bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isolation and characterization of periaxolemmal and axolemmal enriched membrane fractions from the rat central nervous system
Authors: Sapirstein V. S. , Durrie R. , Cherksey B. , Beard M. E. , Flynn C. J. , Fischer I. 
Published: May 2005

AbstractIn this report, we describe the fractionation of crude axolemmal fractions from rat lower brainstem into subfractions enriched in markers for either periaxolemmal myelin or axolemma. These subfractions were isolated on density gradients as bands layering on 0.8M and 1.0M sucrose. Both subfractions consisted of unilamellar vesicles. Relative to myelin purified from the same starting material, the 0.8M subfraction was enriched in MAG, CNPase, carbonic anhydrase and Na+, K+ ATPase but was extremely low in PLP and MBP. In addition, this fraction exhibited a protein profile distinct from myelin. The 1.0M fraction was also highly enriched in Na+, K+ ATPase and had an overall composition similar to the 0.8M subfraction. However, it differed from the 0.8M subfraction by being low in MAG, CNPase, and carbonic anhydrase, but enriched in voltage‐dependent Na+ channel, axon‐specific fodrin, and MAP‐1B. Based on these characteristics we concluded that the 0.8M and 1.0M subfractions were highly enriched in periaxolemmal myelin and axolemmal membrane, respectively. Plasmolipin10 was unique with equally high levels in myelin and in the 0.8M and 1.0M subfractions. Both subfractions were enriched, relative to myelin, in the alpha subunit of the GTP binding protein, Go, and the alpha subunit common to all G proteins, GA/1. Electrophysiology with membrane subfractions fused to lipid bilayers showed that both membranes contained sets of K+ and Cl− channels, which based on channel sizes and open times, are largely distinct from one another. © 1992 Wiley‐Liss, Inc.
Platelet‐activating factor antagonists reduce excitotoxic damage in cultured neurons from embryonic chick telencephalon and protect the rat hippocampus and neocortex from ischemic injury in vivo
Authors: Prehn Jochen H. M. , Krieglstein J. 
Published: May 2005

AbstractThe neuroprotective effects of the platelet‐activating factor (PAF) antagonists BN 52020 and BN 52021 were determined in a temperature‐controlled model of transient forebrain ischemia in the rat (occlusion of both common carotid arteries combined with lowering of the mean arterial blood pressure to 40 mm Hg for 10 min). After 7 days of recirculation, the ischemic neuronal damage was evaluated histologically within the hippocampus and neocortex. Combined pre‐ and post‐treatment with the PAF antagonists (2 × 25 mg/kg, s.c.) significantly reduced the resulting neuronal damage of the CA1 and CA3 hippocampal subfields and of the occipital and parietal cerebral cortex. The two PAF antagonists were also tested for their neuroprotective activity in primary neuronal cultures isoalted from embryonic chick telencephalon. Since an excessive activation of excitatory amino acid receptors is discussed to be of importance for the ischemic brain damage, the cultured neurons were exposed to the excitatory amino acid L‐glutamate (1 mM) for a period of 60 min. Twenty hours after the excitotoxic insult, BN 52020‐ and BN 52021‐ treated cultured (1–100 μM) showed both a better preserved morphology, as well as a dose‐dependent increase in cell viability and protein content compared to the control cultures. Our results demonstrate that the PAF antagonists BN 52020 and BN‐52021 have the capacity to protect brain tissue against ischemic neuronal damge independent of hypothermic effects and are also capable of reducing excitotoxic damage of telencephalic neurons from chick embryos cultured in the absence of glial or endothelial cells. We thus propose that PAF plays an important role in the pathophysiology of ischemic/excitotoxic neuronal injury via a direct action on neurons. © 1993 Wiley‐Liss, Inc.
Brain glutathione reductase induction increases early survival and decreases lipofuscin accumulation in aging frogs
Authors: López‐Torres M. , Pérez‐Campo R. , Fernandez A. , Barba C. , De Quiroga G. Barja 
Published: May 2005

