bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lack of correspondence between mRNA expression for a putative cell death molecule (SGP‐2) and neuronal cell death in the central nervous system
Authors: Garden Gwenn A. , Bothwell Mark , Rubel Edwin W. 
Published: May 2005

AbstractNeuronal death during nervous system development, a widely observed phenomenon, occurs through unknown mechanisms. Recent evidence suggests an active, destructive process requiring new gene expression. Sulfated glycoprotein‐2 (SGP‐2), a secretory product of testicular Sertoli cells has been shown to up‐regulate in several nonneural tissues undergoing programmed cell death and in several types of neuronal degeneration. In order to determine if this message up‐regulates in neurons undergoing developmentally determined cell death, we have studied the expression of SGP‐2 mRNA in the developing and adult rat central nervous system (CNS) with in situ hybridization. We also report on the expression of this message in nonneural tissues from several regions of the developing embryo. The developing and adult rat central nervous system as well as widely varied tissues in the rat embryo express SGP‐2 mRNA in a pattern that does not correlate with regions undergoing developmental cell death. In the nervous system, SGP‐2 mRNA is expressed in neuronal populations including motor neurons, cortical neurons, and hypothalamic neurons at ages when the period of developmental cell death has passed. In a nonneural tissue (palatal shelve epithelium) for which a developmental cell death period has been described, SGP‐2 mRNA was not present in the region where cell death occurs. We conclude that SGP‐2 mRNA expression cannot be correlated with programmed cell death in neural or nonneural tissues. The results of this study as well as recently reported SGP‐2 homologies indicate a possible role for this protein in secretion and lipid transport.
Co‐cultures of inferior olive and cerebellum: Electrophysiological evidence for multiple innervation of Purkinje cells by olivary axons
Authors: Mariani Jean , Knöpfel Thomas , Gähwiler Beat H. 
Published: May 2005

AbstractSlices of inferior olive (IO) and cerebellum were co‐cultured for several weeks by means of the roller tube technique. Recordings were carried out intracellularly from Purkinje cells (PCs) which were identified morphologically by intracellular injection of the fluorescent dye Lucifer yellow, or by immunohistochemical stainings with antibodies raised against the 28 kD Ca2+‐binding protein calbindin. Following stimulation of olivary tissue, an all‐or‐none full complex spike response was recorded in some PCs consisting of a fast rising spike followed by a depolarizing potential. In other PCs, graded stimulation of the olivary explant induced synaptic potentials which were characterized by step‐wise variation in their amplitude and resembled the ones occurring spontaneously. In contrast, only smoothly graded synaptic potentials were observed in cerebellar mono‐cultures. These results indicate that some of the PCs in olivo‐cerebellar co‐cultures are innervated by several olivary neurons.
Sexually dimorphic, androgen sensitive, enkephalinergic afferents to a lumbar motor nucleus of rats
Authors: Coquelin Arthur , Micevych Paul E. , Arnold Arthur P. 
Published: May 2005

AbstractIn male rats, methionine‐enkephalin immunoreactivity (enkephalin‐ir) has been observed in the dorsal lateral nucleus (DLN), a longitudinal pool of motoneurons in the lumbar spinal cord. Within the DLN a mediodorsal crescent of intense enkephalin‐ir staining surrounds the motoneurons innervating the ischiocavernosus muscle of the penis, which suggests a function of the enkephalinergic afferents in male copulatory activities. The present study attempted to determine the roles of gender and adult exposure to androgen in shaping the striking subnuclear distribution of enkephalin‐ir. Transverse sections through L5–6 were obtained from mature male and female rats that were gonadally intact, gonadectomized, or gonadectomized and treated with testosterone, as well as from male rats genetically deficient in androgen receptors (Tfm). The sections were incubated with primary antiserum raised against methionine enkephalin and bound antibodies were visualized using the avidin‐biotin peroxidase technique. A microphotometer was used to compare the staining density in laminae I‐II of the dorsal horn, ventral grey matter, and the DLN. In all groups the DLN stained more darkly than the ventral grey, demonstrating the presence of enkephalin‐ir in the DLN regardless of gender or exposure to androgen. However, the mediodorsal crescent of dense staining in the DLN was obvious only in gonadally intact males, while the entire DLN stained darkly in both sexes of gonadectomized rats treated with androgen. Therefore, the preferential distribution of enkephalin‐ir in the mediodorsal crescent of the DLN is sexually dimorphic though the overall content of enkephalin‐ir within the DLN responds to androgen.
Mapping the early development of projections from the entorhinal cortex in the embryonic mouse using prenatal surgery techniques
Authors: Snyder Dianne C. , Coltman Bert W. , Muneoka Ken , Ide Charles F. 
Published: May 2005

