bluuebunny/crossref_metadata_2025_split huggingface dataset:
α2‐Adrenoceptors are not involved in the regulation of striatal glutamate release: Comparison to dopaminergic inhibition
Authors: Harsing L. G. , Vizi E. S. 
Published: January 2005

AbstractStriatal slices from the rat were loaded with [3H]glutamate ([3H]Glu) superfused measure release of radioactivity at rest and during potassium‐evoked depolarization. Addition of KC1 (22‐40 mmol/liter) to the perfusion fluid enhanced the release of tritium in a concentration‐dependent manner, and this release was abolished by omission of CaCl2. High‐performance liquid chromatography (HPLC) separation coupled with radiochemical delection revealed that 23% and 41% of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respec‐lively, was due to [3H]Glu. At the end of the super‐fusion about 63% of residual tritium content in the tissue was [3H]Glu. Tritium efflux in response to KCI excess was significantly higher from striatum dissected from 6‐hydroxydopamine‐pretreated rats. Apomorphine decreased, the KCl‐evoked release of [3H]Glu haloperidol exerted the opposite effect, Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD‐1015 and γ‐butyrolactone‐pretreated rat caudate nucleus, also reversed the appmprphine inhibition of the, re‐lease of [3H]Glu evoked by depolarization. The selective α2‐adrenoceptor antagonist CH‐38083, however, did not modify the apomorphine inhibition of [3H]GIu release or dopa accumulation, andthe α2‐adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [3H]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and α2‐adrenoceptors are not involved in the regulation of glutamatergic transmission in the rat striatum. The effect of yohimbine on Glu release is attributed to its antidopaminergic rather than α2 adrenoceptor blocking effect.
Role of nucleus basalis in cholinergic control of cortical blood flow
Authors: Scremin O. U. , Torres C. , Scremin A. M. E. , O'Neal M. , Heuser D. , Blisard's K. S. 
Published: January 2005

AbstractThe present investigation was designed to determine the effect of lesions localized to the nucleus basalis/ substantia innominata (NB) on resting and cholin‐ergically activated regional cerebral cortical blood flow (rCBF). Ibotenic acid (l0μg) was infused locally at 1 mm caudal to bregma, 3 mm lateral to the midline, and 8 mm below the cortical surface. Effectiveness of lesions was demonstrated by histological verification of lesion sitesand determination of choline acetyltransferase activity in cerebral cortex homogenates. rCBF was measured with the autoradiographic iodo‐14C‐antipyrine technique. Resting rCBF was similar in the hemisphere that received the NB lesion and in the contralateral (intact) side in all regions examined. Physostigmine intravenous infusion (33 μg kg −1 min −1) enhanced rCBF in frontal, parietal, occipital, and temporal cortex. The increase was symmetrical, however, indicating inability of NB lesion to affect this phenomenon. It is concluded that the cortical cholinergic afferents originating in the NB are not involved in the control of rCBF.
Cerebrospinal fluid catecholamine metabolites in HIV‐infected patients
Authors: Larsson M. , Hagberg L. , Forsman A. , Norkrans G. 
Published: January 2005

AbstractTwenty‐eight HIV‐seropositive individuals—11 asymptomatic cases, 8 with lymphadenopathy syndrome (LAS), and 9 with AIDs—were investigated. Clinical staging of the AIDS dementia complex was done in the 9 AIDS patients. The catecholamine metabolites 3‐methoxy‐4‐hydroxyphenylglycol (MHPG) and homovanillic acid (HVA) in CSF were determined in all the HIV patients and in 20 healthy volunteers. The CSF MHPG levels did not differ significantly between healthy subjects and HIV‐infected patients at any stage of the infection. The CSF concentrations of HVA differed between the groups only during the AIDS stage. The mean CSF HVA value in the AIDS patients was 42% lower than in the healthy subjects and significantly lower than in any other stage of HIV infection (P > .01). Patients with signs cf the AIDS dementia complex had reduced CSF HVA levels, but there was no clear relationship between HVA concentration and stage of the AIDS dementia complex.
Differential taurine uptake in central and peripheral regions of goldfish retina
Authors: Lima L , Matus P. , Drujan B. 
Published: January 2005

