bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sexually dimorphic neuron number in lumbosacral dorsal root ganglia of the rat: Development and steroid regulation
Authors: Mills Alice C. , Sengelaub Dale R. 
Published: January 2005

AbstractRats possess a sexually dimorphic neuromuscular system that controls penile reflexes critical for copulation. This system includes two motor nuclei in the lumbar cord and their target musculature in the perineum. The spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN) motoneuron populations and their target perineal muscles are much larger in males than in females. The sex difference in motoneuron number develops via androgen‐regulated differential cell death during the perinatal period; androgen also regulates retention of the target muscles. The developmental pattern and steroid sensitivity of peripheral afferents to the SNB/DLN motor nuclei were previously unknown. In order to characterize the peripheral sensory component of the dimorphic SNB/DLN system, the neurons of the relevant dorsal root ganglia (DRGs) were quantified in terms of number, size, and androgen sensitivity at various perinatal ages. DRG neuron number is greatest prenatally, then decreases in both sexes after birth; the timing and pattern of neuron number development are similar to those seen in the SNB and DLN. Postnatally, males have more DRG neurons than females, as a result of greater neuron death in the DRGs of females. Females treated with testosterone propionate during the perinatal period exhibit masculine development of DRG neuron number. Thus, the normal development of DRG neuron number parallels that of the SNB/DLN motor nuclei and target muscles in pattern and timing, is sexually dimorphic, and is regulated by androgen. © 1993 John Wiley & Sons, Inc.
Changing synaptic specificities in the nervous system of Caenorhabditis elegans: Differentiation of the DD motoneurons
Authors: Walthall W. W. , Li Lei , Plunkett Jeffery A. , Hsu Chia‐Yu 
Published: January 2005

AbstractDuring postembryonic development, the DD motoneurons in the nematode Caenorhabditis elegans completely reorganize their pattern of synapses. Ablation of a pair of embryonic precursors results in the absence of this entire class of motoneurons. In their absence animals exhibit two developmentally distinct locomotory defects. The transition period from one defect to the other is correlated with the synaptic reorganization of the DD mns. Mutations in a gene (unc‐123) have been isolated that exhibit locomotory defects similar to those of the ablated adult animals. Genetic and cellular analyses of one of these alleles suggest that the unc‐123 gene product may be involved in the reestablishment of functional synapses in these neurons. © 1993 John Wiley & Sons, Inc.
Inhibitory effects of actinomycin D and cycloheximide on neuronal death in adult Manduca sexta
Authors: Fahrbach S. E. , Choi M. Kim , Truman J. W. 
Published: January 2005

AbstractA decline in circulating 20‐hydroxyecdysone permits the emergence of the adult Manduca sexta moth; this endocrine signal also triggers the death of approximately half of the neurons in the unfused abdominal ganglia of the moth central nervous system. This programmed death of neurons was markedly reduced by treatment with either actinomysin D (an RNA synthesis inhibitor) or cycloheximide (a protein synthesis inhibitor). Similar results were found after addition of these agents to ventral nerve cord cultures. The effectiveness of these treatments in delaying or blocking neuronal death depended upon their time of administration relative to the normal time of post‐emergence death in the particular motoneuron under study: late‐dying neurons, for example, could still be saved by these treatments even after early‐dying neurons had already initiated degeneration. In both intact moths and cultured ventral nerve cords, the ability of actinomycin D to prevent neuronal death waned at the same time at which replacement of the steroid hormone could no longer block neuronal death. This suggests that the steroid commitment point represents the time at which the genes that mediate cell death are transcribed. Cycloheximide remained effective in delaying or blocking neuronal death until shortly before the onset of degeneration, suggesting that ongoing protein synthesis is essential for the initiation of the degeneration response. 1994 John Wiley & Sons, Inc.
Substrate‐dependent interactions of leech microglial cells and neurons in culture
Authors: Masuda‐Nakagawa L. M. , Walz A. , Brodbeck D. , Neely M. D. , Grumbacher‐Reinert S. 
Published: January 2005

