bluuebunny/crossref_metadata_2025_split huggingface dataset:
Calcium‐Independent Release of Acetylcholine from Electric Organ Synaptosomes and Its Changes by Depolarization and Cholinergic Drugs
Authors: Doležal Vladimír , Françoise Diebler Marie , Lazereg Sylvie , Israël Maurice , Tuček Stanislav 
Published: October 2006

AbstractChemiluminescent detection was applied to measure the continuous spontaneous Ca2+‐independent liberation of acetylcholine (ACh) from Torpedo electric organ synaptosomes. Differentiation between the release of ACh and choline was achieved by inhibiting cholinesterases with phospholine, and a way to quantify the continuous release was devised. The method permitted measurements during short time intervals from minute amounts of tissue and without an accumulation of ACh in the medium. Synaptosomes continuously liberated small amounts of ACh during incubations in the presence of 3 mM K+ and in the absence of Ca2+. The spontaneous liberation of ACh was similar both quantitatively and qualitatively at pH values of 8.6 and 7.8. It was unaltered by MgCl2 (10.4 mM), 2‐(4‐phenylpiperidino)cyclohexanol (10 μM), ouabain (104 μM), atropine (10μM), and valinomycin (102 nM). Carbamoylcholine brought about a decrease, which could be partially reversed by atropine. The Ca2+‐independent output of ACh was increased considerably when the concentration of K+ ions was raised (eightfold at 103 and 35‐fold at 203 mM K+). Carbamoylcholine (104 μM) blocked the increase in ACh release produced by high K+; this effect of carbamoylcholine was not reversed by atropine (10 μM). When Ca2+ was added to synaptosomes depolarized by a high concentration of K+, the amount of ACh released during the first 1–3 min after the addition of Ca2+ was at least 20 times higher than in the absence of Ca2+, but the release returned rapidly to predepolarization values. Similarly high values of ACh release could be achieved by adding Ca2+ plus the ionophore A23187 and even higher values by adding Ca2+ plus gramicidin. Under the conditions used. the Ca2+‐dependent K+‐evoked release of ACh was not changed by 104 μM carbamoylcholine. It is apparent that the spontaneous Ca2+‐independent liberation of ACh from Torpedo synaptosomes is not a simple diffusion and is mediated by a carrier. The carrier is inhibited by muscarinic activation; the molecular mechanism of the inhibition is unlikely to involve Ca2+ ions or hyperpolarization. During depolarization, muscarinic inhibition of ACh liberation is ineffective, but carbamoylcholine blocks the Ca2+‐independent depolarization‐stimulated ACh output, probably by a direct action on the carriers.
Inability of [125I]Sar1, Ile8‐Angiotensin II to Move Between the Blood and Cerebrospinal Fluid Compartments
Authors: Harding J. W. , Sullivan M. J. , Hanesworth J. M. , Cushing L. L. , Wright J. W. 
Published: October 2006

AbstractThe angiotensin II competitive antagonist [125I]‐Sar1,Ile8‐angiotensin II was not transported from the vascular space to the cerebroventricular space in either intact or nephrectomized rats. In addition [125I]Sar1,Ile8‐angiotensin II lacked the capacity to move in the opposite direction over a 20‐min collection period following cerebroventricular infusion. These data suggest that angiotensins lack the capacity to move freely between the blood and cerebrospinal fluid compartments and are consistent with the notion that blood‐borne and cerebroventricular angiotensins access different receptor populations.
Chromosomal Location of the Mouse Gene that Encodes the Myelin‐Associated Glycoproteins
Authors: D'Eustachio Peter , Colman David R. , Salzer James L. 
Published: October 2006

AbstractThe two myelin‐associated glycoprotein (MAG) species, designated large MAG (L‐MAG) and small MAG (S‐MAG), are believed to be generated by differential splicing from a single RNA transcript. We have now defined the genetic locus encoding the two MAG proteins in the mouse. Analysis of a panel of interspecies somatic cell hybrids indicated that all MAG coding sequences reside on chromosome 7. Following the inheritance of a restriction fragment length polymorphism associated with MAG coding sequences allowed the locus to be positioned 0.5 centimorgans from the locus Abpa (androgen binding protein α) on proximal chromosome 7. These data strongly support the hypothesis that a single gene encodes the two MAG proteins, and we propose the name Mag for this locus. This localization places Mag in close proximity to the neurological mutant locus qv (quivering) and raises the possibility of a functional relationship or identity between Mag and qv. However, an analysis of the MAG gene, its RNA transcripts, and its protein products revealed no abnormalities in homozygous qv mutant mice, suggesting that this chromosomal linkage is not etiologically significant.
Ciliary Neuronotrophic Factor Stimulates Choline Acetyltransferase Activity in Cultured Chicken Retina Neurons
Authors: Hofmann Hans‐Dieter 
Published: October 2006

