bluuebunny/crossref_metadata_2025_split huggingface dataset:
Putative glutamate receptors in membranes obtained from heads of Drosophila melanogaster
Authors: Fiedler J.L. , Inestrosa N.C. , Bustos G. 
Published: January 2005

AbstractThe specific binding of L‐[3H]‐glutamic acid (GLU) was examined in membrance preparations derived from heads of Drosophila melanogaster. L‐[3H]‐GLU bound to the membrane preparation with biphasic in a reversible and saturable way. The specific binding was inhibited by Cl− and Ca2+ ions. Saturation analysis of the data fit a model of two independent binding sites with dissociation constants (KD) of 29 nM and 249 nM and corresponding binding site densities (Bmax) of 5.7 and 24.6 pmol/mg protein. A series of excitatory amino acid receptor agonists and antagonists were tested as inhibitors of L‐[3H]‐GLU specific binding. Some compounds almost totally abolished the specific binding, whereas others reduced the binding to 45% over the concentration range used. Among the first type of inhibitors, L‐GLU was the most potent, D‐aspartate (D‐ASP) and D‐GLU were 10 times less effective than L‐GLU, whereas quisqualic acid had the lowest potency. Among the second type of inhibitors, glutamate diethyl ester, D‐α‐amino adipate, and N‐methyl‐D‐aspartate showed the highest potency, and DL‐2‐amino‐4‐phosphonobutyrate was the less effective. Kainic acid and γ‐amino butyric acid were not able to modify at any concentration used the specific binding of L‐[3H]‐GLU. These data suggest the presence of putative GLU receptors in the brain of Drosophila.
Modifications of light responses in the superior colliculus following cortical cryoblockade
Authors: Molotchnikoff S. , Lamothe L. , Cérat A. , Lachapelle P. 
Published: January 2005

AbstractResponses to light stimuli of cells in the superior colliculus (SC) were studied in anesthetized and paralyzed rabbits after reversible inactivation of corticocollicular impulses by cooling of the visual cortex. The recording of flash‐evoked responses and EEG allowed us to monitor the time course of the inactivation and its recovery. The cell's responses were measured prior to, during, and after cortical blockade. In about half of the collicular cells, disruption of cortical functions resulted in a sharp decline of collicular responsivity. All types of response were affected equally. Hence, the cortex has a global tonic excitatory impact.
Androgen and estrogen receptors in adult zebra finch brain
Authors: Siegel L.I. , Akutagawa E. , Fox T.O. , Konishi M. , Politch J.A. 
Published: January 2005

AbstractAndrogens and estrogens have been implicated in the activation of a variety of sexually‐dimorphic, hormone‐dependent behaviors in the adult zebra finch. In the present report, several biochemical characteristics of two putative sex steroid receptors, androgen‐ and estrogen‐binding activities, were determined by DNA‐cellulose chromatography in brain tissues from these birds. High‐affinity, limited‐capacity receptors for androgens and estrogens were found in cytosolic extracts of telencephalon, diencephalon‐mesencephalon, and metencephalon‐myelencephalon from adult male and female zebra finches. Androgen‐binding activity reproducibly adhered to DNA‐cellulose and was eluted within the 110‐150 mM NaCl region of a linear salt concentration gradient. Estrogen receptors adhered to DNA‐cellulose and exhibited elution maxima between 170 mM and 210 mM NaCl. Collectively these data indicate that brain regions of zebra finches contain steroid receptors that are similar to those found in the brains of other vertebrates and that their biochemical properties are similar in males and females. Quantitatively, males consistently exhibited higher androgen binding than females in both anterior and posterior telencephalic areas. Females treated with estradiol immediately after hatching exhibited adult levels of androgen binding corresponding to those detected in males. Masculinization of the androgen receptor system by early steroid exposure is discussed.
Myelin‐associated glycoprotein (MAG) in the CNS of adult shiverer (Shi/Shi) mice
Authors: Sheedlo H.J. , Siegel G.J. 
Published: January 2005