AbstractBrain catalase was continuously depleted throughout the life span starting with a large population of initially young and old frogs. Free radical‐related parameters were measured in the brain tissue once per year after 2.5, 14.5, and 26.5 months of experimentation. Brain lipofuscin accumulation was observed after 14.5 and 26.5 months, and survival was continuously followed during 33 months. The age of the animal did not decrease endogenous antioxidants nor increase tissue peroxidation either in cross‐sectional or longitudinal comparisons. Continuous catalase depletion similarly affected young and old animals, inducing glutathione reductase, tending to decrease oxidized glutathione/reduced glutathione (GSSG/GSH) ratio, decreasing lipofuscin accumulation in the brain, and increasing survival from 46% to 91% after 14.5 months. At 26.5 months of experimentation the loss of the glutathione reductase induction in catalase‐depleted animals was accompanied by the presence of higher lipofuscin deposits than in controls and was followed by a great increase in mortality rate. Even though the maximal life span (7 years) was the same in the control and treated animals which were already old (4.2 years) at the beginning of the experiment, the treated animals showed a strong reduction in the rates of early death. It is proposed that the maintenance of a high antioxidant/prooxidant balance in the vertebrate brain greatly increases the probability of the individual to reach the final segments of its species‐specific life span. © 1993 Wiley‐Liss, Inc.
Oligodendrocyte proteoglycans: Modulation by cell‐substratum adhesion
Authors: Yim S. H. , Sherin J. E. , Szuchet S. 
Published: May 2005

AbstractThe signals that trigger the cytodifferentiation of oligodendrocytes (OLGs) are largely unknown. Using as a model system cultures of pure OLGs, we have shown that adhesion to a substratum initiates myelinogenesis (Yim SH, Szuchet S, Polak PE, J Biol Chem 261:11808–11815, 1986). It was of interest to investigate whether components such as proteoglycans (PGs) play any role in the biology of OLGs as it pertains to myelinogenesis. We set out to determine first, whether OLGs carry PGs; second, the nature of the association of these components with OLG plasma membrane; and third, if and how these PGs are modulated by OLG–substratum interaction. We compared the expression and characteristics of PGs extracted with different solvents from nonattached (B3.f) and attached (B3.fA) OLGs. B3.f and B3.fA OLG cultures were labeled with carrier‐free 35SO42− in serum‐free medium. After removing excess label, OLGs were treated with heparin to extract susceptible components. Pellets were then exposed to 1% Triton X‐100 plus 0.1 M NaCl and subsequently to 4 M guanidine‐HCl plus 0.5 M NaCl. Solutions containing extracted material were characterized by size‐exclusion chromatography, SDS‐PAGE, and enzymatic degradation. Herein we report that (1) OLGs display [35S]PGs on their surface within 24 hr of substratum adhesion, and (2) these PGs can be operationally classified as peripheral and integral. We further show that the peripheral PGs are of high and intermediate size as assessed by size‐exclusion chromatography and are segregated within the plasma membrane in such a way that the species with intermediate mass are extracted while OLGs remain adhered, whereas the high‐molecular‐weight species are only extracted after OLGs have been detached. Heparin also dislodges a number of sulfated proteins/Gps. Only a single class—high molecular weight—of integral PGs was identified; this PG requires guanidine‐HCl for extraction. All PGs belong to the heparan sulfate class as evidenced by their degradation with heparitinase and their lack of susceptibility to chondroitinase ABC. The common theme of our findings is that these macromolecules have basal levels of expression in the nonadhered OLGs but undergo an adhesion‐induced enhancement in their syntheses. We postulate that these PGs (1) play a role in OLG‐substratum adhesion and hence myelinogenesis, and (2) may be determinants in establishing OLG polarity. Such polarization is the first overt sign of OLG functional differentiation and occurs prior to any morphological differentiation, e.g., extension of processes does not occur until 48 hr later when the plasma membrane is already polarized. © 1993 Wiley‐Liss, Inc.
Localization of bFGF and FGF‐receptor in the developing nervous system of the embryonic and newborn rat
Authors: Weise B. , Janet T. , Grothe Claudia 
Published: May 2005

