bluuebunny/crossref_metadata_2025_split huggingface dataset:
The canary androgen receptor mRNA is localized in the song control nuclei of the brain and is rapidly regulated by testosterone
Authors: Nastiuk Kent L. , Clayton David F. 
Published: January 2005

AbstractSinging in canaries is an androgen‐inducible behavior, under the control of an identified motor pathway, which includes several discrete “song nuclei” in the telencephalon. To determine whether the mRNA for the canary androgen receptor (cAR) is expressed in these song control nuclei, we synthesized probes from the recently cloned cAR cDNA and used in situ hybridization to examine spring male canary brain sections. Concentrations of cAR mRNA are detectable in several of the song control nuclei of the forebrain, including high vocal center (HVC), lateral magnocellular nucleus of the anterior neostriatum and robust nucleus of the archistriatum. In addition, we also show that testosterone treatment rapidly induces a significant reduction of cAR mRNA levels in nucleus HVC of females. Since the effects of androgen on singing behavior occur much more slowly, the behavioral effects are probably a secondary or independent result of androgen's primary and immediate action on target gene transcription. © 1995 John Wiley & Sons, Inc.
Collagen synthesis inhibition reduces clustering of heparan sulfate proteoglycan and acetylcholine receptors but not agrin or p65, at neuromuscular contacts in vitro
Authors: Bixby John L. 
Published: January 2005

AbstractWe have studied presynaptic and postsynaptic differentiation at neuromuscular junctions in vitro by examining the localization of synapse‐specific proteins. In nerve–muscle co‐cultures, the synaptic vesicle protein synaptotagmin (p65) accumulated in the nerve terminal overlying myotubes in association with postsynaptic cluster of acetylcholine receptors (AChRs), heparan sulfate proteoglycan (HSPG), laminin, and agrin. Inhibition of collagen synthesis with cis‐hydroxyproline decreased the nerve‐induced clustering of AChRs in muscle cells as well as that caused by exogenous agrin in muscle‐only cultures. Moreover, accumulation of HSPG at contacts was also inhibited in cis‐hydroxyproline–treated cultures. However, accumulation of p65 in nerve fibers at sites of muscle contact, a sign of presynaptic differentiation, was unaffected by cis‐hydroxyproline treatment. In addition, even in cis‐hydroxyproline–inhibited cultures, agrin was evident at more than 90% of contacts showing accumulation of p65 in the nerve terminal. Therefore, a mechanism exists to maintain agrin concentrations at nerve–muscle contacts, even when at least some extracellular matrix (ECM) proteins are disrupted. Our results suggest that HSPG is not required for the induction of nerve terminal differentiation but are consistent with the idea that HSPG or other ECM proteins are important in both nerve‐and agrin‐induced AChR clustering. In particular, agrin accumulation at sites of nerve–muscle contact is not sufficient to induce AChR clusters when the ECM at these contacts is disrupted. © 1995 John Wiley & Sons, Inc.
Naturally occurring motoneuron cell death in rat upper respiratory tract motor nuclei: A histological, fast dil and immunocytochemical study in the nucleus ambiguus
Authors: Friedland David R. , Eden Avrim R. , Laitman Jeffrey T. 
Published: January 2005

AbstractThe mammalian upper respiratory tract (URT) serves as the common modality for aspects of respiration, deglutition, and vocalization. Although these actions are dependent on coordinated and specific neuromuscular control, little is known about the development of URT control centers. As such, this study investigated the occurrence of naturally occurring motoneuron cell death (MCD) in the nucleus ambiguus (NA) of a developmental series of rats. Standard histological techniques were used to count motoneurons in the ventrolateral brainstem where the mature NA is found. In addition, the neural tracer, fast Dil, was used to determine whether motoneurons were still migrating into the region of the NA during the period that cell counts were first taken. Furthermore, to elucidate the potential effect of inadvertently counting large interneurons on the assessment of motoneuron numbers, an antibody to γ‐aminobutyric acid (GABA) was used. The results of this study have, for the first time, demonstrated that MCD occurs in a URT‐related motor nucleus. Approximately a 50% cell death was observed during the prenatal development of NA, with no further loss seen postnatally. The fast DiI studies showed that by embryonic day 17, NA was fully formed, suggesting that motoneuron migration from the basal plate was complete. In addition, use of the GABA antibody showed a lack of inhibitory interneurons within the NA. The finding of MCD in the NA helps define a critical period in the formation of URT neuromuscular control. As the course of MCD is modifiable by epigenetic signals, insult to the organism during this prenatal period may compromise future URT control. © 1995 John Wiley & Sons, Inc.
Calcium transients in growth cones and axons of cultured Helisoma neurons in response to conditioning factors
Authors: Williams Diana K. , Cohan Christopher S. 
Published: January 2005