AbstractBrain fractions of adult control (+ / +) and shiverer (Shi/Shi) mice were investigated by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDS‐PAGE) and immunoblotting. Immunostaining with specific antisera against rat brain myelin‐associated glycoprotein (MAG) was detected at about the 96‐kD region of gels in electrophoresed samples of the total homogenate, low‐speed supernatant fraction, and low‐ and high‐speed sedimentable portions of brain from +/+ mice. Reduced immunostaining was observed in the corresponding samples of brain fractions from Shi/Shi mice. The cerebrum, cerebellum, and medulla of +/+ and Shi/Shi mice were examined immunocytochemically for MAG on paraffin‐embedded sections. Periaxonal immunostaining for MAG was observed in all the regions and the highest concentrations were in the corpus callosum, in the central cores of cerebellar folia, and in the medulla. Patterns of distribution were similar in +/+ and Shi/Shi mice, although the density of immunostaining around individual axons and the number of immunostained axons were significantly reduced in Shi/Shi mice. In addition, the three brain regions of Shi/Shi mice exhibited oligodendrocyte‐like cells that contained immunostaining for MAG in the cytoplasm and periphery of their perikarya. This type of immunostained cell was not observed in +/+ mice. In this study, immunoblotting with brain fractions and immunocytochemistry revealed strong evidence for reduced concentrations of MAG in the CNS of Shi/Shi mice compared to control mice. In addition, there is immunocytochemical evidence for abnormal accumulation of MAG in perikarya of oligodendroglial‐like cells, suggesting the possibility of a transport block for myelin proteins in the shiverer mutant.
Cellular localization of tyrosine hydroxylase mRNA and its regulation in the rat adrenal medulla and brain by in situ hybridization with an oligodeoxyribonucleotide probe
Authors: Han V. K. M. , Snouweart J. , Towle A. C. , Lund P. K. , Lauder J. M. 
Published: January 2005

AbstractTyrosine hydroxylase (TH) is the rate‐limiting enzyme in the synthesis of catecholamines in neural tissues and adrenal medulla. To study the expression of the TH gene and its regulation in adult and developing neural tissues, we have synthesized an oligodeoxyribonucleotide probe (oligomer) that is specific for TH mRNA. Using Northern blot hybridization of polyadenylated RNAs from adrenal gland, brain stem, liver, and cerebral cortex with the 32P‐labeled oligomer, a single TH mRNA of 1.9 kb was detected in adrenal gland and brain stem but not in liver and cerebral cortex. Using this TH‐specific oligomer, TH mRNAs were localized to the chromaffin cells in the adrenal medulla and to catecholaminergic neurons in locus coeruleus and substantia nigra by in situ hybridization histochemistry. After reserpine administration, the intensity of hybridization signal was increased to threefold that of normal in sections of adrenal medulla and twofold that of normal in locus ceruleus. No difference in hybridization signal intensity was observed in the substantia nigra of normal and reserpine‐treated animals. Use of this specific TH probe in in situ hybridization procedures represents a powerful approach to the study of regulation of TH gene expression at the cellular level.
Ganglioside‐induced alterations in hippocampal cholinergic enzymes and Na, K–ATPase after fimbria–fornix transection
Authors: Fass B. , Ramirez J. J. , Stein D. G. , Mahadik S. P. , Karpiak S. E. 
Published: January 2005

AbstractPrevious biochemical findings suggest that exogenous gangliosides enhance cholinergic sprouting in the hippocampus after partial lesions of the septohippocampal pathway. To assess whether GM1 ganglioside accelerates the onset of this sprouting after complete lesions, we measured cholinergic enzymes and Na, K‐ATPase activity in the hippocampus of rats with unilateral fimbria‐fornix transection. At 14 and 18 days postlesion, histochemical staining showed that acetylcholinesterase (AChE) was almost completely eliminated in the hippocampus ipsilateral to the transection in untreated and GM1‐treated rats. Biochemical assays confirmed that GM1 treaments did not increase AChE activity in the denervated hippocampus. Rather, there were significant reductions of AChE and choline acetyltransferase activities in the ipsilateral hippocampus relative to the contralateral value (P < .001); and the reductions were greater in GMI‐treated rats than in untreated controls (P < .001). Na, K‐ATPase activity in the ipsilateral hippocampus increased by 10.1% in GM1‐treated rats, whereas it decreased by 21.7% in untreated controls (P < .05). Since Na, K‐ATPase is enriched in synaptic membranes, the increased activity of this enzyme may indicate that GM1 treatments stabilize surviving synaptic membranes and/or accelerate the onset of sprouting in the denervated hippocampus. The reductions in cholinergic enyzymes, however, imply that the sprouting pathway must be noncholinergic.
Identification of two cell surface proteins of rat brain oligodrocytes in culture
Authors: Pari F. M. , de los Monteros A. Espinosa , Roussel G. , Nussbaum J. L. 
Published: January 2005