AbstractWe examined the localization of basic fibroblast growth factor (bFGF) in the developing embryonic and newborn rat nervous system using 2 anti‐bFGF antibodies. Embryonic (E13, E14, E15, E16, E17, and E18) and newborn tissues were examined. Between E16 and E17 strong bFGF immunoreactivity (IR) was detectable in the cortex and striatum and, in addition, in almost all neurons of the brainstem, spinal cord, and spinal ganglia. In contrast, in the newborn rat bFGF‐IR was found in neuronal subpopulations of brainstem nuclei, ventral spinal cord, and spinal ganglia as it is known for the respective postnatal/adult parts of the nervous system. At E16 7.0 kb and 3.7 kb bFGF mRNA were present. The identification of bFGF‐responsive cells was performed using immunocytochemistry (anti‐flg antibody) and 125I bFGF for binding studies. The neuronal localization of FGF‐receptor suggests that bFGF mediates its effects in an autocrine or paracrine manner. At the time of strongest bFGF‐staining (E16/17), proliferation of neurons is almost completed in most of the nervous system areas. Therefore, it could also be suggested from previous biological experiments that the physiological functions of bFGF could include trophic and/or differentiating effects on developing neurons rather than mitogenic effects. The change of the bFGF‐staining pattern after birth could indicate a change in the physiological function of bFGF, i.e., different bFGF effects in the immature and mature nervous systems. © 1993 Wiley‐Liss, Inc.
Phospholipid and phospholipid fatty acid composition of mixed murine spinal cord neuronal cultures
Authors: Murphy Eric J. , Anderson D. K. , Horrocks L. A. 
Published: May 2005

AbstractThe phospholipid and phospholipid fatty acid compositions of mixed murine spinal cord neuronal cultures are reported. The phospholipid composition was primarily comprised of ethanolamine glycerophospholipids (44.8%) and choline glycerophospholipids (43.5%). Plasmalogens made up 29.1% of the ethanolamine glycerophospholipids (13.0% of the total phospholipids) and 4.5% of the choline glycerophospholipids (1.9% of the total phospholipids). Other phospholipids ranged from 2.9% for sphingomyelin to 1.0% for phosphatidylinositol 4‐phosphate. The fatty acid compositions of the ethanolamine glycerophospholipids, choline glycerophospholipids, phosphatidylserine, and phosphatidylinositol were also determined. The choline glycerophospholipids were the most saturated and contained the smallest amount of polyunsaturated fatty acids. The ethanolamine glycerophospholipids were the most unsaturated and contained the highest amount of polyunsaturated fatty acids. The phospholipids contained minimal amounts of 20:3 n‐9 (Mead acid) and are not considered polyunsaturated fatty acid deficient. Thus, for the mixed neuronal spinal cord cultures, the phospholipid fatty acid compositions were not polyunsaturated fatty acid deficient and contained a large amount of polyenoic fatty acids of both the n‐3 and n‐6 series. © 1993 Wiley‐Liss, Inc.
Brain‐derived neurotrophic factor selectively rescues mesencephalic dopaminergic neurons from 2,4,5‐trihydroxyphenylalanine‐induced injury
Authors: Skaper Stephen D. , Negro A. , Facci L. , Toso R. Dal 
Published: May 2005