AbstractThe principal aim of the present experiments has been to analyze the properties of microglial cells and their role in nerve regeneration. In the leech, damage to the CNS has been shown to be followed by accumulation of laminin and microglial cells at the site of injury (Masuda‐Nakagawa et al., 1990. Proc. R. Sco. Lond. B. 241:201–206; and 1993. Proc. Natl. Acad. Sci. USA 90:4966–4970). Procedures were devised for isolating these small, wandering cells from the CNS of the leech. In culture, they were reliably identified by their sizes, shapes, and phagocytotic activity. Their morphology, motility, and interactions with neurons were influenced by the substrate molecules on which they were plated. On the plant lectin concanavalin A (Con A) microglia had a rounded shape and remained stationary. By contrast on extracts of leech extracellular matrix (ECM) enriched with laminin the cells were mobile and spindle‐shaped with long processes. On Con A, neuronal growth cones avoided microglial cells, whereas on ECM extract the presence of a microglial cell did not influence neurite growth. Microglial cells showed immunoreactivity on both substrates when stained with a monoclonal antibody against leech laminin. Together these results suggest that microglial cells are influenced in their properties by molecules in the environment and that they could contribute to neuronal outgrowth at the site of any injury. 1994 John Wiley & Sons, Inc.
Regulation of immediate‐early gene expression in rat retinal ganglion cells after axotomy and during regeneration through a peripheral nerve graft
Authors: Hüll Michael , Bähr Mathias 
Published: January 2005

AbstractTo determine mechanisms of structural plasticity in adult CNS neurons, we investigated the expression of immediate early genes (IEGs) in the rat retina. Gene products of different IEG families (JUN and FOS proteins) and cAMP‐responsive element binding protein (CREBP) were examined by immunohistochemistry under three different paradigms. Normal rats which were not axotomized were compared with axotomized animals, where retinal ganglion cells (RGCs) were axotomized by intraorbital optic nerve cut and retrogradely labeled with fluorogold (FG). Under these circumstances, RGCs show only transient sprouting, followed by continuous retrograde RGC degeneration. In the third group, after the optic nerve lesion, adult rats additionally received a sciatic nerve graft to the transected optic nerve stump. This allows some RGCs to regenerate an axon into the grafted nerve. In both groups, the time course of RGC survival and JUN, CREB, and FOS protein expression was monitored. In normal animals, JUN‐Immunoreactivity (JUN‐Ir) was not detectable in the retinal ganglion cell layer. JUN‐Ir was induced in about 70% of all FG‐positive RGCs 5 days after axotomy. The expression of JUN‐Ir started to decline 8 days after axotomy. Only a few JUN‐Ir‐positive RGCs were found after 2 weeks. In transplanted animals, however, the numbers of JUN‐Ir‐positive RGCs were significantly higher 2 and 3 weeks after transplantation compared to animals that exclusively received axotomy. Furthermore, in grafted rats about 70% of the regenerating RGCs expressed JUN‐Ir 2 weeks after grafting as compared to only 38% JUN‐positive RGCs among the surviving but not regenerating RGCs. In normal animals CREBP‐Ir was constitutively expressed in nearly all cells of the retinal ganglion cell layer. The decline in number of CREBP‐Ir‐positive cells paralleled the axotmy‐induced RGC death. FOS‐Ir‐positive cells were not found in the ganglion cell layer at any time. These results demonstrate a selective and transient JUN expression of RGCs after axotomy which is sustained during axonal regeneration. This suggests that sciatic nerve grafts are able to regulate the expression of JUN proteins in axotomized RGCs of adult rats. 1994 John Wiley & Sons, Inc.
Expression of NGF receptor and GAP‐43 mRNA in DRG neurons during collateral sprouting and regeneration of dorsal cutaneous nerves
Authors: Mearow K. M. , Kril Y. , Gloster A. , Diamond J. 
Published: January 2005

