bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of castration and testosterone treatment on the activity of testosterone‐metabolizing enzymes in the brain of male and female zebra finches
Authors: Vockel A. , Pröve E. , Balthazart J. 
Published: May 2005

AbstractRecently, we described the distribution of testosteronemetabolizing enzymes (i.e., aromatase, 5α‐ and 5β‐reductases) in the zebra finch (Taeniopygia guttata) brain using a sensitive radioenzyme assay combined to the Palkovits punch method. A number of sex‐differences in the activity of these enzymes were observed especially in nuclei of the song‐control system. The hormonal controls of these differences have now been analyzed by gonadectomizing birds of both sexes and by giving them a replacement therapy with silastic implants of testosterone (T). Five nuclei of the song system (Area X [X], nucleus magnocellularis of the anterior neostriatum [MAN], nucleus robustus archistriatalis [RA], nucleus intercollicularis [ICo], hyperstriatum ventrale, pars caudalis [HVc]) and three preoptic‐hypothalamic areas (preoptic anterior [POA], periventricular magnocellular nucleus [PVM], and posterior medial hypothalamic nucleus [PMH]) were studied as well as other limbic and control non‐steroid‐sensitive areas. The activity of the 5β‐reductase was higher in males than in females for the five song‐control nuclei and was not affected by the hormonal treatments. The overall activity of this enzyme was not sexually dimorphic in POA and PVM. It was higher in males than in females in intact birds only, and was reduced by gonadectomy and enhanced by T. The activity of the 5β‐reductase was higher in females than in males in all nuclei of the song system and in POA, but was not influenced by the changes in T level. Both sex and treatment effects were observed in the control of aromatase. The production of estrogens was dimorphic (females > males) in RA and PMH. It was increased by T in POA, PVM, and PMH, and also in RA. These data show that some of the sex differences in T‐metabolizing enzymes result from the exposure to different levels of T in adulthood (e.g., 5α‐reductase in POA and PVM or aromatase in PVM), whereas others persist even if birds are exposed to the same hormonal conditions. These are presumably the result of organizational effects of steroids. The steroid modulation of the aromatase might be related directly to the activation of sexual, aggressive, and nest‐building behaviors, whereas the stable dimorphism in 5α‐and 5β‐reductase observed in the nuclei of the song system might be one of the neurochemical bases of the sex differences in the vocal behavior of the zebra finch.
Morphology of pioneer and follower growth cones in the developing cerebral cortex
Authors: Kim Gina J. , Shatz Carla J. , McConnell Susan K. 
Published: May 2005

AbstractIn the developing nervous systems of both invertebrates and vertebrates, neurons must develop precise sets of axonal connections. One strategy used by both orders of animals is to generate a special class of neurons whose axons “pioneer” the first pathways between these cells and their targets. In the developing mammalian telencephalon, the subplate neurons (which are among the first neurons to be generated in development) extend axons to long‐distance subcortical targets before the neurons of the deep cortical layers 5 and 6 have been generated. The axons of layer 5 and 6 neurons later follow a similar pathway to form permanent subcortical projections to the thalamus and tectum, and thereafter the vast majority of subplate neurons die. These results have generated the hypothesis that subplate axons may actually be required for the axons of layer 5 and 6 neurons to innervate their appropriate subcortical targets. The complexity of growth cones has previously been correlated with axonal decision making: differences in growth cone morphologies have been noted in comparisons of leading versus following axons (LoPresti, Macagno, and Levinthal, 1973; Nordlander, 1987; Yaginuma, Homma, Kunzi, and Oppenheim, 1991), and at choice points along axon pathways (Raper, Bastiani, and Goodman, 1983; Tosney and Landmesser, 1985; Caudy and Bentley, 1986a, b; Bovolenta and Mason, 1987; Holt, 1989; Bovolenta and Dodd, 1990; Yaginuma et al., 1991). Thus, as a first step toward addressing the question of whether the axons of deep‐layer neurons simply follow subplate axons to their targets, we have studied the morphology of cortical growth cones at various points along the corticothalamic pathway and at different stages of development. We examined the brains of fetal ferrets and cats at ages ranging from embryonic days (E) 24 to E50, using the fluorescent lipophilic tracer 1,1‐dioctadecyl‐3,3,3′,3′‐tetramethyl indocarbocyanine perchlorate (Dil) to reveal the axons and growth cones of cortical neurons. Growth cones were drawn, and quantitative measurements of their complexity were made by counting filopodia and calculating their surface area. No morphological differences were found among growth cones at different points along the corticothalamic pathway at a given age. However, growth cones belonging to early‐generated cells (likely to be subplate neurons) are significantly larger and more complex than are the growth cones of later‐generated cortical neurons. This evidence is consistent with the suggestion that subplate growth cones actively pioneer the corticothalamic pathway, and that the axons of layer 5 and 6 neurons follow it.
Patterns of cell division and interkinetic nuclear migration in the chick embryo hindbrain
Authors: Guthrie Sarah , Butcher Matthew , Lumsden Andrew 
Published: May 2005