AbstractAccumulating evidence indicates that cytosolic calcium levels regulate growth cone motility and neurite extension. The purpose of this study was to determine if intracellular calcium levels also influence the initiation of neurite extension induced by growth‐promoting factors. An in vitro preparation of axotomized neurons that can be maintained in the absence of growth‐promoting factors was utilized. The distal axons of cultured Helisoma neurons plated into defined medium do not extend neurites until they are exposed to Helisoma brain‐conditioned medium. This provided the opportunity to study the intracellular changes associated with neurite extension. Cytosolic calcium levels were monitored with the calcium‐sensitive dye fura 2 at the distal axon. In control medium calcium levels in the distal axon were constant. However, transient elevations in cytosolic calcium in the axonal growth cone occurred after addition of conditioned medium and coincident with the initiation of neurite extension. Application of calcium channel blockers showed that the transients resulted from calcium influx across the neuronal membrane. The transients, however, were not required for neurite extension, although they did influence the rate and extent of neurite outgrowth. Simultaneous extracellular patch recordings demonstrated that the calcium transients were correlated temporally with an increase in rhythmic spontaneous electrical activity of cells, suggesting that conditioned medium influences ionic membrane properties of these neurons. © 1995 John Wiley & Sons, Inc.
Early isolation from conspecific song does not affect the normal developmental decline of N‐methyl‐D‐aspartate receptor binding in an avian song nucleus
Authors: Aamodt Sandra M. , Nordeen Ernest J. , Nordeen Kathy W. 
Published: January 2005

AbstractEarly effects of experience on synaptic reorganization and behavior often involve activation of N‐methyl‐D‐aspartate (NMDA) receptors. We have begun to explore the role of this glutamate‐receptor subtype in the development of learned birdsong. Song learning in zebra finches occurs during a restricted period that coincides with extensive synaptic reorganization within neural regions controlling song behavior. In one brain region necessary for song learning, the lateral magnocellular nucleus of the anterior neostriatum (lMAN), NMDA receptor binding is twice as high at the onset of song learning as in adulthood. In the present study, we used quantitative autoradiography with the noncompetitive NMDA antagonist [3H]MK‐801 to examine more closely the developmental decline in NMDA receptor binding within lMAN and found that it occurred gradually over the period of song learning and was not associated with a particular stage of the learning process. In addition, early isolation from conspecific song did not affect [3H]MK‐801 binding in lMAN at 30, 60, or 80 days. Since behavioral studies confirmed that our isolate rearing conditions extended the sensitive period for song learning, we conclude that the normal developmental decline in overall NMDA receptor binding within lMAN does not terminate the capacity for song learning. Finally, early deafening, which prevents both stages of song learning, also did not affect [3H]MK‐801 binding in lMAN at 80 days, indicating that the decline in NMDA receptor binding occurs in the absence of auditory experiences associated with song development. © 1995 John Wiley & Sons, Inc.
Regeneration of neuromuscular connections in crayfish allotransplanted neurons
Authors: Krause Kristin M. , Vélez Samuel J. 
Published: January 2005

