bluuebunny/crossref_metadata_2025_split huggingface dataset:
Drug‐induced changes in catecholaminergic cells of the fish retina
Authors: Negishi K. , Laufer M. , Drujan B. D. 
Published: January 2005

AbstractThe changes in fluorescence intensity and number of visible catecholaminergic cells (CA‐cells), as revealed by means of a histofluorescence technique, were used as indicators of the effects of various pharmacological agents upon CA‐cells in the retina of fishes (Cyprinus carpio and Eugerres plumieri). The study includes in vivo and in vitro experiments. In the in vivo experiments, intravitreal injection, two or three hours before eye enucleation, of 10 μg L‐DOPA, dopamine, or noradrenaline accentuated CA‐cell fluorescence and increased the number of visible cells, whereas 10 μg of tyramine, octopamine, synephrine, or adrenaline reduced the endogenous fluorescence. Intramuscular injection of reserpine (3 mg/kg) abolished CA‐cell fluorescence. In the in vitro experiments, pieces of isolated retinas were incubated for three or 30 minutes in media containing different drugs. Only minor changes in fluorescence were detected after three minutes of incubation, but after 30 minutes, dopamine (20 μM) markedly enhanced CA‐cell fluorescence. Carbachol (20 mM), acetylcholine (10 mM) plus BW‐anticholinesterase (1 mM) or substance P (1.6 × 10−2 mM), all reduced CA‐cell fluorescence. Kainic acid (20 μM) abolished fluorescence from CA‐cell somata, while fluorescent fiber networks remain unchanged. L‐aspartate (5 mM) and GABA (10 mM) in the incubation medium did not influence fluorescence intensity. The results are relevant to, and consistent with, electrophysiological observations of dopamine‐mediated spatial effects on horizontal cell potentials.
A new antigen common to the rat nervous and immune systems: II. Molecular characterization
Authors: Rodman Jane Somsel , Akeson Richard 
Published: January 2005

AbstractG5‐IgG is a monoclonal antibody that binds specifically to some cells and tissues of the adult rat nervous and immune systems. The molecular nature of the G5 antigen from adult rat brain is described in this paper. G5 antigen in adult rat brain membrane fractions was trypsin‐sensitive and heat‐labile but not chloroform/methanol‐soluble. It was solubilized by the nonionic detergent NP40 but not by 3 M KCl. Detergent‐soluble rat brain particulate protein inhibited G5‐IgG binding to glutaraldehyde‐fixed rat brain particulate protein. Inhibitory activity could be removed by prior incubation with concanavalin‐A agarose beads. Immunoprecipitates of enzymatically iodinated, detergent‐solubilized brain particulate protein gave a single band on polyacrylamide gels of apparent molecular weight 95,000–105,000 daltons. A band of identical molecular weight was visualized in gels of unlabeled immune precipitates by 125I‐concanavalin A. These results strongly suggest that G5 is an integral membrane glycoprotein in adult rat brain.
Long‐term intracellular retention of hexosaminidase A by Tay‐Sachs disease brain and lung cells in vitro
Authors: Brooks Steven E. , Hoffman Linda M. , Amsterdam Daniel , Adachi Masazumi , Schneck Larry 
Published: January 2005

AbstractEnzyme‐replacement treatment for metabolic storage disorders has been widely studied using model cell culture systems. This study determines the long‐term fate of human hexosaminidase A supplied to Tay‐Sachs disease brain and lung cells. Hex A retention studies showed that the incorporated Hex A is retained in undiminished quantity by TSD lung cells maintained in stationary culture for 14 days. Tay‐Sachs disease brain cells similarly followed for 28 days in stationary culture showed an initial reduction in Hex A for 3 days, after which the Hex A level stabilized and remained relatively constant for the next 25 days. Hexosaminidase B isoenzyme was found to accumulate in both cell lines during extended cultivation, despite the observation that significant amounts were excreted into the extracellular environment. The demonstration of long‐term intracellular retention of exogenously supplied therapeutic enzyme by the target cells offers additional evidence for the feasibility of an enzyme‐replacement approach for study and treatment of lysosomal storage disorders.
Detection of antibodies to central nervous system antigens by solid phase radioimmunoassay
Authors: Linthicum D. Scott , Mackay Ian R. , Wilson Anne , Horvath Leonie B. , Carnegie Patrick R. 
Published: January 2005

