bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased density of perivascular adrenergic innervation in tibial and vagus nerves of spontaneously hypertensive rats
Authors: Koistinaho J. , Wadhwani K. C. , Rapoport S. I. 
Published: January 2005

AbstractAdrenergic innervation of epiperineurial arterioles and of the endoneurium of the tibial and vagus nerves of spontaneously hypertensive rats (SHR) and normotensive controls. (WKY) was studied by glyoxylic acid‐induced fluorescence and paraformaldehyde‐induced fluorescence methods. Adrenergic perivascular innervation of epiperineurial arterioles in both nerves was denser in SHR than in controls. Mean density in the endoneurium also was higher in SHR in both nerve types. These results suggest that adrenergic perivascular innervation, which may influence nerve blood flow, becomes greater in density in peripheral nerves during chronic hypertension.
Progressive restriction in the distribution of the Hox‐1.3 homeodomain protein during embryogenesis
Authors: Tani M. , Odenwald W. F. , Lazzarini R. A. , Friedrich V. L. 
Published: January 2005

AbstractExpression of the murine homeobox containing gene Hox‐1.3 was analyzed in mouse embryos using polyclonal antisera to peptides predicted from cDNA and genomic sequences. At the earliest stage examined, 7.5 days gestation, cell nuclei throughout the three embryonic germ layers and in extraembryonic structures derived from the fertilized ovum were strongly immunoreactive. Rostro‐caudal gradients or other patterns of regional differentiation in levels of expression could not be seen. Surrounding maternal tissue showed only weak immunoreactivity. At 8.5 days gestation, immunoreactivity was present in all embryonic structures including neural tube, somites and lateral plate mesoderm, ectoderm and endoderm. Immunoreactivity was progressively restricted thereafter. At 17 days gestation, strong immunoreactivity was largely restricted to the nervous system, both central and peripheral. Spinal cord was well stained, with a dramatic reduction in intensity near the junction of spinal cord and brain. In addition to this overall pattern, enhanced immunoreactivity appeared in limited populations of newly‐formed neuroblasts of spinal cord and brain, suggesting that Hox‐1.3 might serve to regulate the development of specific types of neurons following cessation of precursor cell mitosis.
Heat stress increases delivery of a unique sub‐population of proteins conveyed by fast axonal transport
Authors: Stone G. C. , Dougher M. M. 
Published: January 2005

AbstractThe effect of heat stress on protein synthesis and fast axonal transport was examined in vitro in bullfrog dorsal root ganglion (DRG) and associated spinal/sciatic nerve. Qualitative and quantitative changes of individual 35S‐methionine‐labelled proteins were determined following DRG labelling and fast transport in respective nerves via two‐dimensional gel electrophoresis/autoradiography. Elevation of temperature from 18°C to 33°C for up to 6 hr resulted in a marked increase in synthesis of five individual DRG species of approximately 74,000 daltons that comigrate with heat shock proteins (HSPs). A quantitative comparison of species within this subset revealed two subgroups differentially affected by stress. The three most basic proteins were induced to approximately 1300% of unstressed controls after 6 hr of stress, while the two most acidic species demonstrated an increase to only 300% of controls over the same period. The relative abundance of 25 additional DRG proteins were uneffected by heat stress. Of 70 35S‐labelled fast‐transported proteins similarly analyzed, 15, comprising 5 families, were consistently transported at >150% of controls following up to 6 hr of heat stress. Over this period all 15 proteins shared a similar profile of abundance relative to non‐induced proteins. Transport was elevated to the greatest extent after 2 hr of stress, declined after 3 hr, and tended to rebound at later times. The remaining 55 fast‐transported protein spots analyzed were unaffected. An increased delivery of this unique sub‐population of 15 fast‐transported proteins suggests a possible involvement in early cellular events that mediate heat stress in the nervous system.
Reduction of glutamine synthetase specific activity in cultured astroglia by ferrous chloride
Authors: Tiffany‐Castiglioni E. , Roberts J. A. , Sheeler‐Gough L. V. 
Published: January 2005