AbstractEarly in its development, the chick embryo hindbrain manifests an axial series of bulges, termed rhombomeres. Rhombomeres are units of cell lineage restriction, and both they and their intervening boundaries form a series that reiterates various features of neuronal differentiation, cytoarchitecture, and molecular character. The segmented nature of hindbrain morphology and cellular development may be related to early patterns of cell division. These were explored by labeling with BrdU to reveal S‐phase nuclei, and staining with basic fuchsin to visualise mitotic cells. Whereas within rhombomeres, S‐phase nuclei were located predominantly toward the pial surface of the neuroepithelium, at rhombomere boundaries S‐phase nuclei were significantly closer to the ventricular surface. The density of mitotic figures was greater toward the centres of rhombomeres than in boundary regions. Mitotic cells did not show any consistent bias in the orientation of division, either in the centres of rhombomeres, or near boundaries. Our results are consistent with the idea that rhombomeres are centres of cell proliferation, while boundaries contain populations of relatively static cells with reduced rates of cell division.
Developmental study of afferented and deafferented bee antennal lobes
Authors: Gascuel Jean , Masson Claudine 
Published: May 2005

AbstractThe role of antennal sensory projections on the ontogeny of the bee antennal lobe was analyzed using both light and transmission electron microscopy. Normal and deafferented developing antennal lobes were examined. The results obtained show that (1) initiation of synaptogenesis in the antennal lobe is independent of the arrival of sensory inputs; (2) sensory inputs are necessary for setting up the glomerular antennal lobe organization; (3) regressive events, such as the reduction of synapse density, occur during the development of the antennal lobe; and (4) glomeruli formation appears as related to glia development.
Migration patterns of sympathetic preganglionic neurons in embryonic rat spinal cord
Authors: Markham Jeffrey A. , Vaughn James E. 
Published: May 2005

AbstractThe displacement of immature neurons from their place of origin in the germinal epithelium toward their adult positions in the nervous system appears to involve migratory pathways or guides. While the importance of radial glial fibers in this process has long been recognized, data from recent investigations have suggested that other mechanisms might also play a role in directing the movement of young neurons. We have labeled autonomic preganglionic cells by microinjections of horseradish peroxidase (HRP) into the sympathetic chain ganglia of embryonic rats in order to study the migration and differentiation of these spinal cord neurons. Our results, in conjunction with previous observations, suggest that the migration pattern of preganglionic neurons can be divided into three distinct phases. In the first phase, the autonomic motor neurons arise in the ventral ventricular zone and migrate radially into the ventral horn of the developing spinal cord, where, together with somatic motor neurons, they form a single, primitive motor column (Phelps P. E., Barber R. P., and Vaughn J. E. (1991). J. Comp. Neurol. 307:77–86). During the second phase, the autonomic motor neurons separate from the somatic motor neurons and are displaced dorsally toward the intermediate spinal cord. When the preganglionic neurons reach the intermediolateral (IML) region, they become progressively more multipolar, and many of them undergo a change in alignment, from a dorsoventral to a mediolateral orientation. In the third phase of autonomic motor neuron development, some of these cells are displaced medially, and occupy sites between the IML and central canal. The primary and tertiary movements of the preganglionic neurons are in alignment with radial glial processes in the embryonic spinal cord, an arrangement that is consistent with a hypothesis that glial elements might guide autonomic motor neurons during these periods of development. In contrast, during the second phase, the dorsal translocation of preganglionic neurons occurs in an orientation perpendicular to radial glial fibers, indicating that glial elements are not involved in the secondary migration of these cells. The results of previous investigations have provided evidence that, in addition to glial processes, axonal pathways might provide a substrate for neuronal migration. Logically, therefore, it is possible that the secondary dorsolateral translocation of autonomic preganglionic neurons could be directed along early forming circumferential axons of spinal association interneurons, and this hypothesis is supported by the fact that such fibers are appropriately arrayed in both developmental time and space to guide this movement.
Influence of altered afferent input on the number of trochlear motor neurons during development
Authors: Sohal G. S. , Hirano S. , Kumaresan K. , Ali M. M. 
Published: May 2005

