bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interaction of ganglioside GM1 with the B subunit of cholera toxin modulates intracellular free calcium in sensory neurons
Authors: Milani D. , Minozzi M.‐C. , Petrelli L. , Guidolin D. , Skaper S. D. , Spoerri P. E. 
Published: January 2005

AbstractThe B subunit of cholera toxin, which binds specifically to GM1 ganglioside on cell surfaces, has previously been shown to modulate intracellular calcium levels and growth in several cell types. To explore a role for such changes in calcium in the growth regulatory function of cell‐associated GM1 in neurons, dissociated neurons from chicken embryonic day 8 dorsal root ganglia were exposed to the B subunit. To enhance sensitivity to B subunit, some neurons were also enriched with added GM1 (100 μM) and then exposed to B subunit. Incubation of naive cultures with 1 μg/ml of the B subunit was sufficient to produce modest increases in intracellular free calcium above basal levels in a minor percentage of cells for at least 5 min, as measured by fura‐2 fluorescence imaging. Pretreatment of the cells with GM1 for 48 hr increased even further the elevations in intracellular free calcium and the percentage of responding neurons observed after B subunit exposure. These in creases in intracellular calcium required the presence of external Ca2+, but were not inhibited by calcium channel blockers. Such changes in calcium were accompanied by fine alterations in morphology affecting mostly the branching of neurites and were more pronounced in the presence of GM1. However, the morphological changes did not result in altered neurofilament protein expression. Immunogold electron microscopy using anti‐choleragenoid depicted extensive aggregations of immunoreactive gold particles on neuronal surfaces, which were more extensive in cells treated with GM1. The results demonstrate that cell incorporated GM1 may modulate calcium fluxes, perhaps accounting for the growth regulatory functions of GM1 in both neuronal and other cell types. © 1992 Wiley‐Liss, Inc.
Treatment of relapsing experimental autoimmune encephalomyelitis with T cell receptor peptides
Authors: Whitham R. H. , Kotzin B. L. , Buenafe A. C. , Weinberg A. D. , Jones R. E. , Hashim G. A. , Hoy C. M. , Vandenbark A. A. , Offner H. 
Published: January 2005

AbstractRestricted T cell receptor (TCR) VB gene usage by T cells for recognition of antigens involved in the production of experimental autoimmune encephalomyelitis (EAE) offers the possibility of selective immunotherapy. We determined the preferential VB gene usage of lymph node‐derived clones from SJL/J mice to recognize the encephalitogenic epitope PLP 139‐151 and from PL/J mice to recognize the newly described encephalitogenic epitope PLP 43‐64. In addition, the VB gene usage for recognition of PLP 139‐151 by T cell lines derived from SJL/J spinal cords was analyzed. Lymph node‐derived SJL/J lines and clones specific for PLP 139‐151 expressed VB2, VB4, and VB17a preferentially, and PL/J lines and clones specific for PLP 43‐64 expressed VB2 and VB8.2 preferentially. A VB4+ SJL/J clone and a VB8.2+ PL/J clone were encephalitogenic. Encephalitogenic SJL/J lines derived from spinal cord expressed VB2, VB10, VB16, and VB17a preferentially, with a predominance of VB2. Candidate TCR peptides were synthesized and tested from the VB gene families VB4, VB8.2, and VB17a, based on our data and previous data on BP‐induced EAE in mice. Treatment of relapsing EAE (R‐EAE) in SJL/J mice with VB4 and VB17a peptides reduced clinical and histological disease severity, and treatment of R‐EAE in (PLxSJL)F1 mice with VB4 and VB8.2 peptides also reduced clinical and histological disease. The use of TCR peptide therapy may have applications for the treatment of human autoimmune diseases such as multiple sclerosis. © 1993 Wiley‐Liss, Inc.
Sp1 binds to the adhesion molecule on glia regulatory element that functions as a positive transcription regulatory element in astrocytes
Authors: Kawakami K. , Watanabe Y. , Araki M. , Nagano K. 
Published: January 2005