AbstractImmature and mature rat astroglia in culture were assayed for glutamine synthetase (GS) activity after a single exposure to the epileptogen FeCl2. Cells were cultured with both standard and elevated extracellular potassium or glutamate (Glu) concentration. FeCl2 reduced GS activity below control levels, whereas high Glu increased GS activity. However, stimulation by high Glu was significantly attenuated in cultures given both FeCl2 and high Glu, indicating that cells treated with FeCl2 were not able to respond as effectively to increased extracellular glutamate by increasing their GS activity. The significance of these findings is that glial regulation of the neuronal environment may be impaired, based on the proposed importance of GS in ammonia detoxification in the brain.
Denervation and hyperinnervation in the nervous system of diabetic animals: III. Functional alterations of G proteins in diabetic encephalopathy
Authors: Abbracchio M. P. , Di Luca M. , Di Giulio A. M. , Cattabeni F. , Tenconi B. , Gorio A. 
Published: January 2005

AbstractG protein‐mediated effects on cAMP production were evaluated in the corpus striatum of diabetic rats 5 and 14 weeks after alloxan injection by measuring both D1‐receptor‐induced stimulation and D2‐receptormediated inhibition of adenylate‐cyclase activity. At 5 weeks of diabetes, no obvious alterations of G protein functions were detected. Both dopamine‐stimulated adenylate cyclase and bromocriptine‐induced inhibition of enzyme activity were indeed similar in control and diabetic animals. Fourteen weeks after alloxan injection, profound alterations were observed. Dopamine‐stimulated cAMP production was markedly increased in diabetic rats, whereas bromocriptine ability to reduce cAMP formation was almost abolished at this late stage of diabetes. Hypoactivity of Gi/Go proteins was also confirmed by the reduced ability of the GTP non‐hydrolyzable analog GTP‐γ‐S to inhibit forskolin‐stimulation of adenylate cyclase. These results show an apparent functional imbalance between Gs and Gi/Go‐mediated transduction mechanisms, with an increased efficacy of Gs activity likely due to the loss of Gi/Go inhibitory functions. Concomitantly with such transductional alteration detected in chronic diabetes, we observed a marked increase of the striatal content of met‐enkephalin, which is known to utilize Gi/Go proteins for inhibition of adenylate cyclase. The measurement of other transmitters (vaso‐active intestinal peptide, substance P, serotonin, noradrenaline, and dopamine) did not reveal any difference with respect to controls. The observed transductional defect in diabetic animals and the increased content and/or hyperinnervation by the metenkephalinergic system could be correlated as mutual compensatory mechanisms.
Platelet‐activating factor stimulates a Fos/Jun/AP‐1 transcriptional signaling system in human neuroblastoma cells
Authors: Squinto S. P. , Block A. L. , Braquet P. , Bazan N. G. 
Published: January 2005

AbstractPlatelet‐activating factor (PAF) elicits a rapid and transient activation of the proto‐oncogenes c‐fos and c‐jun in SH‐SY5Y neuroblastoma cells, but only to a minor extent in Molt‐4 T‐lymphocytes. This effect is inhibited by pretreatment of cells with the PAF antagonist BN 52021, suggesting the involvement of a specific receptor. Moreover, PAF treatment can activate gene expression through an AP‐1 element, and we propose that genomic trans‐activation may occur in target genes containing a functional AP‐1 transcription sequence. These results may further under standing of the molecular mechanisms by which PAF contributes to long‐term phenotypic changes in the nervous system.
Regulation of cAMP levels by protein kinase C in C6 rat glioma cells
Authors: Bressler J. P. , Tinsely P. 
Published: January 2005

