bluuebunny/crossref_metadata_2025_split huggingface dataset:
Kinase requirement for retinal growth cone motility
Authors: Jian X. , Hidaka H. , Schmidt J. T. 
Published: January 2005

AbstractSince cytoplasmic Ca2+ levels are reported to regulate neurite elongation, we tested whether calcium‐activated kinases might be necessary for growth cone motility and neurite elongation in explant cultures of goldfish retina. Kinase inhibitors and activators were locally applied by micropipette to retinal growth cones and the responses were observed via phase‐contrast videomicroscopy. In some cases, growth rates were also quantifed over several hours after general application in the medium. The selective inhibitors of protein kinase C, calphostin C (0.1–1 μM) and chelerythrin (up to 50 μM), caused no obvious changes in growth cones or neurite elongation, and activators of PKC (phorbols, arachidonic acid, and diacylglycerol) also were generally without effects, although phorbols slowed the growth rate. Inhibitors of protein kinase A and tyrosine kinases also produced no obvious effects. The calmodulin antagonists, calmidazolium (0.1 μM), trifluoperazine (100 μM), and CGS9343B (50 μM), however, caused a reversible growth cone arrest with loss of filopodia and lamellipodia. The growth cone became a club‐shaped swelling which sometimes moved a short distance back the shaft, leaving evacuated filaments at points of strong filopodial attachments. A similar reversible growth cone arrest occurred with the general kinase inhibitors: H7 at 200 but not at 100 μM, and staurosporine at 100 but not 10 nM, suggesting possible involvement of a calmodulin‐dependent kinase (camK) rather than PKC. The selective inhibitor of camKII, KN‐62 (tested up to 50 μM), produced no effects but the specific myosin light‐chain kinase (MLCK) inhibitors ML‐7 (3–5 μM) and ML‐9 (5–10 μM) reversibly reproduced the effect, suggesting that MLCK rather than camKII is necessary for growth cone motility. The MLCK inhibitors' effects both on growth cone morphology and on F‐actin filaments (rhodamine‐phalloidin staining) were similar to those caused by cytochalasin D (5 μM), and are discussed in light of findings that inhibiting MLCK disrupts actin filaments in astrocytes and fibroblasts. 1994 John Wiley & Sons, Inc.
Neurotrophic factor therapy for nervous system degenerative diseases
Authors: Hefti Franz 
Published: January 2005

AbstractThe ability of neurotrophic factors to regulate developmental neuronal survival and adult nervous system planticity suggests the use of these molecuales to treat neurodegeneration associated with human diseases. Solid rationales exist for the use of NGF and neurotrophin‐3 in the treatment of neuropathies of the peripheral sensory system, insulin‐like growth factor and ciliary neurotrophic factor in motor neuron atrophy, and NGF in Alzheimer's disease. Growth factors have been identified for neurons affected in Parkinson's disease, Huntington's disease, and acute brain and spinal cord injury. Various strategies are actively pursued to deliver neurotrophic factors to the brain, and develop therapeutically useful molecules that mimic neurotrophic factor actions or stimulate their production or receptor mechanisms. 1994 John Wiley & Sons, Inc.
Target specificity and size of avian sensory neurons supported in vitro by nerve growth factor, brain‐derived neurotrophic factor, and neurotrophin‐3
Authors: Lopresti Patrizia , Scottt Sheryl A. 
Published: January 2005

AbstractTo obtain insight into which subpopulations of sensory neurons in dorsal root ganglia are supported by different neurotrophins, we retrogradely labeled cutaneous and muscle afferents in embryonic day 9 chick embryos and followed their survival in neuron‐enriched cultures supplemented with either nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), or neurotrophin‐3 (NT‐3). We found that NGF is a wide survival factor for subpopulations of both cutaneous and muscle afferents, whereas the survival effects of BDNF and NT‐3 are restricted primarily to muscle afferents. We also measured soma size in each neurotrophic factor. These new data show that BDNF‐ and NT‐3–dependent cells appear to be a mixture of two populations of neurons: one small diameter and the other large diameter. In contrast, based on size alone, NGF‐dependent cells appear to be a single population of only small‐diameter neurons. Thus, BDNF and NT‐3 may have some new, previously unreported effects on small‐diameter afferent neurons. © 1994 John Wiley & Sons, Inc. 1994 John Wiley & Sons, Inc.
Androgen directs sexual differentiation of laryngeal innervation in developing Xenopus laevis
Authors: Robertson John C. , Watson James T. , Kelley Darcy B. 
Published: January 2005