AbstractThe collateral sprouting of intact sensory axons and the regenertion of damaged ones differ in a number of respects. Regeneration is triggered by axotomy‐induced damage, probably involves the loss of a peripheral signal, and appears to occur independently of NGF, while collateral sprouting is evoked and sustained by an increase in a target‐driven signal, namely NGF. New findings strengthen the distinction between these two phenomena. Nerve growth factor receptor (NGFR) mRNA is increased in undamaged DRG neurons whose axons are sprouting into denervated skin. This response is related to an increased availablity of target‐derived NGF, a proposal supported by a number of findings including increased NGF mRNA in the denervated target. In contrast, we observed little or no change in the NGFR mRNA levels in regenerating neurons, consistent with the observations that NGF does not play a role in this process. However, increases in neuronal GAP‐43 mRNA are found during both regeneration and collateral sprouting, a result in keeping with the proposal that GAP‐43 is primarily associated with nerve growth, and the observation that GAP‐43 expression is not especially influenced by NGF. 1994 John Wiley & Sons, Inc.
Calcium regulation of gene expression in neuronal cells
Authors: Ghosh Anirvan , Ginty David D. , Bading Hilmar , Greenberg Michael E. 
Published: January 2005

AbstractLong‐term adaptive changes in neurons following brief periods of neuronal activity are likely to involve changes in gene expression. The mechanisms of activity‐dependent gene expression have been explored in central neurons and the neuronal cell line PC12. Calcium influx through either NMDA receptors or voltage‐sensitive calcium channels leads to the rapid induction of a number of immediate‐early genes including c‐fos. Promoter analysis indicates that Ca2+ influx through different calcium channels activates distinct signaling pathways that either target the serum response element (SRE) or the calcium response element (CaRE) within the c‐fos promoter. Transcription through the CaRE requires the induced phosphorylation of the cAMP response element binding protein (CREB) at Ser133. This site on CREB is also phosphorylated in the suprachiasmatic nucleus in in vivo upon light stimulation. These observations suggest Ca2+ can regulate gene expression by multiple signaling pathways including one that involves the Ca2+‐dependent phosphorylation of the transcription factor CREB. 1994 John Wiley & Sons, Inc.
Excitatory interaction between glutamate receptors and protein kinases
Authors: Soderling T. R. , Tan S. E. , McGlade‐McCulloh E. , Yamamoto H. , Fukunaga K. 
Published: January 2005

AbstractOne of the most active areas of neurobiology research concerns mechanisms involved in paradigms of synaptic plasticity. A popular model for cellular leaning and memory is long term potentiation (LTP) in hippocamus. LTP requires postsynaptic influx of Ca2+ which triggers multiple biochemical pathways resulting in pre‐ and postsynaptic mechanisms enhancing long term synaptic efficiency. This article focuses on an acute postsynaptic Mechanism that can enhance responsiveness of glutamate receptors. Evidence is presented that calcium/calmodulin/dependent protein kinase II, the major potsynaptic density protein at excitatory glutaminergic synapses, can phosphorylate glutamate receptors and enhance ion current flowing through them. 1994 John Wiley & Sons, Inc.
Proteolytic activity, synapse elimination, and the Hebb synapse
Authors: Liu Y. , Fields R. D. , Fitzgerald S. , Festoff B. W. , Nelson P. G. 
Published: January 2005

AbstractThe Hebb synapse has been postulated to serve as a mechanism subserving both regulation of synaptic strength in the adult nervous system (long‐term potentiation and depression) and developmental activity‐dependent plasticity. According to this model, pre‐ and postsynaptic temporal concordance of activity results in strengthening of connections, while discordant activity results in synapse weakening. Evidence is presented that proteases and protease inhibitors may be involved in modification of synaptic strength. This leads to a modification of the Hebb assumptions, namely that postsynaptic activity results in protease elaboration with a consequent general reduction of synaptic connections to the active postsynaptic element. Further, presynaptic activity, if strong enough, induces local release of a protease inhibitor, such as protease nexin I, which neutralizes proteolytic activity and produces a relative preservation of the active input. This formulation produces many of the effects of the classical Hebbian construction, but the protease/inhibitor model suggests additional specific mechanistic features for activity‐dependent plasticity. 1994 John Wiley & Sons, Inc.
Vasopressin‐induced neurotrophism in cultured hippocampal neurons via V1 receptor activation
Authors: Brinton Roberta Diaz , Monreal Alex W. , Fernandez Judivick G. 
Published: January 2005