AbstractWe analyzed cis‐acting elements regulating the expression of the gene encoding adhesion molecule on glia (AMOG) in primary cultured astrocytes from newborn rat cerebrum and cerebellum. The relative promoter activities among the series of 5‐ sequential deletion mutants are similar to those observed in B103 (rat neuroblastoma cell line) cells. The previously identified AMRE (AMOG regulatory element) of the GAGGCGGGG sequence functions as a positive regulatory element, not only in B103 cells, but also in astrocytes. Binding factors to the element were identified as Sp1 based on the following observations using nuclear extracts from the astrocytes and B103 cells: (1) The interaction of the factors with AMRE analyzed by DNase I footprinting and methylation interference analyses was similar to that of Sp1; (2) The binding of the factors to AMRE competed with an oligonucleotide containing the authentic Sp1 consensus sequence; (3) Sp1‐specific antibody interfered with the formation of the AMRE gel retardation complexes. The functional implications of the factors in AMOG gene regulation are discussed. © 1993 Wiley‐Liss, Inc.
Elevated expression of B‐50 (GAP‐43)‐mRNA in a subpopulation of olfactory bulb mitral cells following axotomy
Authors: Verhaagen J. , Zhang Y. , Hamers F. P. T. , Gispen W. H. 
Published: January 2005

AbstractNeurons in the central nervous system regenerate poorly or not at all. In contrast neurons of the peripheral nervous system have the ability to regrow their nerve fibers over considerable distances. Previously it has been suggested that the absence of the reinduction of the expression of growth associated proteins such as B‐50 (GAP43) may be an important factor in the differential response of CNS and PNS neurons to injury. We studied B‐50(GAP43) mRNA expression following lesioning of a class of CNS neurons, the olfactory bulb mitral cells. Expression of B‐50 mRNA in approximately 40% of the mitral cells was upregulated in response to transection of their axons in the lateral olfactory tract (LOT). Enhanced expression persisted for 10 days postlesion but had virtually declined to control levels by 4 weeks after the lesion. A large proportion of the mitral cells gradually degenerated subsequent to LOT transection. Thus a subpopulation of mitral cells maintains their ability to upregulate B‐50, a protein characteristic of growing axons, but enhanced B‐50 expression is not accompanied by regeneration of the severed LOT. © 1993 Wiley‐Liss, Inc.
Development of NMDA receptor‐channel complex and L‐type calcium channels in mouse hippocampus
Authors: Glazewski S. , Skangiel‐Kramska J. , Kossut M. 
Published: January 2005

AbstractIn vitro binding autoradiography was used to examine the pattern and intensity of binding of [3H]glutamate to NMDA receptors, [3H]MK 801 to NMDA receptor associated channels in and [3H]PN‐200 110 to L‐type calcium channels in the hippocampus of mice aged 3–70 days. The distribution of NMDA receptors and NMDA receptor associated channels was similar but not identical at the tested ages. Beginning with postnatal day 8, high binding levels were confined mostly to the hippocampal strata: the oriens and radiatum (CA1 and CA3 with [3H]MK 801 labeling but only CA1 with NMDA displaced [3H]glutamate labeling), the moleculare (higher labeling with [3H]MK 801 than with NMDA displaced [3H]glutamate binding), and the lucidum. The binding values for NMDA receptor‐channel complex rose in the examined period (especially within the second and third week), reaching a plateau at the end of the third postnatal week. Sharp growth of binding within the second and third week of life was about 50% greater with [3H]MK 801 than with NMDA displaced [3H]glutamate labeling. L‐type calcium channels were found to be most abundant in the strata: the oriens of the CA3 field, the moleculare, and the lucidum. The time course of binding value changes for the calcium channel was similar to the time course found for the NMDA receptor‐channel complex. © 1993 Wiley‐Liss, Inc.
Nerve growth factor changes G protein levels and localization in PC12 cells
Authors: Zubiaur M. , Neer E. J. 
Published: January 2005

AbstractGrowth cones at the growing tips of developing neurites contain the machinery to transmit information from receptors to a variety of intracellular enzymes and ion channels. In order to understand how signals are transmitted across the membrane, we asked whether the multiplicity of signalling pathways in the growth cone is reflected by the diversity of G proteins found in this organelle. Our immunohistochemical analysis indicated that growth cones of differentiated PC12 cells contain at least 4 α G protein subunits, 3 that are pertussis toxin substrates (α0, αi−1, αi−2) and 1 that is not (αq). In addition to localization in the neurites and growth cones, α0, αi−1, αi−2, and αq were detected in intracellular perinuclear structures. We also analyzed the temporal change in G proteins in PC12 cells differentiated by treatment with nerve growth factor (NGF). Time course experiments have shown that α0 and β proteins coordinately increase after 2 days of treatment with NGF, reach a maximum at 4 days, and remain elevated. In contrast to α0, αi−2 reached a peak at 4 days, then declined to almost the basal level by day 7 of treatment with NGF. These data indicated that the levels of α0, αi−2, and β are differentially regulated during NGF‐induced neuronal differentiation in PC12 cells. The α0 protein was highly concentrated at the tips of the growth cones before the cellular level of α0 had increased appreciably, suggesting that the α subunits are translocated during the first stage of neurite development. In addition, not every neural process has the same high level of α0, suggesting that G proteins may help define the specialized functions of particular neurites within a single cell. © 1993 Wiley‐Liss, Inc.
Maternal dietary fish oil enriches docosahexaenoate levels in brain subcellular fractions of offspring
Authors: Yeh Y.‐Y. , Gehman M. F. , Yeh S.‐M. 
Published: January 2005

