bluuebunny/crossref_metadata_2025_split huggingface dataset:
Developmental neuroethology of insect metamorphosis
Authors: Truman James W. 
Published: May 2005

AbstractDuring metamorphosis, the insect nervous system must change to accomodate alterations in body form and behavior. Studies primarily on moths have shown that these changes involve the death of some larval neurons, the conservation and remodeling of others, and the maturation of new, adult‐specific cells. The motor and sensory sides of the adult CNS vary in this regard with the former being constructed primarily from remodeled larval components, whereas the latter arises primarily from new neurons.Neuronal remodeling has received considerable attention. Larval‐specific dendritic fields are pruned back during the larval–pupal transition, followed by the sprouting of adult‐specific dendrites. Simple reflexes have been used to correlate these neuronal changes with the acquisition or loss of particular behaviors. The loss of the proleg retraction reflex is associated with the regression of the dendritic arbors of the proleg motoneurons. By contrast, expansion of axon arbors of the gin‐trap afferents is necessary, but not sufficient, for the assembly of the gin‐trap reflex in the pupal stage. The stretch receptor reflex provides a third example in which a new dendritic field in the adult form of a neuron is associated with new adult‐specific connections. Interestingly, these connections are masked by persisting larval contacts until the emergence of the adult moth. For the metamorphosis of more complex behavioral circuits, some, such as that for flight behavior, seem to be assembled de novo, whereas others, like that for adult ecdysis behavior, show conservation of some circuit elements from the larval stage but with the superposition of some adult‐specific components. © 1992 John Wiley & Sons, Inc.
Resealing of the proximal and distal cut ends of transected axons: Electrophysiological and ultrastructural analysis
Authors: Spira Micha E. , Benbassat Dorit , Dormann Ada 
Published: May 2005

AbstractThe fates of the proximal and distal segments of transected axons differ. Whereas the proximal segment usually recovers from injury and regenerates, the distal segment degenerates. In the present report we studied the kinetics of the recovery processes of both proximal and distal axonal segment following axotomy and its temporal relations to the alterations in the cytoarchitecture of the injured neuron. The experiments were performed on primary cultured metacerebral neurons (MCn) isolated from Aplysia. We transected axons while monitoring the changes in transmembrane potential and input resistance (Rn) by inserting intracellular microelectrodes into the soma and axon. Correlation between the electrophysiological status of the injured axon and its ultrastructure was provided by rapid fixation of the neuron at selected times postaxotomy. Axotomy leads to membrane depolarization from a mean of −55.7 S.D. 12.8 mV to −12.7 S.D. 3.3 mV and decreased Rn from tens of MΩ to 1–3 MΩ. The transected axons remained depolarized for a period of 10–260 s for as long as the axoplasm was in direct contact with the bathing solution. Rapid repolarization and partial recovery of Rn was associated with the formation of a membrane seal over the cut ends by the constriction and subsequent fusion of the axolema. Prior to the formation of a membraneous barrier, electron‐dense deposits aggregate at the tip of the cut axon and appear to form an axoplasmic “plug.” Electrophysiological analysis revealed that this “plug” does not provide resistance for current flow and that the axoplasmic resistance is homogenously distributed. The kinetics of injury and recovery processes as well as the ultrastructural changes of the proximal and distal segments are cannot be attributed to differences in the immediated response of the segments to axotomy. © 1993 John Wiley & Sons, Inc.
Brachially innervated ectopic hindlimbs in the chick embryo. II. The role of supraspinal input in the loss of limb motility
Authors: Kitchener P. D. , Laing N. G. 
Published: May 2005