AbstractIn adult Xenopus laevis, innervation of the vocal organ is more robust in males than in females. This sex difference originates during tadpole development; at stage 56, when the gonads first differentiate, the number of axons entering the larynx is the same in the sexes, but by stage 62, innervation is greater in males. To determine if androgen secretion establishes sex differences in axon number, we treated tadpoles with antiandrogen or androgen beginning at stage 48 or 54 and counted laryngeal nerve axons at stage 62 using electron microscopy. When male tadpoles were treated with the antiandrogen hydroxyflutamide, axon numbers were reduced to female‐typical values; axon numbers in females were unaffected by antiandrogen treatment. When female tadpoles were treated with the androgen DHT (dihydrotestosterone), axon numbers were increased to male‐like values. These findings suggest that endogenous androgen secretion during late tadpole stages in males is required for the sexual differentiation of laryngeal innervation observed from stage 62 on. Because androgen treatment and laryngeal innervation affect myogenesis in postmetamorphic frogs, numbers of laryngeal dilator muscle fibers were determined for hormonally manipulated tadpoles. At stage 62, vehicle‐treated males had more laryngeal axons than females; laryngeal muscle fiber numbers did not, however, differ in the sexes. Both male and female tadpoles, treated from stage 54 with DHT, had more muscle fibers at stage 62 than vehicle‐treated controls. Thus, while endogenous androgen secretion during late tadpole stages is subthreshold for the establishment of masculinized muscle fiber numbers, laryngeal myogenesis is androgen sensitive at this time and can be increased by suprathreshold provision of exogenous DHT. A subgroup of tadpoles, DHT treated from stage 54 to 62, was allowed to survive, untreated, until postmetamorphic stage 2 (PM2: 5 months after metamorphosis is complete). Androgen treatment between tadpole stages 54 and 62 does not prevent the ontogenetic decrease in axon numbers characteristic of laryngeal development. In addition, the elevation in stage 62 axon numbers produced by DHT‐treatment at late tadpole stages was not associated with elevated numbers of laryngeal muscle fibers at PM2. Juvenile males normally maintain elevated axon numbers (relative to final adult values) through PM2 and the presence of these additional axons may result from‐rather than contribute directly to—laryngeal muscle fiber addition. 1994 John Wiley & Sons, Inc.
Dual pathways for tactile sensory information to thoracic interneurons in the cockroach
Authors: Pollack Alan J. , Ritzmann Roy E. , Watson James T. 
Published: January 2005

AbstractThe escape system of the American cockroach is both fast and directional. In response to wind stimulation both of these characteristics are largely due to the properties of the ventral giant interneurons (vGIs), which conduct sensory information from the cerci on the rear of the animal to type A thoracic interneurons (TIAs) in the thoracic ganglia. The cockroach also escapes from tactile stimuli, and although vGIs are not involved in tactile‐mediated escapes, the same thoracic interneurons process tactile sensory information. The response of TIAs to tactile information is typically biphasic. A rapid initial depolarization is followed by a longer latency depolarization that encodes most if not all of the directional information in the tactile stimulus. We report here that the biphasic response of TIAs to tactile stimulation is caused by two separate conducting pathways from the point of stimulation to the thoracic ganglia. Phase 1 is generated by mechanical conduction along the animal's body cuticle or other physical structures. It cannot be eliminated by complete lesion of the nerve cord, and it is not evoked in response to electrical stimulation of abdominal nerves that contain the axons of sensory receptors in abdominal segments. However, it can be eliminated by lesioning the abdominal nerve cord and nerve 7 of the metathoracic ganglion together, suggesting that the relevant sensory structures send axons in nerve 7 and abdominal nerves of anterior abdominal ganglia. Phase 2 of the TIAs tactile response is generated by a typical neural pathway that includes mechanoreceptors in each abdominal segment, which project to interneurons with axons in either abdominal connective. Those interneurons with inputs from receptors that are ipsilateral to their axon have a greater influence on TIAs than those that receive inputs from the contralateral side. The phase 1 response has an important role in reducing initiation time for the escape response. Animals in which the phase 2 pathway has been eliminated by lesion of the abdominal nerve cord are still capable of generating a partial startle response with a typically short latency even when stimulated posterior to the lesion. © 1995 John Wiley & Sons, Inc.
Lamina‐specific synaptic connections of hippocampal neurons in vitro
Authors: Frotscher M. , Heimrich B. 
Published: January 2005

