bluuebunny/crossref_metadata_2025_split huggingface dataset:
Touch receptor development and function in Caenorhabditis elegans
Authors: Chalfie Martin 
Published: January 2005

AbstractMutations causing a touch‐insensitive phenotype in the nematode Caenorhabditis elegans have been the basis of studies on the specification of neuronal cell fate, inherited neurodegeneration, and the molecular nature of mechanosensory transduction. © 1993 John Wiley & Sons, Inc.
Local intracerebral implants of estrogen masculinize some aspects of the zebra finch song system
Authors: Grisham William , Mathews Greta A. , Arnold Arthur P. 
Published: January 2005

AbstractThe song system of zebra finches is sexually dimorphic: the volumes of the song control nuclei and the neurons within these nuclei are larger in males. The song system of hatching female zebra finches is masculinized by systemic treatment with estrogen. We investigated the locus of this estrogen action by using microimplants of estradiol benzoate (EB). We implanted female zebra finch nestlings 10–13 days old with Silastic pellets containing approximately 2 μg EB at one of several sites: near the higher vocal center (HVC), in the brain distant from HVC, or in the periphery either under the skin of the breast or in the peritoneal cavity. Controls were either unimplanted or implanted near HVC with Silastic pellets without hormone. The brains were fixed by perfusion at 60 days, and the volumes of the song control regions as well as the sizes of individual neurons were measured. Neurons in HVC were lerger (more masculine) in the HVC‐implanted group than in other groups, which did not differ among themselves. The size of neurons in the robust nucleus of the archistriatum (RA) and the lateral magnocellular nucleus ofthe neostriatum (lMAN) were inversely correlated with the distance of the EB pellet to HVC; neurons in RA and lMAN were larger when the EB pellets were closer to HVC. This result suggests that implants near HVC were at or near a site of estrogen action. To our knowledge, this is the first demonstration that localized brain implants of estrogen cause morphological masculinization in any species. 1994 John Wiley & Sons, Inc.
Dynamics and metamorphosis of an identifiable peptidergic neuron in an insect
Authors: Riddiford Lynn M. , Hewes Randall S. , Truman James W. 
Published: January 2005

AbstractEclosion hormone (EH) is a 7000 Da peptide that triggers ecdysis behavior in insects. In the moth, Manduca sexta, EH is found in two pairs of ventromedial (VM) cells in the brain which send their axons down the ventral nerve cord to a neurohemal site in the proctodeal nerve in the larva and pupa. During adult development, these cells send axon collaterals to the corpora cardiaca where they form a new release site used for adult eclosion. Studies of bioassayable peptide during the 5th larval instar and the larval‐pupal transformation revealed that after depletion at ecdysis, the VM cells showed a transient increase in EH found in their cell bodies and axons. By contrast, their terminals in the proctodeal nerve showed a gradual accumulation of peptide followed by a release of over 90% of the stored material at pupal ecdysis. In situ hybridization analysis on whole mounts of the brains showed that the VM cells always contained EH mRNA with increased accumulation during the larval and pupal molting periods with a slight decline just before ecdysis. High levels of EH mRNA were found in brains of diapausing pupae. During the first two‐thirds of adult development, mRNA accumulated to high levels, then slowly declined until ecdysis. EH mRNA levels up to 3 days after adult eclosion. At no time was EH mRNA found in the lateral neurosecretory cell cluster previously reported to produce EH for adult eclosion. 1994 John Wiley & Sons, Inc.
Effects of testosterone on a sexually dimorphic frog muscle: Repeated in vivo observations and androgen receptor distribution
Authors: Dorlöchter Marlies , Astrow Stephanie H. , Herreta Albert A. 
Published: January 2005