AbstractBrachially innervated grafted hindlimbs display a progressive loss of motility as development proceeds. However, the virtually immobile grafted hindlimbs of E20 embryos exhibited strong, synchronous contractions of gastrocnemius and tibialis muscles upon intraperitoneal injection of strychnine nitrate (20 μg). This result indicated that the marked behavioral deficit was not due to an inability of the motoneurons that innervate the immobile grafted hindlimbs to initiate and propagate action potentials, but was probably the result of an effective loss of motoneuron excitation. To examine the hypothesis that interaction with the supraspinal nervous system is involved in the reduction of grafted hindlimb activity, the normal forelimb and grafted hindlimb movements of chronic spinal embryos were examined. The normal forelimbs of chronic spinal embryos exhibited the same number of movements as normal embryos at all stages examined. Thus the deficit in grafted hindlimb motility is not comparable to the behavior of the normal forelimb in chronic spinal embryos and is, therefore, unlikely to be due to a lack of excitation from the supraspinal nervous system. The possibility of an inhibitory influence via supraspinal projections was examined in chronic spinal embryos that had brachially innervated grafted hindlimbs. After E12, the grafted hindlimbs of chronic spinal embryos displayed significantly fewer movements than the normal forelimbs of chronic spinal embryos but significantly more movements than the brachial hindlimb of embryos with intact spinal cords. By E18, however, both spinal and nonspinal brachial hindlimbs were equally dysfunctional. Thus prevention of supraspinal communication transiently reduces but does not prevent the emergence of motor dysfunction in the brachially innervated hindlimbs, which appears to be due to motoneurons not receiving sufficient net excitation, from spinal circuits, to propagate action potentials to the muscles. © 1993 John Wiley & Sons, Inc.
Acceleration of axonal outgrowth in rat sciatic nerve at one week after axotomy
Authors: Jacob Jane M. , McQuarrie Irvine G. 
Published: May 2005

AbstractFollowing injury of sciatic motor axons in the rat, the rate of axonal outgrowth is faster if there has been a prior “conditioning” axotomy. The acceleration of outgrowth is due to an acceleration of SCb, the rate [slow (SC)] component of axonal transport that carries cytomatrix proteins; this occurs throughout the axon by 7 days after the conditioning axotomy (Jacob and McQuarrie, 1991a, J. Neurobiol. 22:570–583). To further characterize the conditioning lesion effect (CLE), it is important to know (1) the minimum effective conditioning interval (time between conditioning and testing lesions), (2) whether the cell body reaction is required, and (3) whether outgrowth accelerates after a single axotomy. Outgrowth distances were measured by radiolabeling all newly synthesized neuronal proteins and detecting those carried to growth cones by fast axonal transport. When the conditioning and testing lesions were made simultaneously (0 day conditioning interval), there was no CLE. With a conditioning interval of 3 days, there was a shortening of the initial delay (before the onset of outgrowth) without a change in outgrowth rate. With conditioning intervals of 7, 14, and 21 days, the rates of outgrowth were increased by 8%, 22%, and 11%, respectively. To determine whether the cell body reaction to axotomy is necessary for the CLE, a nonaxotomizing stimulus to axonal growth (partial denervation) was used in place of a conditioning axotomy. This had no effect on the rate of outgrowth from a testing lesion made 14 days later. Finally, we examined the possibility that outgrowth accelerates after a single lesion. Outgrowth was faster at 6–9 days after axotomy than at 3–6 days (p < 0.001), and accelerated further at 9–12 days (p < 0.001). We conclude that (1) the shortest effective conditioning interval is 3 days; (2) the cell body reaction is necessary for the CLE; (3) axonal outgrowth from a single axotomy accelerates in concert with the anabolic phase of the cell body reaction. The SCb motor is, in turn, upregulated by this reaction. This suggests that the SCb motor responds to a fast‐transported signal that is a product of the cell body reaction. © 1993 John Wiley & Sons, Inc.
Song‐selective auditory input to a forebrain vocal control nucleus in the zebra finch
Authors: Vicario David S. , Yohay Kaleb H. 
Published: May 2005