AbstractPrompted by the speculated essentiality of docosahexaenoic acid (DHA) for neural development, this study was undertaken to investigate the incorporation of (n‐3) fatty acids in the maternal diet into various phospholipids of infant rat brain subcellular fractions: microsomes (Ms), synaptosomes (Sy), myelin (My), and mitochondria (Mt). Two groups of infant rats were nourished by dams fed diets containing 20% of either corn oil (CO) or menhaden oil (MO) from 2 until 12 days of age. DHA but not eicosapen taenoic acid (EPA) was distributed to all subcellular fractions of infant rats in the CO group. The levels of DHA were higher in Ms and Mt than Sy and My, and higher in phosphatidylethanolamine (PE) and phosphatidylserine (PS) than phosphadylcholine (PC) and phosphatidylinositol (PI). The MO feeding enriched DHA in PE of all subcellular fractions, PS of all subcellular fractions, except My, PC of Sy, My and Mt, and PI of My. EPA was enriched in phospholipids in all subcellular fractions, except mitochondrial PS of the MO group. In the MO group, the ratios of EPA/ DHA, ranging from 0.01 to 0.85, in all subcellular phospholipids were markedly lower than that found in the mother‐s milk (i.e., 1.5), suggesting an ability to elongate and desaturate EPA to DHA and/or disproportional uptake of the fatty acids by the brain. In PE of all subcellular fractions, the increased levels of DHA and EPA, with a concomitant reduction of arachidonic and/or linoleic acid, yielded higher ratios of total (n−3)/(n−6) fatty acids in the MO than the CO group. The inclusion of preformed DHA and EPA in the maternal diet provides an effective means to enrich these fatty acids in developing brains. © 1993 Wiley‐Liss, Inc.
Testosterone regulation of the regenerative properties of injured rat sciatic motor neurons
Authors: Kujawa K. A. , Jacob J. M. , Jones K. J. 
Published: January 2005

AbstractWe have previously demonstrated that systemic administration of testosterone differentially regulates the regenerative properties of injured hamster facial motor neurons, which are androgen receptor‐containing cranial motor neurons. In this investigation the hypothesis that testosterone alters the regenera‐ tive properties of rat sciatic motor neurons, which are androgen receptor‐containing spinal motor neurons, was tested using fast axonal transport of radioactively labeled proteins to assess sciatic nerve regeneration. Adult castrated male rats were subjected to crush axotomy of the sciatic nerve at the level of the gemelli tendons (mid‐thigh). One‐half of the axotomized animals received subcutaneous implants of testosterone propionate (TP), with the remainder of the animals sham implanted with blank capsules. The outgrowth distances of the leading axons were measured at 5, 6, 7, and 11 days postoperative. Linear regression analysis was accomplished, with the slope of the line representing the regeneration rate and the x‐intercept the initial delay of sprout formation. Systemic administration of testosterone resulted in a 13% increase in the rate of regeneration, relative to the control, –TP group. Outgrowth distances were significantly increased in the 4‐ TP group only in the later stages of regeneration. However, TP did not shorten the delay in sprout formation in regenerating sciatic motor neurons, but instead produced a small prolongation in the delay time. This pattern of hormonal regulation of the regenerative properties of spinal motoneu‐ rons is similar to that previously found in cranial motoneurons. The prolongation of the initial delay may have been a factor in the lack of significant outgrowth distances during the early stages of regeneration. The magnitude of the effects of TP on male rat sciatic motor neurons are less pronounced than in male hamster facial motor neurons, but quite similar to those effects observed in female hamster facial motor neurons. Why this is the case is not known, but may be related to a irumber of factors discussed in the text. © 1993 Wiley‐Liss, Inc.
Cerebellar and striatal dopamine receptors: Effects of reeler and weaver murine mutations
Authors: Panagopoulos N. T. , Matsokis N. A. , Valcana T. 
Published: January 2005