AbstractThe purpose of this work was to study the development of specific projections from the postero‐lateral cortex during the third trimester of gestation in the mouse. To do this, we labeled undifferentiated lateral cortex with the fluorescent carbocyanine dye, Dil, in the embryonic day (E) 16 mouse embryo usingexo uterosurgical techniques (Muneoka, Wanek, and Bryant, 1986). Embryos were allowed to develop to term (postnatal day 0, P0) at which time the fiber patterns emanating from the marked regions were studied. Dye placement in the undifferentiated postero‐ventral cortex produced labeled fibers in the hippocampal formation. A robust projection of the angular bundle into the CA1 region of the hippocampus was heavily labeled. In addition, in some animals, cortical tracts, such as the anterior commissure, corpus callosum, and a corticotectal tract, were labeled. These tracts have been described previously as scaffolding pathways in the fetal cat (McConnell, Ghosh, and Shatz, 1989), and other vertebrates (Wilson, Ross, Parrett, and Easter, 1990). Dye placement in adjacent, more anterior or dorsal areas showed strong labeling in cortical structures but no labeling in the hippocampal formation. These data indicate that, by birth, the temporal cortex is subdivided along the rostro‐caudal axis as entorhinal cortex and perirhinal cortex, and along the dorso‐ventral axis, as entorhinal cortex and neocortex. Also, these earliest connections are similar to adult connections in their specificity of target area selection. Therefore, these early, yet specific, connections may play a role in the formation of future connections during postnatal development.
Tamoxifen fails to block estradiol accumulation, yet is weakly accumulated by the juvenile zebra finch anterior hypothalamus: An autoradiographic study
Authors: Mathews Greta A. , Arnold Arthur P. 
Published: May 2005

AbstractIn experiment 1, we used autoradiographic procedures to examine whether tamoxifen could displace 3H‐estradiol labeling in the anterior hypothalamus and the caudal nucleus of the ventral hyperstriatum (HVc) of ovariectomized 20‐day‐old female zebra finches. There was no significant reduction in labeling of cells by 3H‐estradiol in birds preinjected with unlabeled tamoxifen. In experiment 2, we found that injections of 3H‐tamoxifen causedweak labeling of cells in the anterior hypothalamus of 20‐day‐old male and female zebra finches. These results are compatible with the idea that tamoxifen does not block the action of estradiol in the brain of zebra finches, and suggest that the effects of early tamoxifen treatment on the morphology of the song system may reflect central action of tamoxifen.
Hormonally mediated plasticity of motoneuron morphology in the adult rat spinal cord: A cholera toxin‐HRP study
Authors: Kurz E. M. , Brewer R. G. , Sengelaub D. R. 
Published: May 2005

AbstractThe dorsolateral nucleus (DLN) and the spinal nucleus of the bulbocavernosus (SNB) of the rat lumbar spinal cord are sexually dimorphic groups of motoneurons that innervate striated perineal muscles involved in male copulatory behavior. Androgens control the development of these motoneurons and their target muscles, and continue to influence the system in adulthood. Given that several features of SNB motoneuron morphology have been shown to be androgen sensitive in adult male rats, we examined the effects of androgen manipulations on the morphology of motoneurons in the DLN in adult rats. Adult male rats were castrated and implanted with testosterone‐filled or blank implants, or were subjected to a sham‐castration procedure. Six weeks after treatment, motoneurons in the DLN were retrogradely labeled with cholera toxin‐horseradish peroxidase (HRP) after injection into the ischiocavernosus (IC) muscle and their morphology assessed. Measures of the radial extent and coverage of the dendritic arbor of DLN motoneurons projecting to the IC (DLN‐IC motoneurons) were similar across the groups, indicating comparable degrees of HRP transport. However, DLN‐IC motoneurons in castrates with blank implants possessed both shorter dendritic lengths and smaller somas than those of castrates treated with testosterone. Castrates with testosterone implants had DLN‐IC motoneurons that were significantly larger than those of sham castrates in dendritic length and soma area. These results suggest that motoneurons in the DLN, like those in the SNB, possess a significant degree of structural plasticity in adulthood which is influenced by androgens.
Androgen locally regulates rat bulbocavernosus and levator ani size
Authors: Rand Mark N. , Breedlove S. Marc 
Published: May 2005