AbstractBy using slice cultures as a model, we demonstrate here that different target selectivities exist among the various afferent fibers to the hippocampus. As in intact animals, septohippocampal cholinergic fibers, provided by a slice culture of septum, innervate a co‐cultured slice of hippocampus diffusely, that is, without forming distinct layers of termination. As in vivo, the septal cholinergic fibers establish synapses with a variety of target cells. Conversely, fibers from an entorhinal slice co‐cultured to a hippocampal slice display their normal laminar specificity. They preferentially terminate in the outer molecular layer of the fascia dentata, thereby selectively contacting peripheral dendrites of the granule cells. This preferential termination on peripheral dendritic segments is remarkable, since these fibers do not have to compete with commissural fibers, hypothalamic fibers, and septal afferents for dendritic space under these culture conditions. Moreover, in triplet cultures in which first two hippocampal slices were co‐cultured and then, with a delay of 5 days, an entorhinal slice was added, the fibers from the entorhinal slice and those from the hippocampal culture terminated in their appropriate layers in the hippocampal target culture. However, in this approach the normal sequence of ingrowth of these two afferents was reversed. In normal ontogenetic development, entorhinal afferents arrive in the hippocampus before the commissural fibers. The results show that there are different degrees of target selectivity of hippocampal afferents and that the characteristic lamination of certain afferent fibers in the hippocampus is not determined by their sequential ingrowth during development. © 1995 John Wiley & Sons, Inc.
Fos: An immediate‐early transcription factor in neurons
Authors: Curran Tom , Morgan James I. 
Published: January 2005

AbstractIn the past several years a great deal of evidence has accumulated linking neuronal activation events to the regulation of gene expression. We have pursued an analysis of c‐fos regulation in the nervous system to elucidate the molecular mechanisms involved in stimulus‐transcription coupling. The c‐fos gene can be viewed as an archetype of the set of cellular immediate‐early genes encoding transcription factors. These genes are believed to function in coupling short‐term signals elicited by extracellular to long‐term changes in cellular phenotype by orchestrating alterations in target gene expression. Several animal seizure models have been used to demonstrate the activation of gene expression in specific populations of neurons. Using a transgenic mouse approach, based on a foslacZ fusion gene, we now demonstrate an association between c‐fos expression and cell death in the nervous system. A delayed and protracted induction was observed following surgical lesion and in response to neurotoxin exposure. This system allows us to determine, for the first time, the DNA regulatory sequences that are responsible for the induction of gene expression in neurons in vivo. Furthermore, foslacZ transgenic mice provide a unique resource for identifying cell populations that respond to specific stimuli or that are susceptible to particular toxins. © 1995 John Wiley & Sons, Inc.
Plasticity in cultured carotid body chemoreceptors: Environmental modulation of GAP‐43 and neurofilament
Authors: Jackson Adele , Nurse Colin 
Published: January 2005