AbstractNeurons in nuclei on the motor pathway for vocalizations in songbirds are known to responses in one such nucleus, robustus archistriatalis (RA), were characterized by making multi‐unit recordings in awake and anesthetized adult male zebra finches and in birds that had received lesions of the input to RA from the lateral part of the magnocellular nucleus of the anterior neostriatum (LMAN) or the Higher Vocal Center (HVC). In awake birds, RA neurons have a high level of spontaneous activity and vigorous auditory responses to song stimuli. Significantly greater responses are seen to the bird's own song (BOS) than to BOS played in reverse (REV) or to the songs of conspecifics (CON). Under ketamine‐xylazine anesthesia, spontaneous activity is reduced, response latency increases and responses to BOS, REV and CON are indistinguishable. Responses obtained under urethane anesthesia are similar to those seen in awake birds. Thus, the pattern and selectivity of auditory responses in RA depend on the animal's state. Auditory responses in RA are qualitatively unchanged following lesion of the input to RA from LMAN, indicating that this pathway is not required for the sensory processing that underlies the preference for BOS on the vocal production pathway. Our results show that an input other than that from LMAN must be primarily responsible for auditory responses in RA. The direct projection form HVC is the most likely pathway by which song selective auditory information arrives in RA, since lesioning HVC abolished auditory responses in RA. © 1993 John Wiley & Sons, Inc.
Expression of JUN, KROX, and CREB transcription factors in goldfish and rat retinal ganglion cells following optic nerve lesion is related to axonal sprouting
Authors: Herdegen Thomas , Bastmeyer Martin , Bähr Mathias , Stuermer Claudia , Bravo Rodrigo , Zimmermann Manfred 
Published: May 2005

AbstractGoldfish and rat optic nerves were cut and crushed, respectively, and the expression of the transcription factor proteins c‐JUN, JUN B, JUN D, c‐FOS, FOS B, KROX‐24, and CREB was investigated in retinal ganglion cells (RGCs) by immunocytochemistry. Immunoreactivities (IRs) were followed up to 350 days in the goldfish and upto 22 days in the rat. In RGCs of untreated goldfish and rats, all JUN, FOS, and KROX proteins were absent whereas CREB was constitutively expressed. After optic nerve cut in goldfish, a JUN‐like immunoreactivity (JUN‐IR) appeared in a small number of RGCs of central retina after 24 h, reached a maximum within 5 days, declined after 30 days, and was on a half‐maximal level after 50 days. Between 100 and 200 days, JUN‐IR was only visible in a few RGCs and was completely absent after 350 days. Specific antibodies against c‐JUN, JUN B, and JUN D gave no distinct immunoreactive signal. Thus, we could not determine which member of the JUN family contributed to the JUN‐IR. The expression of CREB declined after 5 days. The number of CREB‐labeled RGCs was reduced (not significant) and the intensity of labeling faded out. After 50 days, CREB‐IR had returned to basal level. c‐FOS, FOS B, and KROX‐24 could not be detected in goldfish RGCs following optic nerve cut. After optic nerve crush in the rat, c‐JUN, JUN D, and KROX‐24 appeared in a substantial number of RGCs after 24 h, had a maximal expression after 5 days, and strongly declined after 8 days. c‐JUN and KROX‐24 were completely absent after 22 days whereas JUN D was still present in a few rat RGCs. The number of CREB‐labeled RGCs decreased after 5 days and had declined by 50% after 22 days. Expression of JUN B, c‐FOS, FOS B could not be detected in rat RGCs after optic nerve crush. Our data demonstrate that the decrease of CREB and the increase of JUN and KROX‐24 transcription factors precedes and parallels both the alteration of de novo protein synthesis and the axonal sprouting, which are long lasting in goldfish and transient in rat. © 1993 John Wiley & Sons, Inc.
Target determination of neurotransmitter phenotype in sympathetic neurons
Authors: Schotzinger Robert , Yin Xinghuan , Landis Story 
Published: May 2005