AbstractAdult male rats were gonadectomized, and small Silastic capsules filled with hormone were sutured to each bulbocavernosus and levator ani muscle complex (BC/LA). In the first experiment, one capsule contained testoster one (T), while the capsule on the contralateral muscles contained the antiandrogen hydroxyflutamide (hFI). The intent of this treatment was to provide a focus of androgenic stimulation to the muscles on the muscles on one side. After 30 days, animals were sacrificed, and the BC / LA muscle pairs were removed, weighed, and compared. BC/LAs receiving T treatment were heavier than those receiving hFl treatment (p <0.0001), with an average weight difference of 12%. Muscle fibers from T‐treated BCs were significantly larger in diameter than those from contralateral, hFl‐treated BCs. These results indicate that androgen exerts its anabolic effect by acting locally upon a cell population within or near the BC/LA. When hFl and blank capsules were implanted in castrated males, the hFl‐treated muscles were significantly heavier (by 9%), demonstrating an anabolic effect of hFl in the absence of androgen, and refuting the idea that hFl may have caused local toxic effects in the first experiment. Gonadectomized animals given T versus blank capsules had T‐treated muscles that were 8% heavier than the blank treated side. Muscle weights were also compared in animals receiving bilateral denervation of the BC/LA at the time of T and hFl capsule implantation and gonadectomy; local testosterone treatment failed to affect BC/LA weights in these denervated muscles.
Connections of the forewing tegulae in the locust flight system and their modification following partial deafferentation
Authors: Büschges Ansgar , Ramirez Jan‐Marino , Driesang Robert , Pearson Keir G. 
Published: May 2005

AbstractThe flight motor pattern of the adult locust (Locusta migratoria L.) is able to recover from the loss of the hindwing tegulae. This recovery is due to a functional substitution of the hindwing tegulae by the forewing tegulae (Büschges, Ramirez, and Pearson, 1992). To assess changes in the pathways from the forewing tegulae in the flight system, we investigated the pathways of the forewing tegula in intact locusts and in animals 2 weeks after hindwing tegula removal. The following physiological alterations in these pathways were found to be associated with the recovery: (1) In the intact locusts, the connections of forewing tegula afferents to flight interneurons are variable but this variability did not occur in recovered animals, and (2) larger numbers of forewing tegula afferents connect to interneurons that excite elevator motoneurons (interneurons 566 and 567) and to an interneuron that inhibits depressor motoneurons (interneuron 511). The size of unitary excitatory postsynaptic potentials (EPSPs) evoked by single forewing tegula afferents was found not to be altered in recovered animals. The changes in connectivity of forewing tegula afferents are correlated with morphological alterations in the structure of the terminal processes of the afferents and with sprouting of some branches of interneurons receiving input from these afferents.
Monoclonal M6 antibody interferes with neurite extension of cultured neurons
Authors: Lagenaur Carl , Kunemund Volker , Fischer Gunther , Fushiki Shinji , Schachner Melitta 
Published: May 2005