AbstractStructural enhancement of nerve cell morphology has been postulated to be an integral step in the cellular process leading to information storage in the nervous system. To investigate this postulate, we determined whether vasopressin (AVP), a neural peptide that can enhance memory function, would enhance the cytoarchitectural features of hippocampal neurons in culture. Results of these studies demonstrated that in the presence of serum, vasopressin (1 μM), induced a significant in crease in the number of neurites, in neuritic length, and in neurite diameter following 48 h of exposure. Morphological complexity was also enhanced following vasopressin exposure as indicated by a significant increase in the number of filopodia/branches, in the sum of branch lengths, and in the number of branch bifurcation points. The number of microspikes decorating neuritic branches was also significantly increased following vasopressin exposure. To determine whether the neurotrophic effects of vasopressin was dependent upon factors present in serum, hippocampal nerve cells were cultured in serum‐free media and exposed to 100–1000 nM AVP. Results of these studies demonstrated that in the absence of serum, AVP induced significant enhancement of hippocampal nerve cell growth and that the minimally effective concentration was reduced from 1 μM, as required in the presence serum, to 100 nM. In addition, the time required for a significant increase in nerve cell growth to become apparent decreased from 48 to 24 h. These results demonstrate that AVP‐induced neurotrophism is not dependent upon unidentified factors in serum. AVP‐induced neurotrophism was found to be mediated by V1 receptor activation. Significant enhancement of nerve cell growth occurred following exposure to V1 receptor agonist (100–1000 nM), whereas exposure to V2 receptor agonist (100–1000 nM) did not increase any of the morphological parameters measured. Considered together, these data indicate that vasopressin can exert a significant neurotrophic effect upon hippocampal nerve cells in culture. Moreover, AVP‐induced neurotrophism is a direct effect and not dependent upon unidentified factors present in serum. Enhancement of hippocampal nerve cell growth occurred in the presence of a specific V1 receptor agonist and not following exposure to a V2 agonist, suggesting that activation of the phosphatidyl inositol pathway via V1 receptor activation mediates AVP‐induced neurotrophism. Results of these studies are discussed with respect to their implications for understanding vasopressin involvement during neural development and induction of cytoarchitectual modifications associated with memory formation. 1994 John Wiley & Sons, Inc.
Spatiotemporal pattern of expression of tenascin‐like molecules in a developing insect olfactory system
Authors: Krull Catherine E. , Morton David B. , Faissner Andreas , Schachner Melitta , Tolbert Leslie P. 
Published: January 2005

AbstractDuring the development of the olfactory (antennal)l lobe of the moth Manduca sexta, olfactory sensory axons induce glamerular branching patterns in their target neurons. Glial cells, by surrounding the developing glomerular template, are thought to mediate the developmental influence of olfactory axons on these branching patterns. Previous studies have demonstrated that, in the absence of glia, neurons in the antennal lobe branch in an aglomerular fashino, even in the presence of competent antennal axosn (Oland and Tolbert, 1988, J. Comp. Neurol. 278:377–387; Oland et al., 1988, J. Neurosci. 8:353–367). We have begun to explore the molecular basis by which glial cells could influence patterns of neurite branching. For this work, we have utilized immonocytochemical techniques and a partial biochemical analysis to demonstrate that molecules antigenically similar and comparable in size to mammalian tenascin are localized on the neuropil‐associated glial cells that form borders aroudn glomeruli in the developig antennal lobe. These tenascin‐like molecules associated with neuropilar glia are present at critical stages of glomerulus development; tenascin‐like immunoreactivity declines after glomeruli form and become stabilized. Neither the arrival nor the absence of antennal axons in the lobe induces changes in either the molecular forms or the amounts of tenascin‐like molecules. The spatiotemporal pattern of expression to tenascin‐like molecules suggests that they are in a position to participate in the formation of a glomerular neuropil and could form a molecular barrier that constrains neurite outgrowth strictly to glomeruli. © 1994 John Wiley & Sons, Inc.
Characterization and localization of D1 dopamine receptors in the sexually dimorphic vocal control nucleus, area X, and the basal ganglia of european starlings
Authors: Casto Joseph M. , Ball Gregory F. 
Published: January 2005