AbstractAntibodies specific for the surface of oligodendrocytes were prepared by incubating living cultures of pure oligodendrocytes with a crude anti‐oligodendrocyte antiserum. These specific antibodies, when used in the technique of immunoelectroblotting, led to the characterization of at least two major plasma membrane proteins of 43 kilodaltons (kDa) and 53 kDa, respectively, as accessible at the external surface of the oligodendrocytes. The 53‐kDa protein was also found in oligodendrocyte‐conditioned medium in significant amounts. Additional oligodendrcyte surface proteins were also detected in the Wolfgram protein fraction.
Recovery of cholinesterases in soman‐injected superior cervical ganglion of the rat in the presence and absence of innervation
Authors: Klinar B. , Brzin M. 
Published: January 2005

AbstractWe have previously described the procedure for quantitative separation of extracellular and intracellular ChEs using mild treatment of rat superior cervical ganglion with papain. Here, this procedure was used in order to investigate the recovery of ChEs in the two pools after irreversible inhibition by soman which was directly injected into the ganglion. After such treatment only ganglion ChEs were totally inhibited, whereas the activity of ChEs in preganglionic neurons and their axons remained unaffected. Comparing in innervated and decentralized ganglia the pattern of recovery rate and ultrastructural reappearance of ChEs after local inhibition, it was possibleto distinguish between the indirect effects of innervation on the recovery rate and pattern of ChEs of ganglion origin and the direct contribution to the total ganglion enzyme activity of ChEs originating in the preganglionic elements.The absence of nerve contracts affects mostly extracellular activity, particularly AChE, whereas the intracellular activity of AChE was only slightly decreased and the activity of nsChE was somewhat increased. This increase coincides with the enhanced cytochemical reaction of nsChE in some nonneuronal cells in the ganglion.Actinomycyn D decreased the rate of initial rapid phase of recovery of intracellular ChEs when injected in the ganglion daily for three days, whereas the recovery of extracellular ChEs was already decreased the first day of Actinomycyn D application. This indicates that the externalization of the enzyme is more affected than its synthesis by inhibition the translation step.The results further suggest that functional innervation of the ganglion down‐regulate the rate of reappearance of the new enzyme at the extracellular and intracellular locations and changes the ratio between AChE and nsChE. ChEs synthesized in preganglionic neurons begins to contribute directly to the total ganglion ChEs activity in the late stages of enzyme recovery in spite of the presence of the preganglionic ChEs which was not inhibited after intraganglionic injection of soman. This finding suggests that the externalization and extracellular attachment of ChEs and not their preganglionic resynthesis may be the cause for delayed reappearance of ChEs affiliated with nerve terminals in the ganglion.
Neurite‐promoting activity from fetal skeletal muscle: Immunological comparison with laminin
Authors: Steele J. G. , Dalton B. A. 
Published: January 2005

AbstractPolycation‐binding neurite‐promoting factor (PNPF) from skeletal muscle of bovine fetuses has been compared to mouse tumor laminin by an immunological approach. Antiserum prepared against PNPF blocked the neurite‐promoting activity in a dose‐dependent manner. The anti‐PNPF antiserum bound to Mr = 200,000‐;195,000 bands as well as several components of higher molecular weight, as detected in immunoblots of reduced PNPF. The anti‐PNPF antiserum did not inhibit the neurite‐promoting activity of mouse laminin, although it did bind to native laminin. Antilaminin antiserum bound to PNFP and identified the same Mr = 200,000−195,000 bands and two other higher‐molecular‐weight bands, as did the anti‐PNPF antiserum. The activity of PNPF was confirmed to be sensitive to treatment with heparitinase. It is concluded that PNPF from bovine fetal muscle contains a complex of heparan sulfate and high‐molecular‐weight components, particularly of Mr = 200,000‐195,000, which share antigenic determinants with mouse laminin. However antilaminin antiserum fails to inhibit the activity of PNPF, suggesting that the active site, and/or adjacent regions, of PNPF are antigenically different from the neurite‐promoting site of purified mouse tumor laminin.
Receptors for nerve growth factor on rat spleen mononuclear cells
Authors: Thorpe L. W. , Stach R. W. , Hashim G. A. , Marchetti D. , Perez‐Polo J. R. 
Published: January 2005