AbstractMonoclonal M6 antibody binds to the surface of murine central nervous system neurons as well as to apical surfaces of epithelial cells in the choroid plexus and proximal tubules of the kidney. M6 antigen is expressed in the central nervous system as early as embryonic day 10, most strongly in the marginal zone of the neural tube, and remains detectable in adulthood. IgG or Fab fragments of M6 antibody interfere with the extension of neurites by cultured cerebellar neurons. Effects of the antibody on neurite extension are readily detectable after 24 h. No reduction of cell viability is detected during the first 3 days of antibody treatment. Cultures maintained in the presence of antibody for longer than 5 days exhibit reduced viability of neurons. This reduction in long‐term viability in the presence of M6 antibody is largely avoided when 25 mM KCl is included in the culture medium. The antibody‐mediated perturbation of neurite outgrowth is not blocked by the presence of elevated KCl. The unusually short and flattened appearance of neurites in these cultures suggests that the M6 antibody selectively affects neurite extension. Time‐lapse cinematography of anti‐M6‐treated neurons reveals no apparent effect on movement of lamellipodia and filopdia of growth cones. Only the overall extension of the neurite appears to be inhibited. M6 antigen is a 35 kD glycoprotein that can be isolated from a deoxycholate‐ (DOC) solubilized membrane fraction from adult mouse brain.
Neuron death in the developing avian isthmo–optic nucleus, and its relation to the establishment of functional circuitry
Authors: Clarke P. G. H. 
Published: May 2005

AbstractThe present review covers all the published data on neuron death in the developing avian isthmo–optic nucleus (ION), which provides a particularly convenient situation for studying the causes and consequences of neuron death in the development of the vertebrate central nervous system. The main conclusions are as follows: The naturally occurring neuron death in the ION is related both temporally and causally to the ION's formation of afferent and efferent connections. The ION neurons need to obtain both anterograde and retrograde survival signals in order to survive during a critical period in embryogenesis. They may compete, at least for the retrograde signals, but the nature of the competition is still unclear. The retrograde signals are modified by action potentials. Neurons dying from a lack of anterograde survival signals can be distinguished morphologically from ones dying from a lack of retrograde signals. The neuron death refines circuitry by selectively eliminating neurons with “aberrant” axons projecting to the “wrong” (i.e., ipsilateral) retina or to the “wrong” (topographically inappropriate) part of the contralateral retina. © 1992 John Wiley & Sons, Inc.
Biochemical characterization of programmed cell death in NGF‐deprived sympathetic neurons
Authors: Martin David P. , Ito Akira , Horigome Kazuhiko , Lampe Patricia A. , Johnson Eugene M. 
Published: May 2005

AbstractYoung sympathetic neurons die when deprived of nerve growth factor (NGF). Under such circumstances, cell death is appropriate to the developing nervous system and requires RNA and protein synthesis. We have hypothesized the existence of an endogenous death program within neurons that is suppressed by trophic factors. The extent and timing of required changes in the synthetic events that comprise the death program are unknown. In an effort to characterize the biochemical events that mediate the death program further, we performed several experiments on embryonic rat sympathetic neurons in vitro. The death program was blocked with cycloheximide when total protein synthesis was inhibited ≥80%. When protein synthesis was inhibited within 22 ± 4 h of NGF deprivation, death was prevented in half the neurons. Hence, we define the commitment point for protein synthesis to be 22 ± 4 h. Analogously, the commitment point for RNA synthesis was 26 ± 4 h and that for NGF rescue, 24 ± 4 h. We tested the ability of a wide variety of chemicals to interfere with the death program. Most compounds tested were unable to prevent neuronal death. Some treatments, however, did save NGF‐deprived neurons and were subsequently characterized. These included ultraviolet light and agents that raise intracellular concentrations of cAMP. Finally, we looked for the neuronal expression in vitro and in vivo of genes that have been associated with programmed death in other cell types, including TRPM‐2/SGP‐2, polyubiquitin, TGFβ‐1, c‐fos, and c‐myc. None of these genes showed significant activation associated with neuronal death. © 1992 John Wiley & Sons, Inc.
Cell death in the oligodendrocyte lineage
Authors: Barres B. A. , Hart I. K. , Coles H. S. R. , Burne J. F. , Voyvodic J. T. , Richardson W. D. , Raff M. C. 
Published: May 2005

AbstractWe have recently found that about 50% of newly formed oligodendrocytes normally die in the developing rat optic nerve. When purified oligodendrocytes or their precursors are cultured in the absence of serum or added signalling molecules, they die rapidly with the characteristics of programmed cell death. This death is prevented either by the addition of medium conditioned by cultures of their normal neighboring cells in the developing optic nerve, or by the addition of platelet‐derived growth factor (PDGF) or insulin‐like growth factors (IGFs). Increasing PDGF in the developing optic nerve decreases normal oligodendrocyte death by up to 90% and doubles the number of oligodendrocytes, suggesting that this normally occurring glial cell death might result from a competition for limiting amounts of survival signals. These results suggest that competition for limiting amounts of survival factors is not confined to developing neurons, and raise the possibility that a similar mechanism may be responsible for some naturally occurring cell deaths in nonneural tissues. © 1992 John Wiley & Sons, Inc.
Insect muscle as a model for programmed cell death
Authors: Schwartz Lawrence M. 
Published: May 2005