AbstractA solid phase radioimmunoassay is described which employs 125I‐protein‐A to detect the presence of antibodies against a panel of cellular and soluble central nervous system (CNS) specific antigens coated onto polyvinylchloride Microtiter plates. Serum antibodies from rabbits immunized against myelin, myelin basic protein (MBP), glial acidic fibrillary protein (GFAP), astroglioma cells, and cerebellar cells were easily detected, and high specificity for each antiserum and antigen was also demonstrable. The assay is applicable to cerebrospinal fluid (CSF) from patients with neurological diseases to detect antibodies against CNS‐specific antigens. The assay should be useful for examining cell lines derived from CNS tissue for the presence of brain proteins.
Development and aging of noradrenergic cell bodies and axon terminals in the chicken
Authors: Yurkewicz Lorraine , Marchi Mario , Lauder Jean M. , Giacobini Ezio 
Published: January 2005

AbstractTyrosine hydroxylase activity was measured in the region of locus coeruleus, cerebellum, cervical spinal cord, lumbar sympathetic ganglia, and iris throughout most of the life span of the chicken (8 days of incubation to 5 years) to compare developmental trends in tyrosine hydroxylase activity in noradrenergic cell bodies and in axon terminals in both the central and peripheral nervous system. Fluorescence histochemistry and retrograde transport of horseradish peroxidase were used to characterize further the coeruleo‐cerebellar projections. Tyrosine hydroxylase activity was detected in the cerebellum as early as 8 days of incubation, which is the earliest stage so far reported. The greatest increase in total tyrosine hydroxylase activity in the region of the locus coeruleus and cerebellum occurred during the embryonic period. There was a more pronounced increase in the cerebellum than in the locus coeruleus region. This is in contrast to the cervical spinal cord where tyrosine hydroxylase activity increased at approximately the same rate during the embryonic and post‐hatching periods. Moreover, the cerebellum and cervical spinal cord, two locus coeruleus target sites, displayed different trends in tyrosine hydroxylase activity throughout development and aging.In both structures examined in the peripheral nervous system, the greatest increase in total tyrosine hydroxylase activity occurred during the post‐hatching period, with a greater rise in the cell bodies of the lumbar sympathetic ganglia than in the noradrenergic terminals of the iris. In both the central and peripheral nervous system, total tyrosine hydroxylase activity continued to increase in noradrenergic terminals long after hatching reaching the highest levels at 7 months when the chicken is considered fully mature. During aging, 16 months to 5 years, there was a greater decrease in total tyrosine hydroxylase activity in the terminals of noradrenergic neurons than in the cell bodies in both the central and peripheral nervous system, a phenomenon that was more marked in the peripheral nervous system than in the brain.
Effect of morphine on catecholamine‐stimulated cyclic AMP production in cortex slices from rats and mice
Authors: Slater P. , Blundell C. 
Published: January 2005

AbstractMorphine (10 μM) blocked noradrenaline‐stimulated cyclic AMP production in slices of cerebral cortex from normal rats but not in slices from rats pretreated with 6‐hydroxydopamine (6‐OHDA). In contrast, morphine failed to prevent noradrenaline‐stimulated cyclic AMP production in mouse cortex slices. Levorphanol weakly antagonized the rise in cyclic AMP produced by noradrenaline in both normal and 6‐OHDA‐treated mouse cortex. Morphine had no effect on the adrenaline‐stimulated cyclic AMP accumulation in mouse cortex but it entirely prevented the rise in cyclic AMP produced by isoprenaline. This effect was not observed in brain slices from 6‐OHDA‐treated mice. It is concluded that in slices of rat cortex, morphine stimulates postulated presynaptic, 6‐OHDA‐sensitive, opiate receptors associated with noradrenergic nerve terminals. These opiate receptors alter postsynaptic α‐ and β‐adrenoceptor activity. In the mouse, morphine appears to stimulate presynaptic opiate receptors that modify exclusively β‐adrenoceptor‐mediated cyclic AMP production.
Exaggerated cyclic AMP accumulation and glial cell reaction in the cerebellum during Purkinje cell degeneration in pcd mutant mice
Authors: Ghetti Bernardino , Truex Lewis , Sawyer Barry , Strada Samuel , Schmidt Michael 
Published: January 2005