AbstractA loss of about half of the trochlear motor neurons occurs during the course of normal development. The present investigation was undertaken to examine the role of afferent input in regulating the number of surviving or dying trochlear motor neurons. A majority of the afferent input to the trochlear nucleus comes from the vestibular nuclei of the hindbrain via the medial longitudinal fasciculus. Portions of the hindbrain were lesioned in duck embryos on embryonic day 3, considerably prior to the time motor neurons send their axons out and cell death begins. The effectiveness of hindbrain lesion was verified by electron microscopical examination of synapses. There was a significant decrease in the number of synapses on trochlear motor neurons following hindbrain lesion. Cell counts made after the period of cell death indicated a significant decrease in the final number of surviving trochlear motor neurons. Cell counts made prior to the onset of cell death indicated that there was a drastic reduction in the initial number of trochlear motor neurons produced in hindbrain lesion embryos. In spite of a significant reduction in the initial number of neurons, the percentage loss of neurons was about the same as during normal development. Since trochlear motor neurons are generated prior to the formation of afferent synapses on them, it is unlikely that the reduction in the number of motor neurons initially produced is due to reduced afferent synaptic input. Since the percentage of cell loss in hindbrain lesion and normal embryos is about the same, it seems that the magnitude of cell death is genetically programmed. These observations suggest that the afferent synaptic input to the trochlear motor neurons may not be as important as previously thought in regulating cell number during development. They also suggest that some afferent input, of nonsynaptic type, available at very early stages of development may specify the initial number of trochlear motor neurons produced and that a fixed percentage of that number is programmed to die during development. It is suggested that this early influence may be provided by the embryonic medial longitudinal fasciculus.
Reorganization of sensory regulation of locust flight after partial deafferentation
Authors: Büschges Ansgar , Ramirez Jan‐Marino , Pearson Keir G. 
Published: May 2005

AbstractPrevious investigations have shown that the flight motor pattern of the mature locust (Locusta migratoria L.) relies heavily on the input of the hindwing tegulae. Removal of the hindwing tegulae results in an immediate change in the motor pattern: the wingbeat frequency (WBF) decreases and the interval between the activity of depressor and elevator muscles (D–E interval) increases. In contrast, removal of the forewing tegulae has little effect on the motor pattern. Here we report adaptive modifications in the flight system that occur after the removal of the hindwing tegulae. Over a period of about 2 weeks following hendwing tegula removal, the flight motor pattern progressively returned towards normal, and in about 80% of the animals recovery of the flight motor pattern was complete. We describe the changes in the activity pattern of flight muscles and in the patterns of depolarizations in flight motoneurons and flight interneurons associated with this recovery. In contrast to the situation in the intact animal, the activity of the forewing tegulae is necessary in recovered animals for the generation of the motor pattern. Removal of the forewing tegulae in recovered animals resulted resulted in similar changes in the flight motor pattern as were observed in intact animals after the removal of the hindwing tegulae. Furthermore, electrical stimulation of forewing tegula afferents in recovered animals produced similar resetting effects on the motor pattern as electrical stimulation of the hindwing tegulae afferents in intact animals. From these observations we conclude that recovery is due to the functional replacement of the removed hindwing tegulae by input from the forewing tegulae.
History of the discovery of neuronal death in embryos
Authors: Hamburger Viktor 
Published: May 2005