AbstractBrain‐derived neurotrophic factor (BDNF) supports the survival of sensory neurons as well as retinal ganglion cells, basal forebrain cholinergic neurons, and mesencephalic dopaminergic neurons in vitro. Here we examined the ability of BDNF to confer protection on cultured dopaminergic neurons against the neurotoxic effects of 6‐hydroxyDOPA (TOPA or 2,3,5,‐trihydroxyphenylalanine), a metabolite of the dopamine pathway suggested to participate in the pathology of Parkinson's disease. Cells prepared from embryonic day 14–15 rat mesencephalon were maintained with 10–50 ng/ml BDNF for 7 days prior to addition of TOPA (10–30 μM) for 24 hr. In BDNF‐treated cultures, the extensive loss ( >90%) of tyrosine hydroxylase immunopositive cells was virtually (<10%) eliminated, while the equally drastic loss (>90%) of the overall cell population was limited to only a 25–30% recovery. Furthermore, the monosialoganglioside GM1 (1–10 μM), although inactive alone, acted synergistically with subthreshold amounts of BDNF to rescue tyrosine hydroxylase‐positive cells against TOPA neurotoxicity. These results add impetus to exploring the therapeutic potential of gangliosides and BDNF in Parkinson's disease. © 1993 Wiley‐Liss, Inc.
Differential effects of phorbol myristate acetate and dexamethasone on protein kinase C activity and eicosanoids production in cultured rat astrocytes
Authors: Boneh A. , Shohami E. , Brenner T. 
Published: May 2005

AbstractThe effects of phorbol myristate acetate (PMA) and dexamethasone on protein kinase C (PK‐C) activity and eicosanoid production were characterized in primary cultures of rat glial cells. PMA (1,000 ng/ml) treatment for 2 hr resulted in a maximal effect (a 4‐fold increase in PGE2 production). Longer exposure to PMA (up to 96 hr) resulted in attenuation of PGE2 production. Down‐regulation of PK‐C activity was assessed in glial cell homogenates under these conditions. Although a 70% inhibition of PK‐C activity was measured upon staurosporine treatment, PGE2 production was not affected both under basal conditions and following PMA activation. The production of thromboxane B2 did not change following exposure to PMA. Pretreatment of the cultures with dexamethasone markedly inhibited the PMA‐stimulated production of PGE2 but had only a moderate (approximately 26%) inhibitory effect on PGE2 production under basal conditions. Dexamethasone had no effect on basal or PMA‐stimulated PK‐C activity. Forskolin, which activates adenylate cyclase, did not affect PGE2 production. These data may suggest that activation of PGE2 production by PMA in glial cells is not unequivocally mediated by PK‐C activation. The inhibitory effect of dexamethasone on the PMA‐stimulated synthesis of PGE2 supports previous findings that glucocorticoids are more effective in inhibiting stimulated rather than basal PGE2 production. © 1993 Wiley‐Liss, Inc.
Use‐dependent modification of a slow NMDA receptor‐mediated synaptic potential in rat amygdalar slices
Authors: Gean Po‐Wu , Chang F.‐C. , Hung C.‐R. 
Published: May 2005

AbstractA single stimulus applied to the endopyriform nucleus evoked in 35 of the 101 basolateral amygdaloid (BLA) neurons a slow excitatory postsynaptic potential (s‐EPSP) of varying latencies. The s‐EPSP could be graded by changing the stimulus intensity and, on reaching the threshold, triggered action potentials. At stimulus intensity just subthreshold for evoking a spike, the s‐EPSP has an average amplitude of 16.3 ± 1.4 mV, a time to peak of 25.7 ± 3.8 ms, and a duration of 124 ± 14 ms. The s‐EPSP was reversibly blocked by DL‐2‐amino‐5‐phosphonovaleate (DLAPV) or ketamine, indicating its mediation through N‐methyl‐D‐aspartate (NMDA) receptor activation. However, the s‐EPSP was not able to follow stimulus frequency of 1 Hz, suggesting that APV‐sensitive s‐EPSP is probably generated by a polysynaptic pathway. The s‐EPSP was greatly enhanced by synaptic stimulation in the presence of bicuculline or in Mg++‐free solution leading to the genesis of paroxysmal depolarizing shift (PDS). The s‐EPSP can undergo robust long‐term potentiation (LTP) following tetanic stimulation. These results suggest that the NMDA receptor‐mediated s‐EPSP may play an important role in epileptogenesis and synaptic plasticity in the amygdala. © 1993 Wiley‐Liss, Inc.
Effect of intermittent mild hypoxia and drug treatment on synaptosomal nonmitochondrial ATPase activities
Authors: Benzi G. , Gorini A. , Arnaboldi R. , Ghigini B. , Villa R. 
Published: May 2005