AbstractIt has been demonstrated that cultured choliner‐gic retinal neurons from 8‐day‐old chicken embryos respond to a polypeptide factor present in retinal cell‐conditioned medium (RCM) and in retinal extracts. Compared with control cultures, the activity of acetyl‐CoAxholine O‐acetyltransferase (EC 2.3.1.6; ChAT) is enhanced more than twofold in neuronal retinal cultures grown for 7 days in the presence of RCM. The present study demonstrates that both ciliary neuronotrophic factor (CNTF), which is characterized by its trophic activity on parasympathetic ciliary neurons, and RCM exhibit identical stimulatory effects on ChAT activity in retinal monolayer cultures. Similarly, RCM supports the in vitro survival of ciliary neurons to the same extent as CNTF. The active species in RCM has a molecular weight (20,900 ± 1,000) identical to that of CNTF, as determined by preparative sodium dodecyl sul‐fate gel electrophoresis. The results indicate that cholinergic retinal neurons represent a central neuronal target for CNTF or a closely related protein.
Effects of Taurine and Mitochondrial Metabolic Inhibitors on ATP‐Dependent Ca2+ Uptake in Synaptosomal and Mitochondrial Subcellular Fractions of Rat Retina
Authors: Lombardini John B. 
Published: October 2006

AbstractATP‐dependent Ca2+ uptake was investigated at low Ca2+ concentrations (10 μM) in rat retinal synaptosomal and mitochondrial preparations obtained by differential centrifugation on Ficoll gradients. Ca2+ uptake in the synaptosomal and mitochondrial subcellular preparations was stimulated by ATP and additionally stimulated by ATP plus taurine. The ATP‐dependent and taurine‐stimulated ATP‐dependent Ca2+ uptakes were inhibited by mitochondrial metabolic inhibitors (atractyloside, oligomycin, and ruthenium red). These metabolic inhibitors had a greater effect on the ATP‐dependent and taurine‐stimulated ATP‐dependent Ca2+ uptake activities in the mitochondrial preparation than in the synaptosomal preparation. ATP‐dependent Ca2+ uptake in a synaptosomal subfraction obtained by osmotic shock was only partially inhibited by atractyloside. ATP‐dependent Ca2+ uptake in the synaptosomal subfraction was also stimulated by taurine but to a lesser extent than in either the synaptosomal or mitochondrial preparation. These studies suggest that mitochondria are primarily responsible for taurine‐stimulated ATP‐dependent Ca2+ uptake in synaptosomal preparations.
Sequence of Two mRNAs Encoding Active Rat Tryptophan Hydroxylase
Authors: Darmon Michèle C. , Guibert Bernard , Leviel Vincent , Ehret Mireille , Maitre Michel , Mallet Jacques 
Published: October 2006

AbstractTwo full‐length cDNA clones that encode functional rat tryptophan hydroxylase (EC 1.14.16.4), the key enzyme in serotonin synthesis, have been isolated from a rat pineal gland library. These tv/o clones correspond to the 1.8 and 4‐kilobase mRNA species, respectively. They contain the same coding sequence corresponding to a 51,010 dalton protein and differ in the length of their 3’ untranslated regions.
β‐N‐Oxalylamino‐L‐Alanine Action on Glutamate Receptors
Authors: Ross Stephen M. , Roy Dwijendra N. , Spencer Peter S. 
Published: October 2006