AbstractThe German anatomists, M. Ernst and A. Glücksmann, deserve credit for the discovery of widespread cell death in embryonic tissues, including the nervous tissue. In 1934, V. Hamburger described a significant hypoplasia in dorsal root ganglia (DGR) and lateral motor columns, following the extirpation of limb buds in chick embryos. In the early 1940s, Dr. Rita Levi‐Montalcini in Turin (Italy) repeated the experiment and suggested that the hypoplasia might result from the death of young differentiated neurons. In a joint reinvestigation, published in 1949, large numbers of degenerating neurons were described in brachial DRG, following wing bud extirpations. In the same embryos, Dr. Levi‐Montalcini observed massive neuronal death in cervical and thoracic DRG which had not been affected by the operation. This was the discovery of naturally occurring neuronal death. Long after the discovery of Nerve Growth Factor (NGF) it was recognized that NGF and natural neuronal death are two sides of the same coin: the latter results from an insufficient supply of the former by the target tissues. © 1992 John Wiley & Sons, Inc.
The role of target size in neuronal survival
Authors: Sohal G. S. 
Published: May 2005

AbstractA loss of about half of the trochlear motor neurons occurs during the course of normal development in duck and quail embryos. The role of the size of the target muscle in controlling the number of surviving motor neurons was examined by making motor neurons innervate targets either larger or smaller in size than their normal target. In one experiment the smaller trochlear motor neuron pool of the quail embryo was forced to innervate the larger superior oblique muscle of the duck embryo. This was accomplished by grafting the midbrain of a quail embryo in the place of the midbrain of a duck embyro. Results indicated that no additional quail trochlear motor neurons were rescued in spite of a considerable increase in target size. In another experiment the larger trochlear motor neuron pool of the duck embryo was made to innervate the smaller superior oblique muscle of the quail embryo. This resulted in loss of some additional neurons; however, the number of surviving motor neurons was not proportionate to the reduction in target size. These experiments failed to provide support for the hypothesis that the size of the target muscle controls the number of surviving motor neurons. Although contact with target is necessary for survival of neurons, factors other than the number or size of target cells are involved in the control of motor neuron numbers during development. © 1992 John Wiley & Sons, Inc.
Excitotoxic cell death
Authors: Choi Dennis W. 
Published: May 2005

AbstractExcitotoxicity refers to the ability of glutamate or related excitatory amino acids to mediate the death of central neurons under certain conditions, for example, after intense exposure. Such excitotoxic neuronal death may contribute to the pathogenesis of brain or spinal cord injury associated with several human disease states. Excitotoxicity has substantial cellular specificity and, in most cases, is mediated by glutamate receptors. On average, NMDA receptors activation may be able to trigger lethal injury more rapidly than AMPA or kainate receptor activation, perhaps reflecting a greater ability to induce calcium influx and subsequent cellular calcium overload. It is possible that excitotoxic death may share some mechanisms with other forms of neuronal death. © 1992 John Wiley & Sons, Inc.
Programmed neuronal death in insect development
Authors: Truman James W. , Thorn Robert S. , Robinow Steven 
Published: May 2005

AbstractProgrammed death in the developing nervous system of insects serves to remove obsolete neurons, generate segmental specializations and sexual dimorphism, as well as adjust neuronal number. This diversity is also reflected in the mechanisms which control the death of these neurons. In general, but not without exception, these deaths occur independent of target fate, while endocrine cues, segmental identity, and neural signalling often play critical roles. In addition, the programmed death of at least some neurons can be delayed by behavioral feedback. The study of neuronal death in Drosophila and the cloning of an ecdysteroid receptor bring the promise of understanding the genetic factors and molecular events that regulate this phenomenion. © 1992 John Wiley & Sons, Inc.
Molecular genetics of cell death in the nematode Caenorhabditis elegans
Authors: Driscoll Monica 
Published: May 2005