AbstractSynaptosomal nonmitochondrial ATPases linked to the energy‐utilizing systems were evaluated in cerebral cortex from normoxic rats and rats submitted to mild intermittent normobaric hypoxia [12 hr daily exposure to N2:O2 (90:10) mixture for 4 weeks]. The activities of Na+, K+‐ATPase; high‐ and low‐affinity Ca2+‐ATPase; basal Mg2+‐ATPase; and Ca2+, Mg2+‐ATPase were assayed in synaptosomes and synaptosomal subfractions, namely, synaptosomal plasma membranes and synaptic vesicles. The evaluations were performed either in normoxic rats or in hypoxic rats submitted to 4‐week treatment with saline (controls) or a vasodilator agent (papaverine), an energy‐metabolism interfering agent (theniloxazine), a calcium blocker (nicardipine), and a lipidmetabolism interfering agent (phosphatidylcholine) in order to define the plasticity and the selective changes in individual ATPases. In synaptosomes from rat cerebral cortex, the enzyme adaptation to the daily mild intermittent hypoxia for 4 weeks was characterized by an increase in the activity of Mg2+‐ATPase, concomitant with a decrease in the activities of Na+, K+‐ATPase, high‐affinity Ca2+‐ATPase, and Ca2+, Mg2+‐ATPase. In hypoxic rats the enzyme adaptation to the 4‐week treatment with phosphatidylcholine was characterized by an increase in Ca2+, Mg2+‐ATPase activity and a decrease in Mg2+‐ATPase activity. The action involves the enzymatic form located in the synaptic plasma membranes.In hypoxic rats the adaptation to the 4 week treatment with nicardipine was characterized by an increase in high‐affinity Ca2+‐ATPase activity, while the 4‐week‐treatment with theniloxzine induced an increase in Na+, K2+‐ATPase activity. The actions of both nicardipine and theniloxazine were related to the enzymatic forms located in the synaptic plasma membranes. The effects on the biophase induced by the sequential cycles of hypoxia/normoxia and the treatment with the various agents tested should also be related to the changes induced in the activity of some synaptosomal ATPases. © 1993 Wiley‐Liss, Inc.
Quantification of axotomy‐induced alteration of neuropeptide mRNAs in dorsal root ganglion neurons with special reference to neuropeptide Y mRNA and the effects of neonatal capsaicin treatment
Authors: Noguchi K. , de León M. , Nahin R. L. , Senba E. , Ruda M. A. 
Published: May 2005

AbstractAlteration in mRNA expression in dorsal root ganglia (DRG) neurons encoding 5 neuropeptides was quantitatively compared in normal rats and in those neonatally treated with capsaicin, a selective neurotoxin which destroys a subpopulation of DRG neurons with unmyelinated axons. Adult rats received a unilateral transection of the sciatic nerve and were killed 7 days later. Oligonucleotide probes specific for the genes encoding neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), galanin (GAL), somatostatin (SOM), and calcitonin gene‐related peptide (CGRP) were used for in situ hybridization and RNA blot analysis. Following the nerve cut, RNA blot analysis demonstrated a dramatic induction of NPY, VIP, and GAL mRNA levels from the undetectable constitutive level of expression. Conversely, CGRP and SOM mRNAs, which are constitutively expressed, were reduced 55% and 70%, respectively, following the nerve cut. A unimodal size distribution for neurons expressing NPY mRNA was determined, with a mean cross‐sectional area of 1700 μ2 representing 24.4% of DRG neurons ipsilateral to the nerve cut. Neurons expressing VIP mRNA were mainly small sized, with a cross‐sectional area of approximately 700 μ2, while those expressing GAL mRNA were both small (∼700 μm2) and medium (∼1,300 μm2) sized. The percentages of neurons expressing VIP or GAL mRNA were 19.9% and 33.7%, respectively. In neonatal capsaicin‐treated rats, there was a 10% reduction in neurons expressing NPY mRNA, a 37% reduction for VIP, and a 27% for GAL mRNA compared to vehicle‐treated rats after nerve cut. Capsaicin‐sensitive neurons comprised 37% of CGRP neurons and 83% of SOM neurons. These observations suggest that NPY is primarily induced in myelinated primary afferent neurons, while VIP and GAL mRNA induction occurs in a mixed population, a sizeable percentage of which has unmyelinated axons. Additionally, SOM mRNA expression is associated mainly with unmyelinated primary afferents. Published 1993 by Wiley‐Liss, Inc.
Selection rules for pure rotation and vibration‐rotation hyper‐Raman spectra
Authors: Stanton L. 
Published: May 2005