AbstractWhile the majority of sympathetic neurons are noradrenergic, a minority population are cholinergic. At least one population of cholinergic sympathetic neurons arises during development by a target‐dependent conversion from an initial noradrenergic phenotype. Evidence for retrograde specification has been obtained from transplantation studies in which sympathetic neurons that normally express a noradrenergic phenotype throughout life were induced to innervate sweat glands, a target normally innervated by cholinergic sympathetic neurons. This was accomplished by transplanting footpad skin containing sweat gland primordia from early postnatal donor rats to the hairy skin region of host rats. The sympathetic neurons innervating the novel target decreased their expression of noradrenergif traints and developed choline acetyltransferase (ChAT) activity. In addition, many sweat gland‐associated fibers acquired acetylcholinesterase (AChE) staining and VIP immunoreactivity. These studies indicated that sympathetic neurons in vivo alter their neurotransmitter phenotype in response to novel envronmental signals and that sweat glands play a critical role in the cholinergic and peptidergic differentiation of the sympathetic neurons that innervate them. The sweat gland‐derived cholinergic differentiation factor is distinct from leukemia inhibitory factor and ciliary neurotrophic factor, two well‐characterized cytokines that alter the neurotransmitter properties of cultured sympathetic neurons in a similar fashion. Recent studies indicate that anterograde signalling is also important for the establishment of functional synapses in this system. We have found that the production of cholinergic differentiation activity by sweat glands required sympathetic innervation, and the acquisition and maintenance of secretory competence by sweat glands depends upon functional cholinergic innervation. 1994 John Wiley & Sons, Inc.
Cell‐cell interactions that modulate neuronal development in the leech
Authors: French Kathleen A. , Kristan William B. 
Published: May 2005

AbstractMitotic lineage has been found to determine the cellular identity of leech neurons (reviewed in Stent et al., 1992), Int. Rev. Neurobiol. 33:109–133. However, the details of the adult phenotype of many neurons in the central nervous system of the leech have been shown to be shaped by interactions either with other neurons or with non‐neuronal tissues in the environment. Four effects of cell‐cell interactions will be considered in this article: stimulation of mitosis that generates new neurons, modulation of cell death or axonal retraction, modification of neurotransmitter metabolism, and modification of other physiological properties. In all cases, the interactons that modify development are thought to occur at a location distant from the soma, requiring that signals be transmitted a significant distance from the site of interaction to the metabolic machinery in the soma. 1994 John Wiley & Sons, Inc.
Retrograde determination of motoneuron properties and their synaptic input
Authors: Mendell Lorne M. , Collins William F. , Munson John B. 
Published: May 2005

AbstractBoth motoneurons and the muscle fibers that they innervate can vary widely in their properties. The finding that these properties are highly correlated indicates that these cells are not specified independently, but rather interact in some manner to achieve the observed coherence. The direction of the interaction, i.e., whether orthograde or retrograde, required analysis beyond the simple observation of these correlated properties. Evidence, largely from experiments involving reinnervation of muscle by the original or a foreign motor nerve, suggests the action of retrogradely transported factors from the muscle as well as orthograde ones. Various possible factors, specifically neurotrophins, are advanced as possible candidates for retrograde specification. In addition, synaptic input to motoneurons also varies in a coordianted fashion in a manner that suggests a retrograde determination from the muscle. However, motoneuron properties and their synaptic input change after peipheral nerve manipulations such that they are no longer in register. This indicates some independence in retrograde specification of motoneurons and their synaptic input. 1994 John Wiley & Sons, Inc.
Retrograde signaling in the formation and maintenance of the neuromuscular junction
Authors: Connor Elizabeth A. , Smith Martin A. 
Published: May 2005

AbstractThe neuromuscular junction is characterized by precise alignment between the nerve terminal an the postsynaptic apparatus formed by the muscle fiber. Organization of the neuromuscular junction during embryonic development, growth, and maintenance is coordinated by signals exchanged between motor neurons and their target muscel fibers. Identification of proteins such as agrin, likely to represent neuronal agents that direct the organization of the postsynaptic apparatus, has focused attention on characterization of proteins that mediate retrograde signals that regualte the organization and function of the nerve terminal. The results of these studies implicate a role for both adhesive and diffusible signal in coordinating the development, maturation, and maintenance of the motor nerve terminal. The diversity of molecules identified to date that appear to play a role in these processes implies a considerable level of redundancy in the transduction pathway. However, studies of early nerve‐muscle interactions suggest that a common feature of many of these retrograde agents is activation of a protein kinase coupled with and increase in cytosolic Ca2+ concentration. While the molecular signals that regulate growth and maintenance of neuromuscular junctions are less well understood it seems likely that similar adhesive and diffusible factor will be involved. 1994 John Wiley & Sons, Inc.
Changes in retinal arbors in compressed projections to half tecta in goldfish
Authors: Schmidt John , Coen Timothy 
Published: May 2005