AbstractIn the present study the sexually dimorphic, androgen‐sensitive flexor carpi radialis muscle (FCR) in male Xenopus laevis was viewed repeatedly in vivo to assess the influence of testosterone on muscle fiber size over a period of up to 12 weeks. Regions of the muscle innervated by different spinal nerves responded differently to testosterone treatment. Muscle fibers innervated by spinal nerve 2 (SN2) hypertrophied within 7 days in frogs that had been castrated and given testosterone‐filled implants. This initial hypertrophy was followed by a return to normal fiber size a week late, after which fiber size slowly increased again. In castrated males with empty implants, muscle fibers innervated by SN2 gradually atrophied. Fibers innervated by spinal nerve 3 (SN3) were not affected by androgen replacement or withdrawal. The sartorius, a control muscle that is neither sexually dimorphic nor particularly androgen sensitive, was also unaffected.The in vivo observations were confirmed by measurements of muscle fiber cross‐sectional areas in frozen sections of whole forelimbs. At 8 and 12 weeks after castration, cross‐sectional areas of fibers innervated by SN2 were significantly larger in frogs provided with testosterone than in castrates without testosterone. No difference was found in the SN2 region or in the anconeus caput scapulare (triceps), another control muscle.Immunocytochemistry employing an antibody against the androgen receptor (AR) indicated that the receptor is present in myonuclei of all muscles of the forelimb. While no difference in labeling intensity was detected, the number of AR‐containing nuclei per muscle fiber cross‐section was higher in fibers innervated by SN2 than in those innervated by SN3, and was yet lower in the triceps. This suggests that regulation of androgen sensitivity may occur via muscle fiber. ARs, although an influence of the nerve may also contribute. 1994 John Wiley & Sons, Inc.
Regulation of SC1/DM‐GRASP during the migration of motor neurons in the chick embryo brain stem
Authors: Simon Horst , Guthrie Sarah , Lumsden Andrew 
Published: January 2005

AbstractThe hindbrain of the chick embryo contains three classes of motor neurons: somatic, visceral, and branchial motor. During development, somata of neurons in the last two classes undergo a laterally directed migration within the neuroepithelium; somata translocate towards the nerve exit points, through which motor axons are beginning to extend into the periphery. All classes of motor neuron are immunopositive for the SC1/DM‐GRASP cell surface glycoprotein. We have examined the relationship between patterns of motor neuron migration, axon outgrowth, and expression of the SC1/DM‐GRASP mRNA and protein, using anterograde or retrograde axonal tracing, immunohistochemistry, and in situ hybridization. We find that as motor neurons migrate laterally, SC1/DM‐GRASP is down‐regulated, both on neuronal somata and axonal surfaces. Within individual motor nuclei, these lateral, more mature neurons are found to possess longer axons than the young, medial cells of the population. Labelling of sensory or motor axons growing into the second branchial arch also shows that motor axons reach the muscle plate first, and that SC1/DM‐GRASP is expressed on the muscle at the time growth cones arrive. 1994 John Wiley & Sons, Inc.
Muscarinic acetylcholine responses in the early embryonic chic retina
Authors: Yamashita Masayuki , Yoshimoto Yukiko , Fukada Yutaka 
Published: January 2005

AbstractThe action of acetylcholine on cytoplasmic Ca2+ concentration ([Ca2+]i) was studied in early embryonic chick retinae. Whole neural retinae were isolated from embryonic day 3 (E3) chicks and loaded with a Ca2+‐sensitive fluorescent dye (Fura‐2). Increases in [Ca2+]i were evoked by the puff application of acetylcholine at concentration than 0.1 μM. The Ca2+ response became larger in dose–dependant manner up to 10 μM of acetylcholine applied. The rise in [Ca2+]i was not due to the influx of Ca+2 through calcium channels, but to the release of Ca2+ from internal stores. A calcium channel antagonist, nifedipine, which completely blocks the Ca2+ rise caused by depolarization with 100 mM K+, had no effects on the acetylcholine response and the Ca2+ response to acetylcholine occurred even in a Ca2+‐free medium. The Ca2+ response to acetylcholine was mediated by muscarinic receptors. Atropine of 1 μM abolished the response to 10 μM acetylcholine, whereas d‐tubocurarine of 100 μM had no effects. Two muscarinic agonists, muscarine and carbamylcholine (100 μM each), evoked comparable responses with that to 10 μM acetylcholine. The developmental change of the muscarinic response was examined from E3 to E13. The Ca2+ response to 100 μM carbamylcholine was intense at E3‐E5, then rapidly declined until E8. The muscarinic Ca2+ mobilization we found in the early embryonic chick retina may be regarded as a part of the “embryonic muscarinic system” proposed by Drew's group, which appears transiently and ubiquitously at early embryonic stages in relation to organogenesis. 1994 John Wiley & Sons, Inc.
Structure–function relationships in the neurotrophin family
Authors: Ibáñez Carlos F. 
Published: January 2005