AbstractProgrammed cell death (PCD) is a fundamental component of development in virtually all animals. Despite the ubiquity of this phenomenon, little is known about what tells a cell to die, and less still about the physiological and molecular mechanisms that bring about death. One system that has proven to be very amenable for the study of PCD is the intersegmental muscle (ISM) of the tobacco hawkmoth Manduca sexta. These giant muscle cells are used during the eclosion (emergence) behavior of the adult moth, and then die during the subsequent 30 h. This review uses the ISMs as a model system to address questions that are basic to any cell death system, including the following: (1) how do cells know when to die; (2) what physiological changes accompany death; (3) what are the molecular mechanisms that mediate death; and (4) do all cells die by the same process? For the ISMs, the trigger for PCD is a decline in the circulating titer of the insect molting hormone, 20‐hydroxyecdysone (20‐HE). During cell death there are rapid decreases in both the myofibrillar sensitivity to intracellular calcium and the resulting force of fiber contraction. The ability of the ISMs to under go PCD requires the repression and activation of specific genes. Two of the repressed genes encode actin and myosin. One of the upregulated presumptive cell‐death genes encodes polyubiquitin, which appears to play a critical role in the rapid proteolysis that accompanies ISM death. One curious aspect of ISM death is that these cells display none of the features that are characteristic of apoptosis, suggesting that they may die by a fundamentally different mechanism. © 1992 John Wiley & Sons, Inc.
History of developmental neuroethology: Early contributions from ethology
Authors: Fentress John C. 
Published: May 2005

AbstractEthology has its roots in the natural history of animal behavior. Questions of causation and function have historically been complementary, and each has rested upon a prior appreciation of the behavior of animals in nature. It is thus difficult to place a single time or place where ethology was born. Early evolutionary interests hinted at developmental constraints that continue to guide much research. It has only been relatively recently, however, that the explicit analysis of neural mechanisms in behavior has received the attention it deserves in developmental analyses. A mature developmental neuroethology will require a synthesis of the broad insights of ethology with refined neurobiological technique. Fundamental, however, is the primary focus upon behavior as it normally occurs. © 1992 John Wiley & Sons, Inc.
Pathways in the emergence of developmental neuroethology: Antecedents to current views of neurobehavioral ontogeny
Authors: Oppenheim Ronald W. 
Published: May 2005

AbstractThe historical forces that have contributed to our current views of neurobehavioral development (and thus to the fields of developmental psychobiology and neuroethology) are many and varied. Although similar statements might be made about almost any field of science, it is in particular true of this field, which represents a kind of mongrel discipline derived from at least three major sources (psychology, embryology, and neuroscience) and several more minor ones (including developmental psychology and psychiatry, psychoanalysis, education, zoology, ethology, and sociology). Although I attempt to demonstrate here how each of these sources may have influenced the emergence of a unified field of developmental psychobiology or developmental neuroethology, because the present article represents the first attempt of which I am aware to trace the history of these fields I am certain that there is considerable room for improvement, correction, and revision of the views expressed here. Accordingly, I consider this inaugural effort a kind of reconnaissance intended to trace a necessarily imperfect historic path for others to follow and improve upon. In the final analysis, I will be satisfied if this article only serves to underscore two related points: first is the value derived from historical studies of contemporary issues in development, and the second concerns the extent to which our current ideas and concepts about neurobehavioral development, ideas often considered new and contemporary, were already well known to those who came before us. The first point underscores the arguments expressed in the Introduction that the present must always be reconciled with the past, for the past is never entirely past. The second point returns full circle to an important thought expressed in the opening quotation to this article, namely, that even though our historic predecessors lacked much of the empirical facts available to us they were nonetheless able to attain a surprisingly deep understanding of neurobehavioral ontogeny. © 1992 John Wiley & Sons, Inc.