Abstractβ‐N‐OxalyJamino‐L‐aJanine (L‐BOAA) is a nonprotein excitatory amino acid present in the seed of Lathyrus sativus L. This excitotoxin has been characterized as the causative agent of human neurolathyrism; an upper motor neuron disease producing corticospinal dysfunction from excessive consumption of the lathyrus pea. Previous behavioral, tissue‐culture, and in vitro receptor binding investigations revealed that L‐BOAA might mediate acute neurotoxicity through quisqualate (QA)‐preferring glutamate receptors. The present study demonstrates the stereospecific action of L‐BOAA on glutamate receptor binding in whole mouse brain synaptic membranes. L‐BOAA was most active in displacing thiocyanate (KSCN)‐sensitive specific tritiated (RS)‐α‐3‐hy‐droxy‐5‐methylisoxazole‐4‐propionic acid (AMPA) binding (i.e., QA receptor) (Ki= 0.76 μM) with a rank‐order potency of QA > kainate > N‐methyl‐D‐aspartate (NMDA). By contrast, the nonneurotoxic D‐BOAA isomer (100 μM) was essentially inactive in displacing radioligands for glutamate receptors, except the NMDA site, where it was equipotent with L‐BOAA. Scatchard analysis of L‐BOAA displacement of specific [3H]AMPA binding indicated competitive antagonism (KD: control, 135 nM; L‐BOAA, 265 nM) without a significant change in QA‐receptor density, and Hill plots yielded coefficients approaching unity. Differential L‐BOAA concentration‐dependent decreases in specific [3H]AMPA binding were observed in synaptic membranes, indicating that the neurotoxin was more potent in displacing specific binding from frontal cortex membranes, followed by that for corpus striatum, hippocampus, cerebellum, and spinal cord. Comparative experiments for inhibition of specific [3H]‐AMPA binding in cortex revealed that L‐BOAA was approximately five‐ and 10‐fold less potent than QA and AMPA, respectively, but twofold greater than the endogenous neurotransmitter, glutamate. Parallel studies with KSCN‐treated spinal cord synaptic membranes (compared to cortex controls) indicated that specific [3H]AMPA binding in untreated tissue was (a) approximately 5% of cortex and pharmacologically distinct and (b) differentially sensitive to L‐BOAA and stimulation of binding by KSCN. These data suggest that low levels of L‐BOAA in vivo might initially exert excitotoxicity through sensitive cortex QA‐preferring neurons while eliciting little interference with QA sites in the spinal cord. Although the precise role(s) of the excitatory amino acid synapse in neurodegenerative diseases remains unclear, the cortex QA receptor could be preferentially sensitive to L‐BOAA attack and might represent the initial molecular recognition site responsible for the pathogenesis of this upper motor neuron disease.
Stathmin Is a Major Phosphoprotein and Cyclic AMP‐Dependent Protein Kinase Substrate in Mouse Brain Neurons but Not in Astrocytes in Culture: Regulation During Ontogenesis
Authors: Chneiweiss Hervé , Beretta Laura , Cordier Jocelyne , Boutterin Marie‐Claude , Glowinski Jacques , Sobel André 
Published: October 2006

AbstractStathmin is a ubiquitous soluble protein (Mr˜ 19,000; pI ˜ 6.2–5.5) whose phosphorylation is associated with the intracellular mechanisms involved in the regulations of cell differentiation and functions by extracellular effectors. It is present in various tissues and cell types and has several nonphosphorylated and increasingly phosphorylated forms, and it is particularly abundant in brain. Very high concentrations of stathmin were also detected in mouse embryo striatal neurons grown in primary culture, whereas stathmin was barely detectable in astrocytes from the same source. Stathmin appeared in neurons as a major substjrate for protein phosphorylation and, in particular, for the cyclic AMP (cAMP)‐dependent protein kinase, because its phosphorylation was stimulated by cAMP in cell‐free preparations and in intact cells by forskolin, a potent activator of adenylate cyclase. During brain ontogenesis, stathmin was first detected at embryonic day 12; its concentration increased until birth and then decreased from postnatal day 10 to adulthood. In parallel, its molecular forms shifted from the least phosphorylated to the more phosphorylated ones. This result may reflect the evolution of the activity of stathmin during development and the subsequent maturation of the brain. In conclusion, our results substantiate the likely role of stathmin as an intracellular relay of extracellular regulations, as they point out its specific importance related to neuronal functions and brain differentiation.
Catabolic Regulation of the Expression of the Major Myelin Glycoprotein by Schwann Cells in Culture
Authors: Brunden Kurt R. , Windebank Anthony J. , Poduslo Joseph F. 
Published: October 2006