AbstractThe study of structure–function relationships in the neurotrophin family has in recent years increased our understanding of several important aspects of neurotrophin function. Site‐directed mutagenesis studies have localized amino acid residues important for binding to the low‐affinity (p75LNGFR), as well as to the members of the Trk family of tyrosine kinase receptors. A cluster of positively charged residues has been shown to form a surface for binding to p75LNGFR in all four neurotrophins. Differences in the spatial distribution of these charges among the different neurotrophins may explain some of their distinct binding properties. Elimination of these positive charges drastically reduces binding to P75LNGFR but not to the Trk family members, and it does not impair the biological properties of the neurotrophins in vitro, arguing that binding to and activation of Trk receptors is sufficient to mediate the biological responses of neurotrophins. In contrast. the binding sites to Trk receptors appear to be formed by discontinuous stretches of amino acid residues distributed throughout the primary sequence of the molecule. These include the N‐terminus, some of the variable loop regions and a β‐strand. Despite their apparent distribution, when viewed in the three‐dimensional structure of NGF, these residues appear grouped on one side of the neurotrophin dimer, delineating a continuous surface extending approximately parallel to the twofold symmetry axis of the molecule. Two symmetrical surfaces are formed along the axis of the neurotrophin dimer providing a model for ligand‐mediated receptor dimerization. In the neurotrophin family, co‐evolution of cognate ligands and Trk receptors has developed specific contacts through different residues in the same variable regions of the neurotrophins. Thus, binding specificity is determined by the cooperation of distinct active and inhibitory binding determinants that restrict ligand‐receptors interactions. Binding determinants to the Trk receptors can be manipulated independently in a rational fashion to create neurotrophin analogues with novel ligand‐binding properties. In this way, second‐generation chimeric neurotrophins with multiple specificities (pan‐neurotrophins) have been engineered which may have valuable applications in the treatment of neurodegeneration and nerve damage. 1994 John Wiley & Sons, Inc.
The Trk family of neurotrophin receptors
Authors: Barbacid Mariano 
Published: January 2005

AbstractAccumulating evidence indicates that the Trk family of tyrosine protein kinase receptors, Trk (also known as TrkA), TrkB, and TrkC, are responsible for mediating the trophic effects of the NGF family of neurotrophins. Nerve growth factor (NGF) specifically recognizes Trk, a receptor indentified in all major NGF targets, including sympathetic, trigeminal, and dorsal root ganglia as well as in cholinergic neurons of the basal forebrain and the striatum. Brain‐derived neurotropic factor (BDNF) and neurotrophin‐4 (NT‐4) specifically activate the TrkB tyrosine kinase receptor. trkB transcripts encoding this receptor are found throughout multiple structure of the central and peripheral nervous system. Neurotrophin‐3 (NT‐3) primarily activates the TrkC tyrosine protein kinases, four related isoforns encoded by alternative splicing of trkC, a gene also wildely expressed throughtout the mammalian nervous system. Unlike the other neurotrophins, NT‐3 appears to be somewhat promiscuous since it can activate Trk and TrkB kinase receptors, at least in certain cell systems. The trkB and trkC genes also encode noncatalytic neurotrophin receptor isoforms of an as yet, unknown function. Recently, strains of mice lacking each of these tyrosine kinase receptors have been generated. Preliminary characterization of these mutant mice has provided significant information regarding the role of these receptors in the ontogeny of the mammlian nervous system. For instance, mice deficient for Trk receptors lack most sympathetic neurons and do not display nociceptive and temperature sensations, two defects likely to result from severe neuronal cell loss in their trigeminal and dorsal root ganglia. Mice lacking TrkB tyrosine kinase receptors die postnatally due to their inability to intake food. Neuron cell loss in their trigeminal, nodose and pretrosal sensory ganglia as well as in the facial motor nucleus are likely to contribute to this phenotype. Finally, TrkC‐deficient mice display strikingly abnormal movements consistent with loss of proprioception, a defect likely to be a consequence of the complete loss of Ia muscle afferents observed in this mutant mice. 1994 John Wiley & Sons, Inc.
Activity‐dependent regulation of dendritic spine density on cortical pyramidal neurons in organotypic slice cultures
Authors: Annis Casey M. , K. O'Dowd Diane , Robertson Richard T. 
Published: January 2005