AbstractThis paper describes a general study of the selection rules for pure rotation and vibrationrotation hyper‐Raman spectra. The investigation encompasses the selection rules for the rotational quantum numbers J, K and M for molecules of any symmetry executing any type of allowed vibration. For molecules in which K is not a good quantum number a parity analysis is described. A complete tabulation of allowed K transitions is given for the common point groups. Coriolis effects and their selection rules for degenerate vibrations are discussed for linear and symmetric rotors.
High resolution Raman spectroscopy of gases with laser sources. VII: The rotational spectrum of cyclohexane‐C6H12 and C6D12
Authors: Peters Ralph A. , Walker William J. , Weber Alfons 
Published: May 2005

AbstractThe pure rotational Raman spectra of cyclohexane‐d0 and cyclohexane‐d12 have been photographed under high resolution using a single mode argon laser as the exciting source. The spectra consist of reasonably sharp lines which form well developed R‐ and S‐branches. The molecular constants found from the analysis of the spectra are, for C6H12: B0 = 0.143429 ± 2 × 10−6 cm−1, DJ = (1.56 ± 0.03) × 10−8 cm−1 and, for C6D12: B0 = 0.109469 ± 1 × 10−6 cm−1 and DJ = (0.61 ± ± 0.01) × 10−8 cm−1. These results and possible molecular structures are discussed in terms of the results of recent electron diffraction studies of cyclohexane.
Rotational structure of hyper‐Rayleigh scattering by linear molecules
Authors: Bancewicz T. , Ożgo Z. , Kielich S. 
Published: May 2005

AbstractThe effect of rotational motion of linear molecules on their hyper‐Rayleigh scattering spectra is calculated from angular momentum theory. The expressions derived for the intensities of the hyper‐Raman rotational lines are used to calculate the rotational structure of the hyper‐Rayleigh line of gaseous CO.
Hemoglobin resonance Raman excitation profiles with a tunable dye laser
Authors: Strekas Thomas C. , Spiro Thomas G. 
Published: May 2005

AbstractResonance Raman spectra have been obtained for oxy hemoglobin within the α absorption band, corresponding to the first π – π* transition, using a tunable dye (Rhodamine 6 G) laser. The excitation profiles demonstrate resonance at the electronic origin (0–0), as well as at the vibronic side‐band (0–1) frequency, as predicted by theory. The wavelength dependence of the Raman intensity follows the molar absorptivity, rather than its square. It is suggested, however, that this form of the wavelength dependence may be an artifact of the transition from resonance to pre‐resonance scattering.
Tunable laser resonance Raman spectroscopy of the visual process. I: The spectrum of rhodopsin
Authors: Lewis Aaron , Fager Roger S. , Abrahamson E. W. 
Published: May 2005

AbstractTunable laser resonance Raman spectra have been obained of a solution of bovine rhodopsin. The spectra were obtained without causing the cis‐trans isomerization of the retinylidene chromophore which is the primary photochemical act in vision. The spectra appear to be sensitive to the structure, the environment and the interactions of the retinylidene chromophore in its opsin matrix. The ease with which the spectra were obtained, the experimental flexibility of Raman spectroscopy and the apparent sensitivity of the spectra suggests a wide range of possible applications for resonance Raman spectroscopy in the elucidation of the principal molecular steps in vision.