AbstractTransplantation of whole ganglia was used to study the regeneration of four of the neurons that innervate the superficial flexor muscles of the crayfish Procambarus clarkii. The isolated ganglia containing the somas of these neurons were successfully transplanted from one crayfish to another. Reinnervation proceeded across the muscle surface and by 8 to 10 weeks connections were detected across the entire target field. At different time periods after the transplant, junction potentials (JPs) produced in phase with spontaneous neuronal spikes were recorded. The distribution of JP sizes and their decay times were examined. JPs from transplanted preparations were smaller than JPs from control or normal regeneration animals. These JPs also failed to facilitate when stimulated at 1 and 10 Hz. These are normal characteristics of immature terminals, but in the transplant preparations, once established, they remained stable for the duration of the study. Thus, synaptogenesis appears to be arrested at a stage before synaptic efficacy is established in the allotransplants. In addition, connectivity maps were plotted for each axon over the muscle surface. Some muscle fibers did not receive any contacts, and overall innervation leveled off at around 60% of the muscle fibers, remaining stable for the duration of this study. Despite the incomplete physiological innervation, however, three of the four neurons showed the same medial/lateral preferences observed in control animals, regenerating their original patterns of connectivity across the muscle surface. © 1995 John Wiley & Sons, Inc.
Filarin, a novel invertebrate intermediate filament protein present in axons and perikarya of developing and mature leech neurons
Authors: Johansen Kristen M. , Johansen Jørgen 
Published: January 2005

AbstractThe lan 3–8 monoclonal antibody recognizes a 63 kD antigen that is associated with the cytoskeleton in leech neurons. We have used this antibody to clone a novel invertebrate neuronal intermediate filament protein, filarin, by screening an expression vector library. A full‐length clone of 2.2 kb identified by the antibody was isolated and sequenced. The protein contains a coiled‐coil rod domain typical of the superfamily of intermediate filament proteins flanked by unique N‐ and C‐terminal domains. The highest homology of filarin is to the alternatively spliced squid brain intermediate filament protein (Szaro et al., 1991, J. Biol. Chem. 266:15035–15041), the only other invertebrate neuronal intermediate filament in the data bank. However, apart from extensive homology in the two end regions of the rod domain, the similarity of the two proteins is limited to the general coiled‐coil structure of intermediate filaments. Thus, filarin may represent a novel type of invertebrate neuronal intermediate filament protein. Filarin contains the extra 6 heptads characteristic of lamins and of all cytoplasmic invertebrate intermediate filaments analyzed so far. By Northern analysis, it appears that filarin is not alternatively spliced, since only a single transcript of 2.2 kb is recognized by the clone. Using the lan 3–8 antibody to follow its developmental expression, we found that filarin is present in all known neurons in the central and peripheral nervous system. © 1995 John Wiley & Sons, Inc.
Repair of the central nervous system: Lessons from lesions in leeches
Authors: von Bernhardi Rommy , Muller Kenneth J. 
Published: January 2005

AbstractIn contrast to the limited repair observed in the mammalian central nervous system (CNS), injured neurons in the leech reliably regenerate synapses and restore function with remarkable accuracy at the level of individual neurons. New and recent results reveal important roles for microglial cells and extracellular matrix components, including laminin, in repair. Tissue culture experiments have permitted isolation of neurons and manipulation of their environment, providing insights into the influence of substrate, electrical activity, and other cells, including microglia, on axon growth and synapse formation. The results account for distinctive features of successful repair in the adult leech, where axonal sprouting and target selection can be influenced by unequal competition between neurons. Differences between the formation of connections during embryonic development and repair in the adult include dissimilarities in the roles of glia and microglia in adults and embryos, suggesting that axon growth during regeneration in the CNS is not simply a recapitulation of processes observed during embryonic development. It may be possible in the future to improve mammalian CNS regeneration by recruiting cells whose counterparts in the leech have been identified as instrumental in repair. © 1995 John Wiley & Sons, Inc.
Estrogens and non‐estrogenic ovarian influences combine to promote the recruitment and decrease the turnover of new neurons in the adult female canary brain
Authors: Hidalgo Andrea , Barami Kaveh , Iversen Kristin , Goldman Steven A. 
Published: January 2005