AbstractIn order to examine the effects of activity on spine production and/or maintenance in the cerebral cortex, we have compared the number of dendritic spines on pyramidal neurons in slices of PO mouse somatosensory cortex maintained in organotypic slice cultures under conditions that altered basal levels of spontaneous electrical activity. Cultures chronically exposed to 100 μM picrotoxin (PTX) for 14 days exhibited significantly elevated levels of electrical activity when compared to neurons in control cultures. Pyramidal neurons raised in the presence of PTX showed significantly densities of dendritic spines on primary apical, secondary apical, and secondary basal dendrites when compared to control cultures. The PTX‐induced increase in spine density was dose dependent and appeared to saturate at 100 μM. Cultures exhibiting little or no spontaneous activity, as a result of growth in a combination of PTX and tetrodotoxin (TTx), showed significantly fewer dendritic spines compared to cultures maintained in PTX alone. These results demonstrate that the density of spines on layers V and VI pyramidal neurons can be modulated by growth conditions that alter the levels of spontaneous electrical activity. 1994 John Wiley & Sons, Inc.
Effects of experience and juvenile hormone on the organization of the mushroom bodies of honey bees
Authors: Withers G. S. , Fahrbach S. E. , Robinson G. E. 
Published: January 2005

AbstractThere is an age‐related division of labor in the honey bee colony that is regulated by juvenile hormone. After completing metamorphosis, young workers have low titers of juvenile hormone and spend the first several weeks of their adult lives performing tasks within the hive. Older workers, approximately 3 weeks of age, have high titers of juvenile hormone and forage outside the hive for nectar and pollen. We have previously reported that changes in the volume of the mushroom bodies of the honey bee brain are temporally associated with the performance of foraging. The neuropil of the mushroom bodies is increased in volume, whereas the volume occupied by the somata of the Kenyon cells is significantly decreased in foragers relative to younger workers. To study the effect of flight experience and juvenile hormone on these changes within the mushroom bodies, young worker bees were treated with the juvenile hormone analog methoprene but a subset was prevented from foraging (big back bees). Stereological volume estimates revealed that, regardless of foraging experience, bees treated with methoprene had a significantly larger volume of neuropil in the mushroom bodies and a significantly smaller Kenyon cell somal region volume than did 1‐day‐old bees. The bees treated with methoprene did not differ on these volume estimates from untreated foragers (presumed to have high endogenous levels of juvenile hormone) of the same age sampled from the same colony. Bees prevented from flying and foraging nonetheless received visual stimulation as they gathered at the hive entrance. These results, coupled with a subregional analysis of the neuropil, suggest a potentially important role of visual stimulation, possibly interacting with juvenile hormone, as an organizer of the mushroom bodies. In an independent study, the brains of worker bees in which the transition to foraging was delayed (overaged nurse bees) were also studied. The mushroom bodies of overaged nurse bees had a Kenyon cell somal region volume typical of normal aged nurse bees. However, they displayed a significantly expanded neuropil relative to normal aged nurse bees. Analysis of the big back bees demonstrates that certain aspects of adult brain plasticity associated with foraging can be displayed by worker bees treated with methoprene independent of foraging experience. Analysis of the over‐aged nurse bees suggests that the post‐metamorphic expansion of the neuropil of the mushroom bodies of worker honey bees is not a result of foraging experience. © 1995 John Wiley & Sons, Inc.
A direct comparison of the masculinizing effects of testosterone, androstenedione, estrogen, and progesterone on the development of the zebra finch song system
Authors: Grisham William , Arnold Arthur P. 
Published: January 2005