AbstractIn C. elegans, cell death can be readily studied at the cellular, genetic, and molecular levels. Two types of death have been characterized in this nematode: (1) programmed cell death, which occurs as a normal component in development; and (2) pathological cell death which occurs aberrantly as a consequence of mutation. Analysis of mutations that disrupt programmed cell death in various ways has defined a genetic pathway for programmed cell death which includes genes that perform such functions as the determination of which cells die, the execution of cell death, the engulfment of cell corpses, and the digestion of DNA from dead cells. Molecular analysis is providing insightinto the nature of the molecules that function in these aspects of programmed cell death. Characterization of some genes that mutate to induce abnormal cell death has defined a novel gene family called degenerins that encode putative membrane proteins. Dominant alleles of at least two degenerin genes, mec‐4 and deg‐1, can cause cellular swelling and late onset neurodegeneration of specific groups of cells. © 1992 John Wiley & Sons, Inc.
Neuroethology of olfactory preference development
Authors: Leon Michael 
Published: May 2005

AbstractYoung mammals come to approach the odor of their mother, a response that facilitates their survival during early life. Young rats induce a cascade of events in their mother to induce the emission of her odor. The pups increase circulating prolactin levels, which increases food intake and the emission of large quantities of cecotrophe containing the maternal odor. This odor is synthesized by the action of cecal microorganisms and changes with maternal diet. The diet‐dependence of the odor requires the pups to acquire their attraction to the odor postnatally. The acquisition of this preference occurs when an odor is paired with the tactile stimulation that pups receive during maternal care. The action of the tactile stimulation appears to be mediated by noradrenaline. The development of this type of olfactory attraction is accompanied by changes in the regions of the olfactory bulb that are responsive to the attractive odor. Metabolic, anatomical, and neurophysiological changes in response to the attractive odor emerge in such regions of the bulb after early olfactory preference training. © 1992 John Wiley & Sons, Inc.
Brachially innervated ectopic hindlimbs in the chick embryo. I. Limb motility and motor system anatomy during the development of embryonic behavior
Authors: Kitchener P. D. , Laing N. G. 
Published: May 2005

AbstractThe functional status of brachially innervated hindlimbs, produced by transplanting hindlimb buds of chick embryos in place of forelimb buds, was quantified by analyzing the number and temporal distribution of spontaneous limb movements. Brachially innervated hindlimbs exhibited normal motility until E10 but thereafter became significantly less active than normal limbs and the limb movements were more randomly distributed. Contrary to the findings with axolotls and frogs, functional interaction between brachial motoneurons and hindlimb muscles cannot be sustained in the chick embryo. Dysfunction is first detectable at E10 and progresses to near total immobility by E20 and is associated with joint ankylosis and muscular atrophy. Although brachially innervated hindlimbs were virtually immobile by the time of hatching (E21), they produced strong movements in response to electrical stimulation of their spinal nerves, suggesting a central rather than peripheral defect in the motor system. The extent of motoneuron death in the brachial spinal cord was not significantly altered by the substitution of the forelimb bud with the hindlimb bud, but the timing of motoneuron loss was appropriate for the lumbar rather than brachial spinal cord, indicating that the rate of motoneuron death was dictated by the limb. Measurements of nuclear area indicated that motoneuron size was normal during the motoneuron death period (E6‐E10) but the nuclei of motoneurons innervating grafted hindlimbs subsequently became significantly larger than those of normal brachial motoneurons. Although the muscle mass of the grafted hindlimb at E18 was significantly less than that of the normal hindlimb (and similar to that of a normal forelimb), electronmicroscopic examination of the grafted hindlimbs and brachial spinal cords of E20 embryos revealed normal myofiber and neuromuscular junction ultrastructure and a small increase in the number of axosomatic synapses on cross‐sections of motoneurons innervating grafted hindlimbs compared to motoneurons innervating normal forelimbs. The anatomical data indicate that, rather than being associated with degenerative changes, the motor system of the brachial hindlimb of late‐stage embryos is intact, but inactive. © 1993 John Wiley & Sons, Inc.