐methyl‐D‐aspartate (NMDA) receptor antagonist, NPC 12626. The NMDA receptor was chosen as a target for pharmacological blockade because of the importance of the NMDA receptor in synaptic plasticity and stabilization in development. Chick embryos were given daily injections of NPC 12626 (25 to 100 mg/kg) from embryonic day 14 (E14) to E17. The initial injections of NPC 12626 dramatically blocked embryo movements, but activity levels partially recovered following subsequent injections. Embryo movements were reduced by 24% at the end of the experiment. Embryos were killed on E18, and their brains processed for Golgi‐Cox staining. The morphology of Golgi‐stained Purkinje cells in drug‐treated embryos was similar to control embryos. Morphometric analysis showed, however, that chronic treatment with NPC 12626 resulted in a 19% reduction in Purkinje cell dendritic tree area and a 13% reduction in the number of dendritic branch points. The overall width and height of the drug‐treated dendritic trees were not significantly different from controls, suggesting that NPC 12626 reduced Purkinje cell dendritic area by interfering with branch formation. The volume of the granule cell layer and the heights of the molecular and external granule cell layers was not reduced, suggesting that NPC 12626 treatment did not simply delay development. These results suggest that activation of the NMDA receptor may mediate the afferent‐target interactions in the cerebellum that regulate the elaboration of Purkinje cell dendrites. © 1995 John Wiley & Sons, Inc.