AbstractThe higher vocal center (HVC) of the songbird forebrain exhibits persistent neurogenesis in adulthood, particularly in a region of the mediocaudal neostriatum that is associated with a subventricular layer of estrogen receptive cells. We asked whether estrogens might influence adult neurogenesis, by assessing the effect of ovariectomy on HVC neuronal production in the adult female canary. Fifteen 1‐year‐old females were separated into groups of ovariectomized, estradiol‐replaced ovariectomized, and gonadally intact birds. To label dividing cells and their progency, the birds were given [3H]thymidine for 8 days, killed 32 days later, and their brains autoradiographed. A significant rise was noted in the number of HVC neurons per section in estradiol‐treated birds relative to the untreated control birds. The number of [3H]‐thymidine‐labeled HVC neurons was also higher in the estrogen‐treated birds; however, the neuronal labeling index (LI) did not vary as a function of estradiol replacement, as the total number of HVC neurons rose in parallel with the added new neurons. In contrast, the neuronal LI did rise as a result of ovariectomy, and this ovariectomy‐associated increase in the LI was not reversed by estradiol. Among non‐neuronal cell types, the endothelial LI was higher in estrogen‐treated birds than in their untreated counterparts, suggesting estrogen‐associated angiogenesis. Radioimmunoassay confirmed that serum estradiol was reduced in the castrated birds. Since estrogen appeared to promote the survival of [3H]thymidine+ neurons, we next sought to determine whether estrogen acted directly on the newly generated neurons, or rather indirectly through an intermediary cell population. To this end, we asked whether the new neurons or their precursors expressed estrogen receptor immunoreactivity (ER‐IR). Five adult male canaries were given [3H]thymidine for periods ranging from 2 to 28 days, killed at varying times up to 3 weeks therafter, then probed for ER‐IR and autoradiographed. [3H]thymidine+ cells displayed no detectable ER‐IR within their first 4 weeks of postmitotic life. Rather, during migration from the ventricular zone (VZ), the new neurons traversed a layer of mitotically quiescent, ER+ subventricular cells. Double labeling for ER‐IR and cell‐type selective antigens confirmed that these ER+ cells were neurons. These results indicate that the early survival of new neurons in the adult songbird HVC is promoted by estrogen, and may be mediated by the estrogen‐stimulated paracrine release of neurotrophic agents by ER‐IR subventricular neurons. Our data suggest that estrogen's promotion of neuronal survival may operate concurrently with an estrogen‐independent ovarian suppression of neuronal mitogenesis.
Leukemia inhibitory factor influences the timing of programmed synapse withdrawal from neonatal muscles
Authors: Kwon Young W. , Abbondanzo Susan J. , Stewart Colin L. , Gurney Mark E. 
Published: January 2005

AbstractWe show that leukemia inhibitory factor (LIF) plays a physiological role in the programmed withdrawal of synapses form neonatal muscles. First, LIF mRNA is present in embryonic skeletal muscle and is developmentally regulated. We detect high levels of LIF mRNA at embryonic day 17 (E17) in mouse hind leg muscles. The content of LIF mRNA falls 10‐fold between E17 and birth and then remains low in the neonate and adult. The decrease in LIF mRNA in skeletal muscle coincides with the end of secondary myogenesis and the completion of the adult number of myofibers. Second, treatment of the mouse tensor fascia latae (TFL), a superficial muscle of the hind leg, with LIF from birth (100 ng/day), transiently delays the withdrawal of excess inputs from polyneuronally innervated myofibers by approximately 3 days. The midpoint of the process is shifted from 7.5 ± 0.5 to 10.2 ± 0.6 days of age. LIF treatment delays synapse withdrawal by altering its timing without an appreciable effect on its rate. Third, in mice homozygous for a distruption of the LIF gene, the midpoint in the reduction of multiply innervated TFL myofibers occurs 1 day earlier, at 6.5 ± 0.5 days of age. Muscle fiber number is unchanged in LIF null mice. Treatment with LIF does not alter the rate of neonatal growth, the number of muscle fibers in the TFL, or the reappearance of inputs that have been eliminated. Instead, LIF appears to delay maturation of the motor unit by transiently delaying the onset of synapse withdrawal. We hypothesize that this is a necessary component of a selective process that will operate simultaneously and equally on multiple, competing motor units. © 1995 John Wiley & Sons, Inc.
Pharmacological analysis of heartbeat in Drosophila
Authors: Gu Gang‐Guo , Singh Satpal 
Published: January 2005