AbstractThe presence and the binding characteristics of D1 and D2 receptors were investigated in normal‐reeler and normal‐weaver mutant mice utilizing [3H]spiperone (D2 antagonist), [3H]SKF 38393 (D1 agonist), and [3H]DA as ligands. Analysis of the binding data showed that in the cerebellum there are two binding components for all [3H]ligands. Comparison of the binding constants from cerebellum and striatum showed that in cerebellum the high affinity‐low capacity component has similar affinity with that of striatum. The reeler and weaver mutations affected the binding of all ligands: In reeler, total cerebellar specific binding sites for [3H]spiperone and [3H]SKF 38393 decrease significantly (≈50% and ≈70%, respectively), while those for [3H]DA show a small (≈10–15%) but not significant decrease. In weaver, total cerebellar specific binding sites for [3H]spiperone, [3H]SKF 38393, and [3H]DA also decrease significantly (≈60%, ≈70%, and ≈50%, respectively). In reeler striatum [3H]SKF 38393 binding (Bmax) is significantly decreased (≈24%), while [3H]spiperone and [3H]DA binding (Bmax) is not affected. In weaver striatum, [3H]SKF 38393 binding is significantly increases significantly (≈40%), while [3H]DA binding (Bmax) decreases significantly (≈70%). On the basis of the cytoarchitectural aberrations that characterize the cerebellum of these mutants and some well‐established information regarding the dopaminergic system of the cerebellum, the above results indicate that in this region (a) D1 receptors are mainly localized on granule cells and (b) D2 receptors are localized postsynaptically on granule cells and presynaptically on the DA fibers innervating the cerebellum. © 1993 Wiley‐Liss, Inc.
Molecular cloning of the myelin basic proteins in the shark, Squalus acanthias, and the ray, Raja erinacia
Authors: Spivack W. D. , Zhong N. , Salerno S. , Saavedra R. A. , Gould R. M. 
Published: January 2005

AbstractMyelin basic proteins (MBPs) are a family of alternatively spliced isoforms present in myelin sheaths of most vertebrates. A reverse transcriptase‐polymerase chain reaction (RT‐PCR) approach was used to clone MBP isoforms in species representing two superorders of elasmobranchs: Squalus acanthias, representing Squalomorph sharks, and Raja erinacia, representing Batoidea rays. Two products were generated from each species. The larger product encoded a 155 amino acid protein, the same size as MBPs from two Galeomorph sharks, Heterodontus francisci and Carcharhinus obscurus, which, based upon alignment with other vertebrate MBPs, contained six of the seven MBP exons; only exon II was absent. The smaller product encoded a 141 amino acid protein that lacked exon II and exon V. There were 26 and 30 nucleotide differences between Squalus and Heterodontus, and Raja and Heterodontus, respectively. Sequences from Squalus and Raja were far more similar, having only five nucleotide differences. Both isoforms of elasmobranch MBP contain 18.5% basic (lysine plus arginine) amino acids, compared with 17.5% in mammalian MBPs comprised of the corresponding exons. Northern blot analysis of whole brain total RNA revealed a single band of 2.5 kb in Squalus, and three bands of 1.2, 1.4, and 2.3 kb in Raja. The finding that MBPs of a Squalomorph shark and a Batoidea ray are closer to one another than either is to the Galeomorph sharks suggests that MBP sequence information may prove useful in classifying modern day Chondrichthytes. © 1993 Wiley‐Liss, Inc.
Myelin basic protein mRNA translocation in oligodendrocytes is inhibited by astrocytes in vitro
Authors: Amur‐Umarjee S. , Phan T. , Campagnoni A. T. 
Published: January 2005

AbstractMyelin basic protein (MBP) mRNAs are translocated from cell bodies into the slender processes connecting oligodendrocyte somas with the myelin sheath in vivo. This translocation was observed in mixed glial cultures prepared from newborn mouse brains and it occurred in approximately 25% of the cells expressing the gene. However, when “enriched” oligodendrocytes were prepared by shaking them free of other glial cells, MBP mRNA translocation occurred into the processes of essentially all of the cells. When enriched oligodendrocytes were plated back onto astrocytes, MBP mRNA was observed to be confined to the cell bodies of almost all the cells, indicating a marketd inhibition of translocation of the mRNA. This inhibition of mRNA translocation did not appear to be mediated through soluble factors secreted by astrocytes or by “astromatrix,” but rather through physical contact between the oligodendrocytes and astrocytes. Intact, but not necessarily live, astrocytes were required for the inhibition of mRNA translocation in the oligodendrocytes. Fibroblasts and a neuroblastoma cell line, SKN‐SH, did not inhibit MBP mRNA translocation in oligodendrocytes suggesting that astrocyte surface‐specific components might be involved in the interaction between astrocytes and oligodendrocytes in culture. These results suggest that contact between these two cell types can influence intramolecular events related to myelinogenesis. © 1993 Wiley‐Liss, Inc.
Nerve growth factor stimulates GAP‐43 expression in PC12 cell clones independently of neurite outgrowth
Authors: Burry R. W. , Perrone‐Bizzozero N. I. 
Published: January 2005