Abstract:Previous studies have suggested that neonatal Schwann cell cultures deprived of axonal contact do not express components of the myelin membrane, including the major myelin glycoprotein, P0. In contrast, Schwann cells from permanently transected, adult nerve exhibit continued biosynthesis of P0 after culture, suggesting that the ability to express the myelin glycoprotein may depend on the degree of cellular differentiation. To examine further the ability of Schwann cell cultures to express P0 as a function of age, we have performed precursor incorporation studies on endoneurial explants from 4‐ to 12‐day‐old rat sciatic nerves after 5 days in culture. The data reveal that explants from 12‐day‐old animals synthesize detectable levels of this integral myelin protein when assayed by [3H]mannose incorporation, even though there is no apparent myelin assembly in the cultures. Pulse–chase analysis of cultures from 12‐day‐old rats demonstrates that [3H]mannose‐labeled P0 is substantially degraded within 3 h. This catabolism largely can be prevented by the addition of swainsonine, ammonium chloride, or L‐methionine methyl ester to the pulse‐chase media. The former agent alters oligosaccharide processing whereas the latter two compounds inhibit lysosomal function. The P0 synthesized by the 12‐day explant cultures following the addition of swainsonine is readily fucosylated, implying that the protein has progressed at least as far as the medial Golgi before its exit and subsequent catabolism. If cultures from 4‐, 6‐, and 8‐day‐old animals are analyzed for P0 biosynthesis by [3H]mannose incorporation in the presence of swainsonine, detectable levels of the glyoprotein are seen. The inability to demonstrate the presence of P0 in earlier studies of neonatal cultures was presumably due in part to the rapid lysosomal catabolism of the protein after translation.
Development of Benzodiazepine and Picrotoxin (t‐Butylbicyclophosphorothionate) Binding Sites in Rat Cerebellar Granule Cells in Culture
Authors: Squires Richard F. , Saederup Else , Damgaard Inge , Schousboe Arne 
Published: October 2006

Abstract:The specific bindings of [3H]flunitrazepam ([3H]FLU), [3H]CGS 8216, and t‐[35S]butylbicyclophosphorothionate ([35S]TBPS) to sites on rat cerebellar granule cells all increase from 4 to 15 days in culture, although their time courses differ. Specific [3H]FLU binding doubles, [3H]CGS 8216 binding triples, and [35S]TBPS binding increases about fourfold from 4 to 15 days in culture. Displacement studies, using the type I‐selective ligand CL 218,872, indicate that at 4 days the [3H]FLU binding sites are almost entirely “type II,'’judging from an IC50 value near 300 nM and a pseudo‐Hill number near 1. By 10 days, approximately equal numbers of type I and type II binding sites are present in the cultured cells, and this ratio remains constant thereafter (12 and 15 days). At days 10–15, both the IC50 value for CL 218,872 (near 100 nM) and the pseudo‐Hill number (near 0.7) remain constant and are significantly different from the values at culture day 4. The development of specific [35S]TBPS binding parallels that of [3H]CGS 8216 binding more closely than the development of [3H]FLU binding. The [3H]CGS 8216/[3H]FLU ratio increased by a factor of 1.6 from day 4 to day 15 (p < 0.001). Taken together, our data suggest the existence of several γ‐aminobutyric acidA (GA‐BAA) receptor subunits, the relative proportions of which change during development. The presence of the GABA‐mimetic 4,5,6,7‐tetrahydroisoxazolo[5,4c]pyridine‐3‐ol (THIP) in the culture medium had no apparent effect on any of the binding sites studied, although THIP was shown previously to induce low‐affinity GABA binding sites.
Treatment with Oxiracetam or Choline Restores Cholinergic Biochemical and Pharmacological Activities in Striata of Decorticated Rats
Authors: Consolo S. , Salmoiraghi P. , Amoroso D. , Kolasa K. 
Published: October 2006

Abstract:Interruption of the corticostriatal pathway by undercutting the frontal cortex resulted after 2 weeks in a 40% reduction of basal acetylcholine (ACh) release in vivo, and in inhibition of the striatal sodium‐dependent high‐affinity uptake of choline (SDHACU) to the same extent. The lesion, too, completely prevented the rise (about 35%) in striatal ACh content induced by oxotremorine and apomorphine acting at muscarine and dopamine receptors, respectively. Acute intraperitoneal injections of 100 mg/kg of either oxiracetam or choline chloride resulted in time‐dependent recovery of ACh output from the striata of decorticated rats to control levels. Oxiracetam also normalized the ex vivo striatal SDHACU activity of decorticated rats 2 h after administration without any effect in sham‐operated rats. Oxiracetam or choline chloride administered before oxotremorine (0.8 mg/kg, i.p.) or apomorphine (1 mg/kg, i.p.) reinstated the ACh‐increasing effect of these agonists. It is suggested that choline chloride acts directly simply by being the precursor for ACh, whereas oxiracetam may act indirectly, possibly by increasing the availability of choline chloride for ACh synthesis. Furthermore, the frontally decorticated rat could constitute a useful model for studying means to restore the deficit in striatal cholinergic neurotransmission.
Selective Increase in S‐100β Protein by Aging in Rat Cerebral Cortex
Authors: Kato Kanefusa , Suzuki Fujiko , Morishita Rika , Asano Tomiko , Sato Tsuneko 
Published: October 2006