AbstractD1 dopamine receptors were pharmacologically characterized and localized by quantitative autoradiography in the basal ganglia of male and female European starlings (Sturnus vulgaris). The D1 selective antagonist SCH 23390 was used to label this receptor subtype. Starlings are songbirds and possess a neural circuit implicated in the learning and production of song. This circuit includes a sexually dimorphic nucleus, area X, that is a subregion of the parolfactory lobe of the basal ganglia and is known from work on zebra finches to receive dopaminergic input from the area ventralis of Tsai. We focused our investigation on the D1‐like receptor subtype because they are abundant in the basal ganglia. Competition studies indicate that a variety of dopaminergic ligands compete with [3H] SCH 23390 for the binding site in an order of potency characteristic of a D1‐like receptor. Autoradiographic studies of the basal ganglia revealed high D1 receptor densities in the avian homologues of the caudate‐putamen and relatively low‐receptor densities were observed in the avian homologue of the globus pallidus. In male starlings, area X could be reliably discerned on the autoradiograms by the higher density of D1 receptors compared to the surrounding parolfactory lobe (LPO). This was also true for females, though nt as reliably as in males. When we compared the mean D1 receptor density in area X for males and females we did not find a significant sex difference. However, we also analyzed the data by comparing sex differences in the degree to which area X has a higher receptor density in comparison with the surrounding LPO. When we normalized D1 receptor density in area X relative to the LPO, we did find a significant sex difference. This sex difference in relative receptor density represents another neural sex difference in the song circuit that may mediate sex differences in the learning and production of song in starlings and other songbirds. 1994 John Wiley & Sons, Inc.
The molecular cloning and characterization of potential chick DM‐GRASP homologs in zebrafish and mouse
Authors: Kanki John P. , Chang Susannah , Kuwada John Y. 
Published: January 2005

AbstractA full‐length zebrafish cDNA clone and a partial mouse cDNA clone similar to chick DM‐GRASPwere isolated and analyzed. The nucleotide sequence of the full‐length zebrafish clone shares 54% identity, and predicts 39% amino acid identity, with chick DM‐GRASP. The partial mouse clone shares 76% nucleotide identity, and predicts 76% amino acid identity, with chick DM‐GRASP. The predicted proteins encoded by both of these clones exhibit conserved structural domains that are characteristic of the chick protein. These features may identify them as a distinct subfamily within the immunoglobulin superfamily of cell adhesion molecules. Express of the zebrafish DM‐GRASP protein is similar to chick DM‐GRASP and is principally restricted to a small subset of developing sensory and motor neurons during axonogenesis. Zebrafish DM‐GRASP expression was temporally regulated and limited to specific axon domains. This regional expression correlated with fasciculated axon domains. These results suggest that the zebrafish and mouse cDNA clones represent the respective fish and mammalian homologs of thick DM‐GRASP. The highly selective expression of zebrafish DM‐GRASP suggests that it is involved in the selective fasciculation and guidance of axons along their normal pathways. 1994 John Wiley & Sons, Inc.
Neurotrophin‐4/5 (NT‐4/5) increases adult rat retinal ganglion cell survival and neurite outgrowth in vitro
Authors: Cohen A. , Bray G. M. , Aguayo A. J. 
Published: January 2005

AbstractRetinal ganglion cell (RGC) survival and neurite outgrowth were investigated in retinal explants from adult rats. Neutrotrophin‐4/5 (NT‐4/5) caused dose‐dependent increases in neurite outgrowth with one‐half maximal effects at approximately 0.5 ng/ml and maximal effects at 5 ng/ml. In explants treated for 7 days, the actions of NT‐4/5 were similar to those of brain‐derived neurotrophic factor (BDNF); with either neurotrophin, nearly twice as many RGCs survived and there was a two‐ to threefold increase in the number of neurites formed by RGCs. Combinations of saturating concentrations of NT‐4/5 and BDNF did not enhance these in vitro effects, implying that both neurotrophins share a common signaling pathway. In contrast, nerve growth factor (NGF), neurotrophin‐3 (NT‐3), or ciliary nuerotrophic factor (CNTF) appeared to exert minimal influences on RGC survival or neurite outgrowth. 1994 John Wiley & Sons, Inc.