AbstractIn adult goldfish, electrophysiological studies have shown that the retinotectal projection reorganizes, following removal of half of the tectum, to form a complete but compressed projection over the remaining half tectum. As a result, each fiber terminates more rostrally than normal. Electron microscopic studies suggest a competition between retinal fibers for a fixed number of synaptic sites. The current study examines whether retinal arbors in the compressed projection are smaller than normal in extent or branching and whether the fiber paths in the tectum show the rostral movements and the search strategy that the retinal fibers use. The caudal half tectum was removed without cutting retinal fibers except those at the cut edge. At 3 to 19 months afterward, retinal fibers were labeled with horseradish peroxidase. In whole‐mounted tecta, fibers and terminals were drawn under camera lucida and compared with normal arbors. The axonal paths were also traced across the tectum to their termination sites. At 3 to 6 months (early stages of compression), the arbors were rather normal in appearance, although they were actually significantly larger (23%) than normal in linear extent, arborized somewhat deeper and had fewer branches (18%). The fibers normally terminating in the rostral tectum followed normal stereotyped paths, whereas those cut at the edge had grown back and forth loops (apparent searching behavior) with little branching. By 10 months when compression is complete, arbors were significantly smaller than normal (19%), were arborizing significantly deeper, and had significantly fewer branches (19%). The differences were more pronounced in arbors of coarse and medium caliber than in fine caliber axons. The axons still ran in stereotyped fascicles, but included an extrafascicular portion that, unlike any axons in normals, turned back in a rostral direction before branching. This striking effect, present even in far rostral tectum, indicated that arbors had been forced to move rostrally to accomodate those from the ablated half. The small effect on arbor extent suggests that this is influenced by factors other than the magnification factor of the map, perhaps postsynaptic dendritic extent. The increased depth of termination is consistent with the increased thickness of the retinal terminal layer. The decreased number of branches is consistent with the conclusion that the remaining fixed number of synaptic sites shared among the full complement of retinal fibers should result in fewer synapses per retinal fiber. © 1995 John Wiley & Sons, Inc.
Acetylcholine receptor clustering in C2 muscle cells requires chondroitin sulfate
Authors: Mook‐Jung Inhee , Gordon Herman 
Published: May 2005

AbstractProteoglycans have been implicated in the clustering of acetylcholine receptors (AChRs) on cultured myotubes and at the neuromuscular junction. We report that the presence of chondroitin sulfate is associated with the ability of cultured myotubes to form spontaneous clusters of AChRs. Three experimental manipulations of wild type C2 cells in culture were found to affect both glycosaminoglycans (GAGs) and AChR clustering in concert. Chlorate was found to have dose‐dependent negative effects both on GAG sulfation and on the frequency of AChR clusters. When extracellular calcium was raised from 1.8 to 6.8 mM in cultures of wild‐type C2 myotubes, increases were observed both in the level of cell layer‐associated chondroitin sulfate and in the frequency of AChR clusters. Culture of wild‐type C2 myotubes in the presence of chondroitinase ABC eliminated cell layer‐associated chondroitin sulfate while leaving heparan sulfate intact and simultaneously prevented the formation of AChR clusters. Treatment with either chlorate or chondroitinase inhibited AChR clustering only if begun prior to the spontaneous formation of clusters. We propose that chondroitin sulfate plays an essential role in the initiation of AChR clustering and in the early events of synapse formation on muscle. © 1995 John Wiley & Sons, Inc.