AbstractIn this study we use dissociated cell cultures of the rat carotid body to investigate the adaptive capabilities of endogenous oxygen chemoreceptors, following chronic stimulation by various environmental factors. These oxygen chemoreceptors are catecholamine‐containing glomus cells, which derive from the neural crest and resemble adrenal medullary chromaffin cells. Using double‐label immunofluorescence, we found that chronic exposure of carotid body cultures to hypoxia (2% to 10% oxygen) caused a significant fraction of tyrosine hydroxylase‐positive (TH+) glomus cells to acquire detectable immunoreactivity for growth‐associated protein gap‐43. The effect was dose‐dependent and peaked around an oxygen tension of 6%, where approximately 30% of glomus cells were GAP‐43 positive. Treatment with agents that elevate intracellular cyclic adenosine monophosphate (cAMP) (i.e., dibutyryl cAMP or forskolin) also markedly stimulated GAP‐43 expression. Since hypoxia is known to increase cAMP levels in glomus cells, it is possible that the effect of hypoxia on GAP‐43 expression was mediated, at least in part, by a cAMP‐dependent pathway. Unlike hypoxia, however, cAMP analogs also stimulated neurofilament (NF 68 or NF 160 kD) expression and neurite outgrowth in glomus cells, and these properties were enhanced by retinoic acid. Nerve growth factor, which promotes neuronal differentiation in related crest‐derived endocrine cells, and dibutyryl cGMP were ineffective. Thus, it appears that postnatal glomus cells are plastic and can express neuronal traits in vitro. However, since hypoxia stimulated GAP‐43 expression, without promoting neurite outgrowth, it appears that the two processes can be uncoupled. We suggest that stimulation of GAP‐43 by hypoxia may be important for other physiological processes, e.g., enhancing neurotransmitter release or sensitization of G‐protein–coupled receptor transduction. © 1995 John Wiley & Sons, Inc.
Proliferating hair cell precursors in the ear of a postembryonic fish are replaced after elimination by cytosine arabinoside
Authors: Presson Joelle C. , Smith Tamara , Mentz Lynn 
Published: January 2005

AbstractIdentified, proliferating S‐phase cells in the postembryonic fish ear are known to be the precursors to new hair cells. It is not known, however, whether the ability to proliferate is restricted to a small population of cells. The ability of cells that are not normally in the cell cycle to enter S‐phase was examined using the antimitotic drug cytosine arabinoside (ara‐C). The normal population of S‐phase cells in the saccule was destroyed by a single large dose of ara‐C. Two weeks later, the prsence of S‐phase cells was evaluated using the S‐phase marker bromodeoxyuridine. The results strikingly demonstrate that S‐phase cells are replaced, since S‐phase cells returned to the saccule in the same number as found in normal fish. The data are interpreted to suggest that a large number of nonsensory support cells are capable of entering the cell cycle and that some mechanism must regulate which of these are actually cycling at any given time. © 1995 John Wiley & Sons, Inc.
Distribution of androgen receptor immunoreactivity in the spinal cord of wild‐type, androgen‐insensitive and gonadectomized male rats
Authors: Freeman Louise M. , Padgett Barbara A. , Prins Gail S. , Breedlove S. Marc 
Published: January 2005

AbstractThe polyclonal antiserum PG21 was used to detect androgen receptor (AR) protein in three motoneuronal pools of the male rat lumbar spinal cord. In gonadally intact, wild‐type males, the spinal nucleus of the bulbocavernosus (SNB), dorsolateral nucleus (DLN), and retrodorsolateral nucleus (RDLN) all displayed immunolabeling of cell nuclei. The percentage of motoneurons displaying such labeling was highest in the SNB and lowest in the RDLN. This pattern of AR immunocytochemical labeling agrees well with previous steroid autoradiographic studies of androgen accumulation in the rat spinal cord. In contrast, virtually no motoneurons in any of the three pools displayed nuclear AR immunostaining in long‐term gonadectomized males or in gonadally intact males carrying the Tfm mutation, which renders the AR incompetent. In gonadectomized males, labeling was restored in the SNB and DLN, but not the RDLN, 30 min after an injection of replacement testosterone. Eight hours of testosterone exposure restored immunolabeling in all three motor nuclei. Apparent cytoplasmic staining was seen in SNB motoneurons of untreated castrates and Tfm rats, but not intact rats, suggesting that AR residing in the cytoplasm translocates to the nucleus on binding to androgen in these motoneurons. © 1995 John Wiley & Sons, Inc.
Imaging of caffeine‐inducible release of intracellular calcium in cultured embryonic mouse telencephalic neurons
Authors: Tsai Ti Dao , Barish Michael E. 
Published: January 2005