AbstractExpression of the growth associated protein GAP‐43 (B‐50, F1, neuromodulin) increases with the onset of neuronal development as seen by the growth of axons. To investigate the relationship of the signaling events leading to GAP‐43 expression and neurite outgrowth, we examined PC12 clones with different phenotypes. Three clones, PC12‐NO9, PC12‐N15, and PC12‐N21, responded to NGF with increased expression of GAP‐43, but only two clones, PC12‐N15 and PC12‐N21, responded with growth of neurites. Similar increases in expression of GAP‐43 were obtained when these clones were exposed to the phorbol ester PMA. Thus, NGF and PMA induced GAP‐43 expression in PC12‐NO9 cells in the absence of neurite outgrowth. In contrast, all three clones, were able to respond to forskolin (FOR) by initiation of long neurites which had synaptophysin in the growth cones, but showed only low levels of GAP‐43. Combined stimualtion of PC12‐NO9 cells with FOR and PMA both initiated neurites and increased expression of GAP‐43 as seen in normal PC12 clones were also able to respond to FOR with increased neurite outgrowth in the presence of low levels of GAP‐43. The dissociation of GAP‐43 expression and growth of neurites observed in PC12‐NO9 cells suggests that signaling mechanisms can independently regulate GAP‐43 expression and neurite outgrowth during neuronal differentiation. © 1993 Wiley‐Liss, Inc.
Bradykinin and capsaicin stimulate cyclic GMP production in cultured rat dorsal root ganglion neurons via a nitrosyl intermediate
Authors: Bauer M. B. , Simmons M. L. , Murphy S. , Gebhart G. F. 
Published: January 2005

AbstractDorsal root ganglion (DRG) neurons express receptors for bradykinin and capsaicin, both algesic substances. Administration of bradykinin or capsaicin to neurons cultured from embryonic rat DRG stimulated the production of cyclic GMP but in nonneuronal DRG cultures. Bradykinin‐evoked Cyclic GMP production was mediated by B2 receptors and was unaltered by indomethacin. Both bradykinin‐ and capsaicin‐stimulated cyclim GMP production required Ca2+ and was inhibited by methylene blue. Furthermore, methylene blue attenuated basal cyclic GMP production in DRG neurons, suggesting tonic cyclic GMP production in these Cells. L‐NG‐monomethyl arginine inhibited both bradykinin‐and capsaicin‐stimulated cylic GMP production as well as basal cyclic GMP production. These findings suggest the involvement of a nitrosyl compound in bradykinin‐and capsaicinstimulated cyclic GMP production and in tonic cyclic GMP production in DRG Neurons. © 1993 Wiley‐Liss, Inc.
Retinal morphology and visual pigment levels in 6‐and 12‐month‐old rhesus monkeys fed a taurine‐free human infant formula
Authors: Imaki H. , Jacobson S. G. , Kemp C. M. , Knighton R. W. , Neuringer M. , Sturman J. 
Published: January 2005

AbstractRhesus monkey infants were raised from birth until 6 or 12 months of age on a taurine‐free soy protein based human infant formula or on the same formula supplemented with taurine. An additional group received taurine‐free formula until 6 months. The densities of rod and cone visual pigments were measured by fundus reflectometry at 6 and 12 months, and retinal morphology was then examined by light and electron microscopy. The densities of rhodopsin, measured in the near periphery after a white bleach, and of cone pigment, measured in the macula after a red bleach, were significantly reduced in the taurine deprived monkeys at 6 months but not at 12 months. The retinas of 6‐month‐old taurine‐deprived infants showed degenerative morphological changes in photoreceptors, particularly in cones in the foveal region, which were somewhat less severe than those seen in a previous study at 3 months of age. The prevalence and degree of these abnormalities continued to decrease with age in taurine‐deprived animals, but changes persisted in some animals at 12 months. Recovery was more complete in monkeys reversed to the supplemented diet from 6 to 12 months. Thus, monkey infants are dependent on dietary taurine to maintain normal retinal structure until at least 6 months of age; the effects of taurine deprivation regress spontaneously but incompletely by 12 months. © 1993 Wiley‐Liss, Inc.