Abstract:Changes in the cocentrations of nervous tissuerelated proteins and their isoproteins, such as S‐100 proteins (S‐100α and S‐100β), enolase isozymes (α‐enolase and γ‐enolase), and GTP‐binding proteins (Goα, Gi2α, and β‐subunits), were determined in the CNS of male rats of various ages (from 2 to 30 months old) by means of enzyme immunoassay. The weights of brains and the concentrations of soluble proteins in the cerebral cortex, cerebellum, and brainstem were constant during the observation period. The concentration of S‐100β protein, which is predominantly localized in glial cells, increased gradually in the cerebral cortex with age; levels in the 25‐month‐old rats increased to approximately 150% of the levels in the young (2‐month‐old) rats. However, the S‐100β concentrations in the cerebellum and brainstem were relatively constant, showing similar values in rats 2–30 months old. Levels of other proteins, including both neuronal (γ‐enolase and Goα) and glial (α‐enolase and S‐100α) marker proteins, did not change significantly with age in the cerebral cortex, cerebellum, and brainstem. These results suggest that there is a close relation between the age‐dependent changes of the CNS function and S‐100β protein levels in the cerebral cortex.
Quantification of metamorphopsia in a macular hole patient using M‐CHARTS™
Authors: Arimura Eiko , Matsumoto Chota , Okuyama Sachiko , Takada Sonoko , Hashimoto Shigeki , Shimomura Yoshikazu 
Published: October 2006

Abstract.Purpose:  In cases of macular hole, metamorphopsia is one of the most important symptoms, along with decreased visual acuity and a central scotoma. We investigated the relationship between the degree of metamorphopsia and the morphological appearance of macular holes.Methods:  Using M‐CHARTS™ developed by ourselves, we quantified the metamorphopsia scores in 35 eyes with an idiopathic macular hole in 35 patients. Metamorphopsia in eyes with macular hole was characterized by straight lines recognized by the subject as bending toward the central scotoma. We also evaluated best corrected visual acuity (VA) and the central 10 degrees of differential light sensitivity using the Octopus 101 program M2. The size of the macular hole and the fluid cuff were measured using a scanning laser ophthalmoscope. We also evaluated the improvement in metamorphopsia scores after surgical treatment for macular hole in 22 patients.Results:  A significant correlation was found between metamorphopsia score and fluid cuff size, but not diameter of the macular hole. After vitrectomy, VA improved in 14 of 22 patients and metamorphopsia scores improved in 19 of 22 patients. M‐CHARTS™ is a simple and useful method for the quantification and follow‐up of metamorphopsia in patients with macular hole.
Strontium-Calcium Movement from Soil to Man
Authors: Comar C. L. , Russell R. Scott , Wasserman R. H. 
Published: October 2006

The calcium reservoirs of the biosphere are becoming labeled to varying degrees with strontium-90 from nuclear weapons. These reservoirs include the human and animal skeleton, the milk, the vegetation, the upper layers of soil, and the waters. The degree of labeling is governed by the dilution that occurs, or the differential behavior of calcium and strontium in various steps of the food chain. This differential behavior normally provides a factor of protection against strontium-90 in the soil and vegetation that may be as high as 25 for the newborn and is most likely not less than 6 for adults, depending on food habits.
The physiological steps that are important in the movement of the two elements in the biosphere are described to provide a basis for an approach toward increase of the discrimination against strontium in favor of calcium. Some aspects of agricultural practices are discussed from this standpoint. The matter of hazard from levels now existing and the present need to undertake remedial measures are not discussed, in major part because of lack of experimental data on which to base such considerations.
Poleward Migration of Early Angiosperm Flora
Authors: Axelrod Daniel I. 
Published: October 2006

1) During the opening phase of the Early Cretaceous (Neocomian), angiosperms commenced to invade lowland basins of deposition at generally lower latitudes. They reached high northern and middle southern latitudes at the close of the epoch (Albian) and only replaced the relict Jurassic-type vegetation at high latitudes during the early part of Late Cretaceous time.
2) This poleward migration of angiosperms is consistent with the theory that the phylum had its center of origin and dispersal at tropical latitudes, which ranged between 45°N and 45°S in pre-Cretaceous time.
3) Recognition of the time-space factor involved in the Early Cretaceous poleward migration of angiosperms removes most of the conflicts in the testimony on age supplied by fossil plants and by marine invertebrates-conflicts which have persisted for nearly a century.