AbstractThe transport system of taurine was investigated in fragments of goldfish retina prepared from the total tissue and from concentric regions: center and periphery. A high‐affinity, saturabie, sodium‐dependent system was demonstrated in the three types of fragments. The Kmfor one‐site analysis was similar in the two regions and the total retina. The analysis for two sites revealed a significant higher Km, for the high‐affinity site in fragments from the central region. The maximal uptake rate was higher in the central zone than in the total retina or the periphery. The Hill slopes obtained from saturation experiments of fragments of total retina, center, and periphery were similar to one other and near to 1. The slope of the time course uptake was intermediate for total retina and higher in the center than in the periphery. Hy‐potaurine and beta‐alanine were found to inhibit taurine uptake, but GABA was a weak inhibitor. The values of Kifor hypotaurine by one‐ and two‐site analysis were lower in the central region. The disruption of photoreceptors by shaking did not modify significantly the uptake of the amino acid. Remotion of endogenous taurine by dialysis of central and peripheral fragments increased the uptake in the periphery, but not in the center. The differences observed among the three samples revealed less affinity and high capacity for taurine uptake in the center, plus a higher sensitivity of inhibition. In addition, the peripheral zone had a greater affinity for taurine, and the maximal velocity of the entrance seems to bg inhibited by the higher concentration of the amino acid in this zone. These observations may reflect differences between proliferating and non‐proliferating regions of : The retina (i.e., periphery and center).
Purinergic stimulation of astroblast proliferation: Guanosine and its nucleotides stimulate cell division in chick astroblasts
Authors: Kim J.‐K. , Rathbone M. P. , Middlemiss P. J. , Smith R. W. , Hughes D. W. 
Published: January 2005

AbstractA highly active fraction that was mitogenic for astroblasts but which contained no amino acids was identified during the purification of peptides from chick embryo brains. This material was purified by ultracentrifugation, ultrafiltration through Diaflo PM‐30 and YM‐2 membranes and retention on Diaflo YC‐05, followed by ion exchange chroniatography and reversed phasehigh performance liquid chromatography (HPLC) on a C18 Deltapak column. On thin layer chromatography and HPLC the material co‐chromatographed with authentic commerciallyobtained GMP. Its ultraviolet absorption spectrum was also identical with that of GMP. 1H and 31P nuclear magnetic resonance spectra of the isolated material were identical with those of GMP. The close match between the fast atom bombardment (FAB) mass spectra of the unknown material and authentic GMP indicated that the unknown material was GMP of molecular weight 363 Da. Authentic, commercial GMP stimulated the growth of cultured chick astroblasts in the same dose‐dependent manner as the material from chick embryo brains; maximal stimulation was at 50 μM. Guanosine, GDP, and GTP also stimulated cell proliferation. The nucleotides were equally as effective as guanosine. 5′‐Guanylyl imido‐diphosphate, guanosine 5′‐O‐(2‐thiodiphosphate), and guanosine 5′‐N‐(3‐thiotriphosphate), guanine nucleotides which are relatively resistant to enzymatic hydrolysis, were also mitogenic, indicating that the nucleotides do not need to be degraded to nucleosides to be active and that they probably act extracellularly. Guanine nucleosides and nucleotides prompted astroblast growth when other growth factors were removed from the culture medium. The mitogenic effects of guanosine and its nucleotides were inhibited in a dose‐dependent fashion by micromolar concentrations of theophylline, a characteristic of phenomena mediated by purinergic receptors. Guanosineand its nucleotides are released in micromolar concentrations by hypoxic ordying cells. Under these circumstances these compounds may stimulate division of adjacent cells in vivo.
Differentiation of PC12 cells with K‐ras: Comparison with nerve growth factor
Authors: Simpson D. L. , Dickens G. , Doll S. , Koizumi S. , Tocco M. , Okuda O. , Oshima M. , Rudkin B. B. , Brightman M. , Guroff G. 
Published: January 2005