AbstractTo gain a better understanding of Ca2+‐induced Ca2+ release in central neurons, we have studied the increase in intracellular Ca2+ concentration ([Ca2+]i) induced by application of caffeine to cells cultured from embryonic mouse telencephalon (hippocampus or cortex). The magnitudes and distributions of changes in [Ca2+]i in neuron somata were measured by quantitative video microscopy. We observed that application of caffeine to pyramidally shaped neurons typically initiated an increase in [Ca2+]i in the cytoplasmic region between the nucleus and the base of a major dendrite. [Ca2+] in this region increased over a period of 3 to 6 s and was followed by, with a slight delay, a surge of Ca2+ that moved across the soma and into or over the nucleus. Similar Ca2+ that moved across the soma and into or over the nucleus. Similar Ca2+ responses to caffeine were observed in Ca2+‐containing and nominally Ca2+‐free external solutions, suggesting that caffeine was inducing Ca2+ release from intracellular stores. Ca2+ responses to caffeine were potentiated by inducing a tonic Ca2+ influx through N‐methyl‐D‐aspartate (NMDA)‐type glutamate receptors activated by 0.3 μM glutamate and multiple responses to caffeine could be elicited by using this Ca2+ influx to refill the intracellular stores. Ryanodine inhibition of caffeine‐induced Ca2+ release was use‐ and concentration‐dependent; the median effective concentration EC50 for ryanodine declined from 22 μM for the first application of caffeine to 20 nM for the fourth. We conclude, based on these responses to caffeine, that ryanodine‐sensitive mechanisms of intracellular Ca2+ release are active in hippocampal and cortical neurons and may be involved in generation of directed Ca2+ waves that engulf the nucleus. © 1995 John Wiley & Sons, Inc.
Multiple strategies for directed growth cone extension and navigation of peripheral neurons
Authors: Jellies John , Johansen Jørgen 
Published: January 2005

AbstractLeeches have a diverse constellation of peripheral neural elements that are challenged to extend growth cones in highly specific ways in a constantly changing embryonic environment. Two major systems are reviewed here. In one, peripheral afferents extend growth cones toward the central nervous system (CNS), forming common pathways, and then segregate into particular tracts within the CNS. A majority of these afferents depend on CNS‐derived guidance cues and projections from the CNS to guide their way. However, not all of the nerves are established this way and at least one of the peripheral nerves is likely to be pioneered by sensillar sensory afferents. The distribution of particular antigens (such as the lan3–2 antigen) suggests the identity of molecules involved in homophilic adhesion along common pathways, whereas others (such as the lan4–2 and 3–6 antigens) are candidates for mediating specific pathway choices. In the second system, the myo‐organizing Comb cell (C cell) projects multiple growth cones simultaneously along oblique trajectories not influenced by segmental or midline boundaries. Its parallel growth cones exhibit space‐filling as well as directional growth and are guided by local cues to extend in discrete phases that are coordinated with the development of the environment. Both systems exhibit highly directed outgrowth orchestrated by a hierarchy of cues, establish patterns of neurites used to direct later migrating cells, and seem to be regulated temporally and spatially by interactions with the embryonic environment. These systems illustrate the strengths of examining neural development in vivo across several levels of analysis. © 1995 John Wiley & Sons, Inc.
Sequential steps in axonal targeting are mediated by carbohydrate markers
Authors: Zipser Birgit 
Published: January 2005

AbstractMannose and hybrid/complex‐type oligosaccharides serve as markers for both the full set of peripheral sensory afferent neurons in the leech and also for disjoint subsets of these neurons. We have shown that these various surface carbohydrates play crucial roles in the multistep process by which afferents meet their synaptic parterns in the central nervous system (CNS). The carbohydrate marker common to all these afferents allows their projections (which are fasciculated as they enter the CNS) to disperse and search out target regions. Carbohydrate markers specific for subsets of these afferents subsequently allow each subset to consolidate the position of its projections in appropriate regions of the CNS where it contacts its synaptic partners. ‐ 1995 John Wiley & Sons, Inc.
Cell–cell interactions define the innervation patterns of central leech neurons during development
Authors: Wolszon Laura 
Published: January 2005

AbstractIn the last 20 years, the nervous system of the developing leech has been used to great advantage to study the processes by which neurons seek and finally innervate their targets. This review summarizes what is presently known about how neurons of the CNS interact with each other and with their targets during embryogenesis. ‐ 1995 John Wiley & Sons, Inc.