AbstractThe Purkinje cell degeneration mutant (pcd) is characterized by a complete loss of cerebellar Purkinje cells. Norepinephrine causes an accumulation of cyclic AMP in the cerebellum of pcd that is far greater than in normal mice. Experiments were conducted (1) to correlate changes in the cyclic‐nucleotide response with a histologic examination of the cerebellum during neuronal loss and (2) to examine the role of cyclic AMP catabolism and adenosine receptor interactions in the phenomenon. The greatest elevation in cyclic AMP occurred between 30 and 128 days of age when a severe astrocytic response was demonstrated throughout the cerebellar cortex. Purkinje cells had degenerated by 45 days of age. Norepinephrine elicited a smaller increase in cyclic AMP from 155‐day‐old mice than at earlier ages, and the response continued to decrease with age; at 270 days, equal accumulation, and at 365 days, lower accumulation of cyclic AMP was detected in pcd cerebella. During this time, the Purkinje cell debris had been removed, the granule cell layer was depleted of granule cells, and the molecular layer was deprived of a large number of parallel fibers. However, although phagocytosis of neuronal debris was completed, large numbers of astrocytic processes were still seen in the neuropil.Biochemical experiments in vitro established that the exaggerated accumulation of cyclic AMP in the presence of norepinephrine was not due to lower catabolism of cyclic AMP, a synergistic interaction with adenosine, or a result of lower protein in the pcd cerebellum. The correlates of heightened norepinephrine‐stimulated accumulation of cyclic AMP with neuronal loss and the glial cell reaction might indicate that cyclic nucleotides play a role in controlling some glial cell functions, ie, proliferation, migration, and phagocytosis.
Electroblot analysis of the myelin proteolipid protein
Authors: Macklin Wendy B. , Braun Peter E. , Lees Marjorie B. 
Published: January 2005

AbstractThe myelin proteolipid has been studied by the electroblot method of Towbin et al [1979]. Samples were separated by SDS–polyacrylamide gel electrophoresis, transferred to nitrocellulose, and incubated with proteolipid antibody. The proteolipid band could be identified immunologically in CNS myelin and in whole brain homogenates. No proteolipid was detected in PNS myelin. Proteolipid from human, bovine, rat, and mouse myelin all cross‐react when analyzed by this method. No cross‐reactivity was indicated between proteolipid and myelin basic protein.
Effects of methadone on ornithine decarboxylase and cyclic nucleotide phosphohydrolase in neuronal and glial cell cultures
Authors: Vernadakis Antonia , Estin Charles , Gibson D. Ann , Amott Susan 
Published: January 2005

AbstractMixed neuronal and nonneuronal cell cultures were obtained from 8‐day‐old chick embryos cerebral hemispheres and glial‐enriched cultures were obtained from fifteen‐day‐old chick embryo cerebral hemispheres. Cultures were exposed to methadone, a narcotic drug, from days four to six. The activity of ornithine decarboxylase (ODC) was determined at day eight and the activity of cyclic nucleotide phosphohydrolase (CNP) was determined at day fifteen. Both ODC and CNP activity were higher in mixed neuronal‐nonneuronal cell cultures treated with methadone as compared to control. No effect was observed in the neuronal‐enriched or glial‐enriched cultures. These findings are interpreted to reflect that neuronal‐glial interaction is important in the response of primary neural cells to methadone.
Inhibitory action of high formamide concentrations on excitation‐contraction coupling in skeletal muscle
Authors: de Motta Gladys Escalona , Códoba F. , de León M. , del Castillo J. 
Published: January 2005

AbstractStrips of guinea pig ileum lose over 70% of their contractility when bathed in Krebs‐Ringer solution containing 0.4–0.9 M formamide (FMD). This effect is not accompanied by an appreciable loss of tissue water and is totally reversed by washing the preparation in normal solution. Frog sartorius muscles also paralyze when immersed in Ringer containing FMD, but higher concentrations (1.0–2.0 M) and longer exposure times are required. Contractility is not recovered upon transferring these muscles to normal Ringer. However, the contractile proteins still respond to activator calcium as shown by the fact that these muscles still contract in the presence of caffeine. The membrane of muscles uncoupled by FMD retain electrical excitability, and neuromuscular transmission appears to be unimpaired. However, alterations in the early after‐potential of the spikes suggest the occurrence of a sarcotubular disruption. Therefore, FMD appears to exert two separate effects on muscle: a reversible inhibition of contractility, as observed in ileal strips and an irreversible blockade due to an osmotic shock observed when frog muscles are returned to normal Ringer. The reversible effect is probably related to interference with the availability of activator calcium, since no marked inhibitory effects on the activities of the actomyosin‐like and the calcium‐dependent and ‐independent ATPases could be observed on FMD‐treated subcellular fractions.
Effect of phospholipase A2 on calcium transport in brain synaptosomes
Authors: Noremberg Krystyna , Łazarewicz Jerzy W. 
Published: January 2005