AbstractThe cell line PC12, derived from a rat pheochromocytoma, has served as a model for studies on the mechanism of action of nerve growth factor, as well as for the exploration of neuronal differentiation in general. When treated with nanomolar concentrations of nerve growth factor, these neoplasticchromaffin‐like cells stop dividing and acquire, for all intents and purposes, the phenotype of mature sympathetic neurons. This phenotype is characterized by the extensive outgrowtb of electrically excitable neurites, the ability to form functional synapses, and the acquisition of a number of biochemical markers.Treatment of PC12 cells with retro viral vectors encoding the K‐ras, the N‐ras, or the v‐src oncogenes also produces a marked morphological differentiation very similar to that seen upon treatment with nerve growth factor. Treated cells stop dividing and develop an extensive network of neurites. It has recently been shown that PC12 cells differentiated with v‐src, while resembling, morphologically, those treated with nerve growth factor, differ substantially in the biochemical characteristics normally associated with nerve growth factor‐induced differentiation.Cells infected with K‐ras also develop a neurite network similar to that seen after treatment with nerve growth factor. In addition, such cells develop tetanus toxin‐binding sites and saxitoxin‐binding sites, as do cells treated with nerve growth factor. Decreases in the binding of epidermal growth factor and in the activity of calpain also occur and these, as well, are characteristic of nerve growth factor‐treated cells. But the adhesive properties of cells infected with K‐ras are different than those of nerve growth factor‐treated cells, and the former do not show an increase in the NILE glycoprotein. Finally, K‐252a, an inhibitor of the actions of nerve growth factor on PC 12 cells, has no effect on the neurite outgrowth produced by infection with K‐ras. Thus, many of the key markers of nerve growth factor‐induced differentiation of PC 12 cells also appear upon differentiation with K‐ras, but there are, nevertheless, some crucial differences in the properties of these two sets of cells.
α Isoform of smooth muscle actin is expressed in astrocytes in vitro and in vivo
Authors: Lecain E. , Alliot F. , Laine M. C. , Calas B. , Pessac B. 
Published: January 2005

AbstractWe have previously reported that astroglial cell lines derived from spontaneously immortalized mouse cerebellar cultures as well as primary astrocyte cultures express the mRNA of the α isoform of smooth muscle actin. In this report, we have used an antiserum specific for the α smooth muscle actin protein to investigate the presence and the pattern of expression of a smooth muscle actin protein at the cellular level with immunocytochemical methods. The results show that an anti‐smooth muscle vessels α actin antiserum labels a typical actin network in the D19 astroglial cell clone and in flat astrocytes of primary cultures derived from various CNSregions of embryonic and postnatal mice. Furthermore, this antiserum labels distinct populations of astrocytes in the adult mouse brain, in particular in the corpus callosum and the fornix. However, in the corpus callosum, astrocytic processes are strongly labeled by anti‐SMV α actin antibodies only in parasagittal planes. Thus, a smooth muscle actin represents a newmarker for subsets of astrocytes.
Inhibition of mouse T‐cell proliferation by CGRP and VIP: Effects of these neuropeptides on IL‐2 production and cAMP synthesis
Authors: Boudard F. , Bastide M. 
Published: January 2005