AbstractTo assess which hormones are capable of masculinizing the neural song system of zebra finch hatchlings, we implanted female hatchlings with estrogen (estradiol [E2], 75 μg, n = 9), testosterone (T, 75–88 μg, n = 13), androstenedione (AE, 75 μg, n = 7), progesterone (P, 117 μg, n = 10), or nothing (Blanks, n = 10) and compared these to unimplanted males (n = 7). Implants, consisting of a hormone and Silastic mixture encased in polyethylene tubing, were placed under the skin of the breast on the day of hatching. Birds were killed when they were subadult (58 to 68 days old). We measured volumes of area X, the higher vocal center (HVC), and the robust nucleus of the archistriatum (RA); measured soma sizes in the lateral magnocellular nucleus of the neostriatum (IMAN), HVC, and RA: and counted RA neurons. E2 masculinized all measures in the song system and nearly sex‐reversed the size of RA neurons. T masculinized volumes of nuclei and soma sizes but not the number or spacing of RA neurons. E2 was always at least as effective as T in masculinizing measures of the song system and was usually more effective. AE and P did not significantly masculinize any measure. These data suggest that E2 is more potent than aromatizable androgens or P in masculinizing the female song system in development and that the action of E2 alone may be sufficient to masculinize the volume of song control nuclei and the size and number of neurons. © 1995 John Wiley & Sons, Inc.
Calcium‐activated proteolysis of neurofilament proteins in goldfish Mauthner axons
Authors: Raabe Tim D. , Nguyen Tri , Bittner George D. 
Published: January 2005

AbstractWe have examined the proteolytic breakdown of neurofilament proteins (NFPs) in isolated Mauthner axoplasm (M‐axoplasm). Documentation of proteolytic breakdown of NFPs in M‐axoplasm is important because NFPs are not degraded in distal segments of severed Mauthner axons (M‐axons) maintained in vivo for up to 62 days at 20°C. By incubating M‐axoplasm with 2 mM calcium in vitro, we have demonstrated that M‐axoplasm contains an endogenous calcium‐activated neutral protease that degrades NFPs. This calcium‐activated proteolysis of M‐axoplasm NFPs produced novel bands on silver‐stained gels. These novel bands were presumed to be NFP breakdown products because they reacted with antibodies to the α‐intermediate filament antigen (anti‐IFA) on immunoblots from these gels. Incubations of M‐axoplasm with 2 mM calcium plus exogenous calpain produced novel bands similar to those observed for M‐axoplasm incubated with 2 mM calcium. Incubations of M‐axoplasm with 2m M calcium plus calpain inhibitors did not produce these novel bands. These in vitro data indicate that M‐axoplasm contains calpain that degrades NFPs and produces novel bands similar to those observed from distal segments of severed M‐axons maintained in vivo longer than 62 days postseverance. Factors that affect the activity of calpain or affect the ability of calpain to degrade NFPs could account for the delayed degradation of NFPs in distal segments of severed M‐axons maintained in vivo. © 1995 John Wiley & Sons, Inc.
Electric field‐directed growth and branching of cultured frog nerves: Effects of aminoglycosides and polycations
Authors: Erskine L. , Stewart R. , McCaig C. D. 
Published: January 2005

AbstractThe direction and rate of earliest nerve growth are critical determinants of neuronal architecture. One extrinsic cue that influences these parameters is a small direct current electric field, although the underlying mechanisms are unclear. We have studied the orientation, rate of growth, and branching behavior of embryonic Xenopus spinal neurites exposed to aminoglycoside antibiotics, to raised external cations, to applied direct current electric fields, and to combinations of these treatments. Field‐induced cathodal turning and cathodal branching of neurites were blocked by the aminoglycosides, by raised extracellular calcium ([Ca2+]0) and by raised extracellular magnesium ([Mg2+]0). Neomycin together with high external Ca2+, by contrast, induced a reversal in the polarity of turning and branching, with neurites reorienting and branching more frequently anodally. Aminoglycosides decreased neurite growth rates, and for neomycin this was partially reversed by high external Ca2+. Raised [Ca2+]0 alone but not raised [Mg2+]0 altered growth rates in a field‐strength dependent manner. Modulation of membrane surface charge may underlie altered galvanotropic orientation and branching. Such an effect is insufficient to explain the changes in growth rates, which may result from additional perturbations to Ca2+ influx and inositol phospholipid metabolism. © 1995 John Wiley & Sons, Inc.