AbstractPretreatment of isolated brain synaptic endings with commercial phospholipase A2 isolated from venom of Apis mellifera, followed by a BSA washing, selectively inhibited the depolarization‐dependent portion of 45Ca uptake.Phospholipase A2 initially caused an increase of synaptosome respiration and subsequently inhibited their oxygen uptake, but this effect was completely abolished in BSA‐containing media.The classical uncoupler of oxidative phosphorylation, DNP, produced release of 45Ca or [3H]GABA from superfused synaptosomes previously loaded with radioactive calcium or GABA. The treatment of synaptosomes with phospholipase A2 had no effect on the spontaneous efflux of 45Ca or [3H]GABA. However, depolarization‐dependent release of [3H]GABA from synaptosomes treated with phospholipase A2 was significantly inhibited.We suggest that the inhibition of depolarization‐dependent influx of 45Ca into synaptosomes treated with phospholipase A2 may be attributed to the lesion of the specific function of plasma membrane rather than to the impairment of the calcium‐sequestrating function of intraterminal structures.
Kanic acid alters cholinergic responses in the rat retina: A 2‐deoxyglucose study
Authors: Gomez‐Ramos P. , Nelson S. , Walter D. , Cross R. , Samson F. E. 
Published: January 2005

AbstractIntraocular injections of the neuroexcitatory toxin, kainic acid, did not alter the output of the retinal ganglion cells, as determined by the rate of glucose use in the stratum griseum superficialis of the superior colliculus. However, significant differences were observed in cholinergic interactions of the ganglion cells after kainic acid treatment. Intraocular injection of kainic acid prevented the increase in the stratum griseum superficialis activity typically produced by systemic injection of the acetylcholinesterase inhibitor diisopropylfluorophosphate (DFP). In addition, the retinal ganglion cells were strikingly sensitive to intraocular injections of acetylcholine 1 week after exposure to kainic acid, reflected in the marked increased glucose utilization in the stratum griseum superficialis. This responsiveness to acetylcholine may be entirely due to the 80% decrease in acetylcholinesterase in the retina observed 1 week after kainic acid exposure or in part to a supersensitivity of the ganglion cells following the period of acetylcholine depletion.
Presynaptic effects of sodium bisulfite at the frog neuromuscular junction
Authors: Steinacker Antoinette 
Published: January 2005

AbstractBoth spontaneous and evoked transmitter release from the frog neuromuscular junction can be modified by application of sodium bisulfite, a reagent specific for disulfide bonds. An increase in miniature endplate frequency is produced that is not dependent on external calcium, sodium, or presynaptic terminal depolarization. The increased release can be halted by application of the sulfhydryl oxidizing agent DTNB. The response of bisulfite can be prevented by prior treatment of the endplate with acetylcholine or an anticholinesterase. It is concluded that bisulfite produces its effects by acting on a protein in the presynaptic membrane that is involved in regulation of transmitter release.
Cell surface‐mediated cellular interactions: Effects of B104 neuroblastoma surface determinants on C6 glioma cellular properties
Authors: Ciment Gary , de Vellis Jean 
Published: January 2005

AbstractTo study the influence of cell surface‐associated molecules on intercellular communication, C6 glioma cells were cultured both on plastic and on substrata of paraformaldehyde‐fixed B104 neuroblastoma cells. By then comparing the phenotypic expression of these “cocultured” C6 cells with cells cultured on tissue culture plastic, the influence of the cellular substratum was determined.The beta‐adrenergic‐responsive cyclic AMP‐generating system of C6 cells was compared on these various substrata. We found that fixed beds of dibutyryl cyclic AMP (dbcAMP)‐treated B104 cells uncoupled beta‐receptors from adenylate cyclase, whereas fixed beds of similarly treated C6 cells did not. However, other cellular properties were not affected by growth atop fixed dbcAMP‐treated B104 cell beds including the rate of C6 cellular proliferation and their rate of protein synthesis. The cell surface‐associated determinant on B104 cells capable of uncoupling the beta‐responsive cyclase system of C6 cells is probably a protein, as judged by its susceptibility to protease treatment.Other properties of C6 cells were also affected by the various substrata including basal and hydrocortisone‐induced levels of glycerol phosphate dehydrogenase (GPDH; an oligodendroglial marker) and the rate of RNA synthesis in these cells.
The ratio of 3‐hydroxyacyl‐CoA dehydrogenase to lipoamide dehydrogenase activity in individual muscle fibers: Mitochondrial specialization for source of energy
Authors: Hirsch Hilde E. , Parks Mary Ellen , Blanco Cesar E. , Simpson Donald R. 
Published: January 2005