AbstractWe compared the effect of two neuropeptides, calcitonin generelated peptide (CGRP) and vasoactive intestinal peptide (VIP), on mitogen‐induced murine splenocyte proliferation. Both neuropeptides exerted their maximal effect within 24 hr after activation by Con A. The combination CGRP‐VIP caused an additive inhibitory effect on T‐cell proliferation. The inhibitory effect of VIP could be correlated with a decrease in interleukin 2 (IL‐2) production, whereas CGRP did not affect this production. Since we also observed an additive inhibitory effect on T‐cell proliferation by the theophylline and CGRP or VIP combination, we measured the effect of each neuropepntide on intracellular cAMP production by enriched T‐cells: CGRP, but not VIP, strongly stimulated cAMP synthesis. Taken together, our results indicate that inhibition of murine T‐cell proliferation by CGRP and VIP is mediated by different mechanisms.
Population‐specific modulation of 5‐HT expression in cultures of embryonic rat rhombencephalon
Authors: Becquet D. , Héry F. , Héry M. , Drian M. J. , Faudon M. , König N. 
Published: January 2005

AbstractThis study aimed at analyzing the regulation of in vitro serotonin expression by neurons taken from different regions of the embryonic rat rhombenceph‐alon. We studied the influence of co‐culture with alar‐plate tissue using immunocytochemical and biochemical methods.Computer‐assisted densitometry was used to estimate the co‐culture effects on the serotonin content of the cell bodies. The more dynamic aspects of serotonin expression, such as synthesis and release, were studied by measuring (3H)serotonin newly synthe‐sized from (3H) tryptophan.The density of the immunostaining was significantly decreased in B1, B2 cells by co‐culture with both caudal and rostral alar‐plate tissue. For B4–B9 cells, only co‐culture with rostral alar‐plate tissue produced a significant decrease. The de novo synthesis of serotonin was significantly decreased in B1, B2 neurons co‐cultured with caudal alar‐plate tissue only. Once again, the B4–B9 cells proved to be less influenced by the experimental conditions, as co‐culture with both types of alar‐plate tissue produced no significant effect.We concluded that the in vitro expression of serotonin can be modulated by environmental factors, but the relative influence of these factors is very different in rostral versus caudal serotonin expressing cell populations.
Monoclonal antibody Br4 recognizes specific neuronal celltypes
Authors: Saito Mitsuo , Saito Mitsuo 
Published: January 2005

AbstractA monoclonal antibody termed as Br4 was prepared by a fusion of the myeloma P3 x 63‐AG8‐653 with spleen cells from BALB/c mice immunized with chick embryonic brain cells. Immunocytochemically, it reacts strongly with certain neurons in cerebral cortex, hippocampus, substantia nigra, and granular layer of cerebellum from rat brain but does not react with the white matter, A monoclonal antibody Br4 also reacts with primary cultured chick neurons, but not with cultured astrocytes. Western blots show that Br4 recognizes three proteins of 145,000, 108,000, and 97,000 molecular weight from the rat brain. The protein with molecular weight 145,000 (p145) and the protein with 97,000 molecular weight (p97) are essentially soluble; p145 is especially enriched in the synaptosomal soluble fraction. The protein with 108,000 molecular weight (p108) is found in both membranebound and soluble forms. Western blots show that among the tissues examined the three proteins are found most abundant in brain and especially enriched in the cerebral cortex and hippocampus. The Br4 antigens may be useful in identifying neuronal cell subpopulations in the central nervous system.
Substance P gene expression is regulated by interleukin‐1 in cultured sympathetic ganglia
Authors: Hart R. P. , Shadiack A. M. , Jonakait G. M. 
Published: January 2005

AbstractWe have investigated the effects of interleukin‐1β (IL‐1β) on the induction of substance P (SP) in cultured sympathetic ganglia. Northern blot analysis reveals that SP increases are secondary to an increase in mRNA coding for the preprotachykinin (PPT) precursor of SP. Nuclear transcription assays detect an early increase in PPT‐specific nascent transcripts, suggesting that the ultimate effect of IL‐1 is on transcription itself. Depolarizing agents, interferon‐γ glucocorticoid hormones, and prostaglandin synthesis inhibitors all diminish the induction of SP and PPT mRNA by IL‐1. Since SP has stimulatory effects on the immune system, the IL‐1–induced increase in ganglionic SP may be one means by which the nervous and immune systems interact during an acute response to ganglionic injury.
Protein kinase C‐induced redistribution of the cytoskeleton and phosphorylation of vimentin in cultured brain macrophages
Authors: Ciesielski‐Treska J. , Ulrich G. , Aunis D. 
Published: January 2005