AbstractConsiderable evidence is mounting to support the concept of a modulatory role for the brain and neuroendocrine system on the immune response. This neuroimmunomodulation occurs in part through the interaction of specific neurosubstances with receptors on lymphocytes and monocytes. Nerve growth factor (NGF) is a neuronotrophic factor necessary for the development and maintenance of sympathetic and embryonic sensory neurons. This trophic effect is initiated through binding of NGF at specific cell surface receptor sites on NGF‐responsive cells. Several recent studies suggest that NGF may interact with cells of the immune system and may play a role in the regulation of some immunologic reactions. In this study we report on the presence of specific receptors for NGF on the surface of mononuclear cells from rat spleens. The NGF‐binding sites are of the low‐affinity type with Kd's in the 10−9 M range. These receptors migrate on SDS‐PAGE as two molecular species of approximately 190 and 125 kilodaltons. Our findings of receptors for NGF on lymphocytes and accessory cells support other evidence that NGF may influence immunoreactivity in vivo.
Is the muscarinic receptor that mediates potentiation of dopamine release negatively coupled to the cyclic GMP system?
Authors: Marchi M. , Paudice P. , Gemignani A. , Raiteri M. 
Published: January 2005

AbstractDopamine (DA) terminals in rat corpus stratum and frontal cortex possess muscarinic receptors that mediate enhancement of the depolarization‐evoked release of the catecholamine. The effects of the membrane‐permeating cyclic guanosine monophosphate (cyclic GMP) analog 8‐Br‐cyclic GMP and of the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) on the muscarinic‐induced increase of DA release were investigated in striatal synaptosomes prelabeled with [3H]DA and exposed in superfusion to 15 mM KCl and to acetylcholine (ACh). Preincubation of synaptosomes with 8‐Br‐cyclic GMP (10‐200 μM) or with IBMX (200 μM) prevented the ACh‐induced enhancement of [3H]DA release, without affecting the K+ ‐evoked release of the [3H]amine. No significant decrease of the ACh effect was observed when 8‐Brcyclic GMP or IBMX were added concomitantly with ACh to the superfusion medium. The data suggest that stimulation of presynaptic muscarinic receptors on DA terminals may produce enhancement of 3HDA release through a decrease of the intraterminal cyclic GMP content.
Glial fibrillary acidic protein immunohistochemistry of spinal cord astrocytes after induction of ischemia or anoxia in culture
Authors: Goldberg W. J. , Connor J. R. , Bernstein J. J. 
Published: January 2005

AbstractThe effects of ischemia (removal of oxygen and glucose for 4 h) and anoxia (removal of oxygen alone) on astrocytes were studied in dissociated cultures of E14 spinal cord containing both neurons and astrocytes. In addition, a group of cultures was treated with a low Na+, low Ca2+, and high K+ medium during the 4‐h ischemic period (ischemia‐protected group), a process that protects neurons from ischemic damage under identical conditions. Astrocytes were examined immunohistochemically using glial fibrillary acidic protein (GFAP) antiserum 24 h after insult. Densitometry and statistical analysis (1‐way analysis of variance [ANOVA], a priori; 2‐tailed Tukey‐t, a posteriori) of the digitized images of the somata and processes of astrocytes in the anti‐GFAP reacted cultures showed significant differences between the groups; a significant increase (P<0.01) in the GFAP‐positive reaction in the somata of ischemic astrocytes and a significant decrease (P<0.01) in the GFAP‐positive reaction in the processes of ischemic, ischemia‐protected, and anoxic astrocytes. There were no significant differences in the GFAP immunoreactivity of somata between control, ischemia‐protected, and anoxic astrocytes or of processes from ischemic, ischemia‐protected, and anoxic astrocytes. These data show that following ischemia cultured astrocytes increase somatic GFAP immunoreactivity compared to all other groups tested whereas the staining intensity for GFAP was decreased in the processes of all three experimental groups compared to controls. Ischemia protection resulted in the absence of the enhancement of somatic GFAP immunoreactivity. The relationship of the astrocytic response and the type of cellular stress is discussed.
The macroglial cells of the leech are molecularly heterogeneous
Authors: Flaster M. S. , Zipser B. 
Published: January 2005

AbstractMonoclonal antibodies derived from fusions employing either whole leech nerve cords or frationated proteins (gel bands) bind to the macroglial cells of the nerve cord. Three different antibodies bind to either one, two, or three of the four macroglial cell types in the leech CNS, serving as markers and showing that these four cell types, which differ primarily by anatomical position, all differ molecularly as well. Conventional microscopy confirms the existence of a novel macroglial cell type first noted because it binds antibody. Western (immunoblot) blot analyses demonstrate a polypeptide antigen of 77 kD in the macroglial cells of the connectives and a 130‐kD polypeptide antigen associated with the macroglial cells of the connectives, of the root nerves, and of the ganglionic neuropil. The extensive molecular heterogeneity of leech neurons demonstrated by monoclonal antibody techniques is shared by macroglia.
Dehydroepiandrosterone and its sulfated derivative reduce neuronal death and enhance astrocytic differentiation in brain cell cultures
Authors: Bologa L. , Sharma J. , Roberts E. 
Published: January 2005