AbstractCultures of rat C6 rat glioma cells exhibit a diminished response to isoproterenol and forskolin after being treated with phorbol 12,13‐dibutyrate (PDbU). An IC50 for PDbU of 38±5 nM and 62±8 nM was observed in the isoproternol and forskolin response, respectively. Similarly, C6 cultures exhibited a diminished response to isoproternol and forskolin after an overnight incubation with phospholipase C. We previously demonstrated that this treatment will increase diacylglycerol levels in these cells (Bressler: J Neurochem 48:181–186, 1987). An IC50 for phospholipase C of 6.0±0.1 × 10 −1 and 7.0±0.1 × 10−1 units/ml was observed for the isoproterenol and forskolin response, respectively. A kinetic analysis suggests that the site of PDbU‐mediated inhibition to beta‐adrenergic and forskolin stimulation was different. Degradation of cAMP was a contributory factor since elevated cAMP levels decreased faster in PDbU treated cells than in nontreated cells. In addition, PDbU treated cells exhibited a significantly higher level of phosphodiesterase activity. We conclude that activation of protein kinase C and subsequent stimulation of phosphodiesterase activity contributes to the inhibition of the beta‐adrenergic and forskolin mediated increase in cAMP levels in intact C6 rat glioma cells. The consequences of lower cAMP levels in sustaining differentiated function in the C6 rat glioma cell line will be discussed.
Effect of low‐dose lead acetate exposure on the metabolism of nucleic acids and lipids in cerebellum and hippocampus of rat during postnatal development
Authors: Agodi A. , Viola M. , Alberghina M. , Stella A. M. Giuffrida 
Published: January 2005

AbstractPostnatal exposure (from the second day after birth to 30 days) of rat pups to low levels of lead acetate (50 mg/kg body weight/day), administered by gastric intubation, yielded a maximum blood level of 76.1μg/100 ml, at day 15 of age. Cerebellar and hippocampal lead contents were 8.67μg/100 mg and 11.7μg/100 mg, respectively, at day 30 of age. This lead exposure has been shown to elicit little change in some biochemical parameters in cerebellum and hippocampus. At the three ages investigated (5,15, and 30 days after birth) there were no alterations of body weight; brain, cerebellum, and hippocampus wet weight; and DNA, RNA, protein and phospholipid content, either in total tissue or in mitochondria. A similar invariance following lead exposure was observed in mitochondrial succinate dehydrogenase and cytochrome oxidase activities. After intraperitoneal administration, the incorporation of [methyl‐14C]thymidine into DNA and [5,6‐3H]uridine into RNA of cerebellum and hippocampus showed a significant decrease only at day 5, reaching the control value at 15 and 30 days of age. After intraperitoneal injection, [2‐3H]glycerol incorporation into total lipids and phospholipids of cerebellum and hippocampus also showed no significant changes in Pb‐treated pups compared to controls at all three postnatal ages.We concluded that subclinical lead administration exerts its effect by slowing cell proliferation in the very early growth phase of the brain. It is likely that a metabolic compensative response to subtoxic effect of lead acetate may be brought about in cerebellum and hippocampus during critical phases of nervous system development between days 15 and 30.
Molecular cloning of cDNAs that encode the chicken Po protein: Evidence for early expression in avians
Authors: Barbu M. 
Published: January 2005

AbstractAs the major transbilayer glycoprotein of peripheral myelin, Po is believed to play a prominent role in the formation of this structure by Schwann cells. The amino acid sequence of the chicken Po molecule, deduced from the nucleotide sequence of cDNA clones, is reported here. Comparison with the mammalian molecule reveals an extensive overall homology, thus underlining the importance both of the cytoplasmic and of the extracellular domains of this protein in the stablishment and preservation of peripheral myelin structure. Unexpectedly, an avian Po cDNA probe was found to hybridise with several mRNA species, in exclusively in peripheral nerve and in proportions that varied according to the developmental stag. The expression of these transcripts was detected significantly earlier than that of po mRNA in nammals.
Developmental expression of glial fibrillary acidic protein mRNA in the rat brain analyzed by in situ hybridization
Authors: Landry C. F. , Ivy G. O. , Brown I. R. 
Published: January 2005