AbstractAnalysis of the mechanisms underlying cardiac excitability can be faciliated greatly by mutations that disrupt ion channels and receptors involved in this excitability. With an extensive repertoire of such mutations, Drosophila provides the best available genetic model for these studies. However, the use of Drosophila for this purpose has been severely handicapped by lack of a suitable preparation of heart and a complete lack of knowledge about the ionic currents that underlie its excitability. We describe a simple preparation to measure heartbeat in Drosophila. This preparation was used to ask if heartbeat in Drosophila is myogenic in origin, and to determine the types of ion channels involved in influencing the heart rate. Tetrodotoxin, even at a high concentration of 40 μM, did not affect heart rate, indicating that heartbeat may be myogenic in origin and that it may not be determined by Na+ channels. Heart rate was affected by PN200–110, verapamil, and diltiazem, which block vertebrate L‐type Ca2+ channels. Thus, L‐type channels, which contribute to the prolonged plateau of action potentials in vertebrate heart, may play a role in Drosophila cardiac excitability. It also suggests that Drosophila heart is subject to a similar intervention by organic Ca2+ channel blockers as the vertebrate heart. A role for K+ currents in the function of Drosophila heart was suggested by an effect of tetraethylammonium, which blocks all the four identified K+ currents in the larval body wall muscles, and quinidine, which blocks the delayed rectifier K+ current in these muscles. The preparation described here also provides an extremely simple method for identifying mutations that affect heart rate. Such mutations and pharmacological agents will be very useful for analyzing molecular components of cardiac excitability in Drosophila. © 1995 John Wiley & Sons, Inc.
Projection pattern of sensory neurons in the central nervous system of a homeotic mutation of the moth Manduca sexta
Authors: Booker Ronald , Miles Carol I. 
Published: January 2005

AbstractOctopod (Octo) is a mutation of the moth Manduca sexta, which transforms the first abdominal segment (A1) in the anterior direction. Mutant animals are characterized by the appearance of homeotic thoracic‐like legs on A1. We exploited this mutation to determine what rules might be used in specifying the fates of sensory neurons located on the body surface of larval Manduca. Mechanical stimulation of homeotic leg sensilla did not cause reflexive movements of the homeotic legs, but elicited responses similar to those observed following stimulation of ventral A1 body wall hairs. Intracellular recordings demonstrated that several of the motoneurons in the A1 ganglion received inputs from the homeotic sensory hairs. The responses of these motoneurons to stimulation of homeotic sensilla resembled their responses to stimulation of ventral body wall sensilla. Cobalt fills revealed that the mutation transformed the segmental projection pattern of only the sensory neurons located on the ventral surface of A1, resulting in a greater number with intersegmental projection patterns typical of sensory neurons found on the thoracic body wall. Many of the sensory neurons on the homeotic legs had intersegmental projection patterns typical of abdominal sensory neurons: an anteriorly directed projection terminating in the third thoracic ganglion (T3). Once this projection reached T3, however, it mimicked the projections of the thoracic leg sensory neurons. These results demonstrate that the same rules are not used in the establishment of the intersegmental and leg‐specific projection patterns. Segmental identity influences the intersegmental projection pattern of the sensory neurons of Manduca, whereas the leg‐specific projections are consistent with a role for positional information in determining their pattern. © 1995 John Wiley & Sons, Inc.
Ciliary neurotrophic factor arrests muscle and motoneuron degeneration in androgen‐insensitive rats
Authors: Forger Nancy G. , Wong Vivien , Marc Breedlove S. 
Published: January 2005

AbstractSteroid hormones and neurotrophic factors exert profound and widespread effects on the developing nervous system, including regulation of the size, connectivity, and survival of neurons. Androgenic control of the survival of motoneurons in the spinal nucleus of the bulbocavernosus (SNB) of rats has been well documented. We previously found that ciliary neurotrophic factor (CNTF) mimics many effects of androgen on the developing SNB. Whether effects of CNTF depend on the presence of a functional androgen receptor was evaluated in the present study. Androgen‐insensitive male rats bearing the testicular feminization mutation, Tfm, and female littermates were treated with CNTF or with vehicle alone from embryonic day 22 through postnatal day 3. On postnatal day 4 SNB cell number was elevated in both groups receiving CNTF. Volumes of the bulbocavernosus (BC) and levator ani (LA) muscles, targets of SNB motoneurons, were also markedly increased by CNTF. Since the BC appears to degenerate completely in untreated females, these results indicate that CNTF can delay or prevent muscle fiber death. The relative sparing of muscles and motoneurons did not differ for Tfm males and females, demonstrating that effects of CNTF on the SNB neuromuscular system do not require functional androgen receptors. © 1995 John Wiley & Sons, Inc.