AbstractHuman studies of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA‐S) have shown age‐related changes in serum levels of these two sex hormone precursors. The levels of both DHEA and DHEA‐S are characterized by monotonic decreases after puberty in females and after 20–24 yr of age in males. Further studies have shown that DHEA and DHEA‐S levels are significantly low or close to minimal at ages when the incidence of senile dementia of Alzeimer's type (SDAT) begins to increase. We propose that DHEA and DHEA‐S play a significant role in normal function of neuronal cells and that supplementation with them may prevent neuronal loss and/or damage. In the present study, using methods of immunocytochemistry, autoradiography, and scanning electron microscopy, we show that a supplement of as little as 10−8 M DHEA or DHEA‐S greatly increases neuronal survival and differentiation and reduces astroglial proliferation rates in mouse brain cells in cultures. These results suggest that correcting the DHEA and the DHEA‐S deficit may prevent and/or improve the SDAT condition in humans.
Effect of purkinje cell loss on cerebellar gangliosides in nervous mutant mice
Authors: Seyfried T. N. , Bernard D. J. , Yu R. K. 
Published: January 2005

AbstractThe distribution of cerebellar gangliosides was studied in adult (73 ± 2 days) nervous (nr/nr) mutant mice which lose 50–90% of their Purkinje cells. This neuronal loss is associated with significant reductions in cerebellar weight and ganglioside concentration. The cerebellar dry weights (mg) and the ganglioside concentrations (μg N‐acetylneuraminic acid per 100 mg dry weight) in nr/nr mice and age‐matched normal littermates (+/?) are 7.4 ± 0.3 mg and 13.2 ± 0.4 mg; and 411.7 ± 4.8 μg and 438.5 ± 2.1 μg, respectively. Abnormalities were also observed for the concentration of certain ganglioside species. Most notably, GT1a is significantly reduced by 42%, and GD3 is significantly increased by 29% in the nr/nr mice compared to the +/? mice. The nr/nr mice also express a slight but significant reduction in GT1b. No ganglioside abnormalities were observed between the nr/nr and +/? mice in cerebral cortex. We previously found reduced cerebellar GT1a content in other mutants that also lose Purkinje cells, i.e., sg/sg, pcd/pcd, and Lc/+. GT1a is not reduced, however, in wv/wv mice that lose mostly granule cells. The findings in nr/nr mice are therefore consistent with our hypothesis that GT1a is enriched in Purkinje cells. GD1a, which is enriched in mature granule cells, is not reduced in the nr/nr mice. Since we previously found that GD3 is a good marker for reactive glia in neurological disease, the elevated GD3 concentration in the nr/nr mice indicates a mild gliosis. Our findings with nr/nr and the other neurological mutants indicate that gangliosides can be useful as cell‐surface markers for monitoring changes in the cytoarchitecture of the mouse cerebellum.
Effect of ascorbic acid on the synaptosomal uptake of [3H]MPP+, [3H]Dopamine, and [14C]GABA
Authors: Sershen H. , Debler E. A. , Lajtha A. 
Published: January 2005

AbstractThe effects of ascorbic acid on the synaptosomal uptake of [3H]MPP+, [3H]dopamine, and [14C]GABA were examined in attempts to understand the mechanism of ascorbic acid attenuation of MPTP neurotoxicity. [3H]Dopamine uptake was increased at lower levels (0.01 and 0.1 mM) and decreased at higher levels (10 mM) of ascorbic acid. Ascorbic acid inhibited [3H]MPP+ uptake (IC50 = 0.1 mM) and [14C]GABA uptake (IC50 = 10 mM). Washout of ascorbic acid restored uptake of [3H]dopamine and [3H]MPP+, suggesting that ascorbic‐acid‐induced lipid peroxidation was not involved in the effect on uptake. In addition to the possible involvement of antioxidant mechanisms in the in vivo attenuation of the neurotoxicity of MPTP by ascorbic acid, the present results indicate a direct effect of ascorbic acid in inhibiting the uptake of MPP+ into dopaminergic nerve terminals.