AbstractGlial fibrillary acidic protein (GFAP) accumulates in astrocytes during development. We have characterized the increase in GFAP mRNA during development of the rat brain by using Northern blotting and in situ hybridization histochemistry and have found a caudal to rostral gradient of expression, consistent with overall brain maturation. GFAP mRNA was first obseved at embryonic day 16 (E16) in the glial limitans of the ventral hindbrain. During brain development message levels increased rostrally and by postnatal day 5 (P5) the entire glial limitans showed a positive signal which persisted into adulthood. GFAP mRNA was also found to accumulate in a caudal to rostral direction within the Purkinje cell layer of cerebllum beginning shortly after birth. By P5 the entire layer was positive and signal in this region could be localized to Bergmann glia by P15. A transient elevation in GFAP mRNA was apparent during the second postnatal week in cerebellum and cerebrum. Using in situ hybridization, a peak in message levels was observed at P15 and could be localized primarily to the deep white matter of cerebellum, to the corpus callosum, and to certain hippocampal fiber tracts. The pattern of GFAP expression in these regions is consistent with the differentiation of interfascicular glia and the appearance of type‐2 astrocytes during the initial events of myelination. GFAP mRNA levels in white matter were greatly reduced in the adult. The pronounced regional differences in GFAP mRNA expression during development may reflect the differentiation of subpopulations of astrocytes.
Alterations in glutamine synthetase activity by FeCl2‐induced focal and kindled amygdaloid seizures
Authors: Tiffany‐Castiglioni E. C. , Peterson S. L. , Castiglioni A. J. 
Published: January 2005

AbstractThe purpose of this study was to determine the effects of two experimental models of chronic epilepsy in rats on the activity of the astroglial enzyme glutamine synthetase. FeCl2‐induced cortial lesions that increased the sensitivity to pentylenetetrazol‐induced generalized seizures also significantly increased glutamine synthetase activity in the homotopic site of the contralateral cortex. A decrease in cortical glutamine synthetase was found in the cortex ipsilateral to the stimulated amygdala in electrically kindled animals. These findings provide evidence that increased glutamine synthetase activity is associated with developing, submaximal seizures and that decreased activity is characteristic of mature, chronic seizure states such as that associated with kindled amygdala seizures.
Prevention of chemically induced synaptosomal changes
Authors: Bondy S. C. , McKee M. 
Published: January 2005

AbstractThe ability of altered environmental conditions to modulate some properties of synaptosomes has been studied. Incubation conditions used included the presence of methyl mercury or an organochlorine insecticide: chlordecone. Other adverse chemical conditions during incubation were the absence of calcium salts from the incubation medium or the addition of agents bringing about enhanced oxidative conditions. Synaptosomal parameters studied were the cytosolic level of free, ionic calcium, [Ca2+]i, the extent of depolarization‐induced uptake of radioactive calcium, and the permeability of the limiting membrane. In addition, peroxidative activity was estimated by quantitation of thiobarbituric acid‐reactive material. All these facets of synaptosomal function were responsive to the presence of these potentially deleterious changes in the incubation medium. While the response of [Ca2+]i, was potentially in either direction, all adverse conditions increased synaptosomal permeability as evaluated by leakage of fura‐2 into the extracellular compartment. Pretreatment with ganglioside GM, in some situations or α‐tocopherol in others could either wholly or partially prevent the onset of such altered synaptosomal characteristics.
Phosphorylation of proteins of the postsynaptic density: Effect of development on protein tyrosine kinase and phosphorylation of the postsynaptic density glycoprotein, PSD‐GP180
Authors: Curd James W. , Bissoon N. 
Published: January 2005