Abstract3‐Hydroxyacyl‐CoA dehydrogenase (HAD) has been widely used to assess the capacity for fatty acid oxidation by different muscle fiber types, with various Krebs cycle enzymes as a base for comparison. We have measured this enzyme in individual lyophilized fibers of the guinea pig soleus and the white and red portions of the vastus lateralis, and compared its activity in each fiber with that of lipoamide dehydrogenase (LAD), which as a part of the pyruvate dehydrogenase complex fulfills a function similar to HAD in forming acetyl‐CoA, but from pyruvate and, thus, mainly from a carbohydrate source. The mean HAD/LAD ratio was 17.2 ± 3 in the red vastus, 24.9 ± 3 in the white vastus, and 43.7 ± 10 in the soleus, all differences being highly significant. The two types of fast fibers were not distinguished from one another by the enzyme ratio within either the white or the red portion of the vastus lateralis. Data from all of the fast fibers taken together indicate a close correlation (0.93) between the two enzymes, whereas values from the soleus indicate a specialization of the mitochondria of the slow muscle fibers for the oxidation of fatty acids.
Gonadal influences on the inhibition of monoamine oxidase type B activity
Authors: Vaccari Andrea , Biassoni Roberto 
Published: January 2005

AbstractMonoamine oxidase type B (MAO‐B) was similarly active in the hypothalamus of 60‐day‐old male and female Charles River rats. A single, 2 mg/kg IP injection of deprenyl, however, resulted in a significantly greater inhibition of hypothalamic MAO‐B in normal males than in normal females. Repeated administration of estrogen (estradiol valerate) to intact males postnatally, a treatment which disrupts the masculinization process, although not provoking true “feminization,” decreased the inhibition of MAO‐B, thus abolishing the sex‐specific difference. The intensity of deprenyl‐provoked hypothermia and ptosis in males exceeded that of females; neonatal and postnatal estrogenization of males resulted in diminution of these effects. Androgen administration to neonate females did little affect the biochemical and in vivo parameters of MAO inhibition. It is concluded that sex‐specific, biochemical differences in MAO‐B inhibition may have pharmacological correlates, and both facets of MAO inhibition are sensitive to neonatal exposure to estrogen.
Tay‐Sachs disease and normal cerebellar cells in culture: Elevated levels of lysosomal enzymes in Tay‐Sachs disease cells
Authors: Hoffman Linda M. , Brooks Steven E. , Schneck Larry 
Published: January 2005

AbstractTay‐Sachs disease and normal fetal cerebellar cells were maintained in culture for up to four weeks. Elevated levels of the lysosomal enzymes hexosaminidase B, β‐galactosidase, and acid phosphatase were observed in the Tay‐Sachs cells in long term cultures although elevated lysosomal enzyme levels were not observed in the normal cultures. Similarly, elevated lysosomal enzyme activities were observed in Tay‐Sachs cultures which had been treated with Concanavalin A.
ATPase activities in myelin and oligodendrocytes isolated from the brains of developing rats and from bovine brain white matter
Authors: Zimmerman Thomas R. , Cammer Wendy 
Published: January 2005

AbstractOf the Na, K‐ATPase activity in brain homogenates from 20‐, 60‐, and 120‐day‐old rats, 1.4 to 2.6% was recovered in myelin. The relative specific activities, at 0.2 to 0.3 times the specific activities in the rat brain homogenates, did not decrease during development, and myelin from bovine brain white matter had a similar relative specific activity. Oligodendrocytes from rat brains and bovine white matter had approximately one third the Na, K‐ATPase specific activities found in myelin from the respective sources. The Mg‐ATPase activity in rat brain myelin decreased during development and, in myelin from adult rats, was much lower than the Na, K‐ATPase activity. Notably, oligodendrocytes from both the forebrains of 10‐ to 120‐day‐old rats and from bovine white matter had high Mg‐ATPase activities. Whereas Na, K‐ATPase may be intrinsic to certain regions of the myelin sheath, the Mg‐ATPase in isolated myelin probably arises from fragments of oligodendrocyte membranes.