AbstractThe effect of development on the tyrosine kinase activity of postsynaptic densities (PSDs) has been determined. PSDs were prepared from the forebrains of rats ranging in postnatal age from 13 to 90 days and the phosphorylation of both exogenous and endogenous substrates by tyrosine kinase measured. PSDs exhibited tyrosine kinase activity at all ages examined. Phosphorylation of the exogenous substrates polyglutamyltyrosine (4:1) and [val5] angiotensin II increased twofold between days 30 and 90 to levels̀ slightly lower than those present at 13 days. The phosphorylation of endogenous PSD proteins on tyrosine residues, assessed by alkali digestion of polyacrylamide gels of 32P‐labelled PSD proteins and by measuring the formation of [32P] phosphotyrosine by PSDs incubated in the presence of [γ‐32P] ATP, closely paralleled the changes in total tyrosine kinase activity. Tyrosine phosphorylation of the PSD‐specific glycoprotein, PSD‐GP180, also showed a transient increase between days 22 and 30, although its concentration within the PSD continued to increase slowly up to 90 days. The results indicate that the tyrosine kinase activity of PSDs is developmentally regulated and that tyrosine phosphorylation of PSD proteins is limited by enzyme rather than substrate availability.
Thy‐1‐like immunoreactivity in developing chicken skeletal muscle: Identification of a cross‐reactive slow‐fiber specific molecule that is not Thy‐1
Authors: Shahin S. , Jeffrey P. L. , Rostas J. A. P. 
Published: January 2005

AbstractWe investigated the Thy‐1‐like immunoreactivity during the development of chicken skeletal muscle using a group of monoclonal antibodies raised and characterised against purified chicken brain Thy‐1.The immunoreactivity attributable to bona fide Thy‐1 in muscle was present in nerves, connective tissue associated with the intrafusal capsule and blood vessels, and the extracellular matrix of the muscle fibres. During development there was no change in the staining of nerves, blood vessels or intrafusal capsules. However, the extracellular staining of muscle first appeared around hatching and gradually increased in intensity reaching maximal levels in the adult. The intensity of staining varied within and between the muscles examined. One of the antibodies (SB1 20.11)recognised an additional molecule that is not Thy‐1 and that was localised in the cytoplasm of slow muscle fibres. This immunoreactivity was first detectable at E10 in all myotubes that contained both alkali and acid stable mvosin ATPase activity (presumptive slow), but not in those myotubes with only alkalistable myosin ATPase activity (presumptive fast). Thereafter, the staining increased to a maximum in the newly hatched animal and then decreased until reactivity was undetectable in the adult (>25 weeks). All positive fibres initially stained with a uniform intensity but the time of commencement and the rate of loss of staining was variable. Those fibres that contained both acid stable and acid labile myosin ATPase activity lost the antigen much faster than the fibres containing only acid‐stable myosin ATPase activity, which also tended to increase in intensity for a longer period. These may represent, respectively, the slow tonic type III fibres and the slow twitch type I fibres classified by Barnard et al. (1982).
Influence of oxidative stress on the age‐linked alterations of the cerebral glutathione system
Authors: Benzi G. , Marzatico F. , Pastoris O. , Villa R. F. 
Published: January 2005

AbstractThe glutathione system (reduced and oxidized glutathione; redox index) was studied in the forebrain of male Wistar rats of 5, 15, and 25 months of age following the administration for 2 months in drinking water of chemicals that induce oxidative stress: paraquat and diethyldithiocarbamate (DDC) to increase superoxide radical formation, aminotriazole and hydrogen peroxide to increase hydroxyl radical generation, as well as diamide and ferrous chloride to decrease the glutathione cycle activity. Chronic oral administration of phosphatidylcholine for 2 months was evaluated in 25‐month‐old rats. Aging accentuated the changes produced by chemicals that induce oxidative stress; i.e., the changes in the glutathione redox index were most pronounced in the forebrains of the older paraquat‐, DDC‐, H2O2−, and diamidetreated rats. Markedly different adaptative changes occurred within the various drug groups. The reduced glutathione was increased (by paraquat, DDC and aminotrazole), decreased (by H2O2) or unchanged (by iron and diamide). Furthermore, in older rats, paraquat and DDC increased the glutathione redox index, whereas H2O2 and diamide decreased the glutathione redox index or were ineffective (i.e., aminotriazole, iron). The glutathione redox index alterted by chronic drug administration was modified by the concomitant administration of phosphatidycholine.