AbstractThe phorbol ester 12‐O‐tetradecanoyl‐acetate (TPA) induced prominent and transient changes in the organization of the cytoskeleton in cultured amoeboid microglial cells including redistribution of actin toward the center of the cells and in the subplasmalemmal region, appearance of fine actin filaments, retraction of micro tubules (MT), and rearrangement of intermediate filaments (IF) containing vimentin. The possible implication of protein kinase C (PKC) in mediating the effects of TPA was suggested by a parallel shift of PKC activity from the soluble to membrane fractions and phosphorylation of several microglial proteins.The rearrangement of IF closely correlated with increased vimentin phosphorylation, detected by pulse labeling of intact cells. Two monoclonal antivimentin antibodies, B3 and V9, showed different staining patterns. Immunoreactivity with the antibody B3 was more restricted and could be abolished by treatment of fixed, permeabilized cells with alkaline phosphatase, thus suggesting that the antibody reacts with a phosphorylated epitope. Using this antibody, rearrangement of IF involving vimentin phosphorylation was detected within 15 to 60 min of treatment with 50 nM TPA and consisted in the appearance of intense perinuclear fluorescent label. This perinuclear fluorescence persisted up to 24 hr after TPA removal and gradually diminished during the following 2 to 3 days. Immunochemical analysis of nonionic detergent‐soluble and ‐insoluble extracts from untreated and TPA‐treated cells revealed no differences in vimentin solubility suggesting that TPA induced vimentin phosphorylation does not result in notable vimentin filament disassembly. However the extent of vimentin degradation was more prominent in TPA‐treated cultures indicating a higher sensitivity of vimentin to proteolytic degradation.The data show that PKC‐mediated phosphorylation of vimentin results in precise spatial and temporal rearrangement of IF which are not associated with altered vimentin solubility, but possibly changes the mechanical properties and interactions of vimentin filaments.
Cloning of a human cDNA expressing a high voltage‐activating. Tea‐sensitive, type‐a K+ channel which maps to chromosome 1 band p21
Authors: Rudy B. , Sen K. , De Miera E. Vega‐Saenz , Lau D. , Ried T. , Ward D. C. 
Published: January 2005

AbstractOver ten different mammalian genes related to the Drosophila Shaker gene (the Sh gene family) have been identified recently. These genes encode subunits of voltage‐dependent K+ channels. The family consists of four subfamilies: ShI genes are homologues of Shaker; ShII, ShIII, and ShIV are homologues of three other Shaker‐like genes in Drosophila, Shab, Shaw, and Shal, respectively We report here the cloning of a human K+ channel cDNA (HKShIIIC) obtained from a brain stem cDNA library. HKShIIIC transcripts express an atypical voltage‐dependent transient (A‐type) K+ current in Xenopus oocytes. This current is activated by large membrane depolarizations and is extremely sensitive to the K+ channel blocker TEA unlike most A‐type currents. The gene encoding HKShIIIC maps to chromosome 1p21.
Sequence of the rabbit neurofilament protein L
Authors: Soppet D. R. , Beasley L. L. , Willard M. B. 
Published: January 2005

AbstractIn the course of screening a rabbit brain cDNA library with a probe for the H neurofilament protein, we identified a neurofilament L‐cDNA. Its nucleotide sequence is 88% identical to that of human, indicating that L is highly conserved among species. The similarities between the sequences of L from rabbit and mouse suggest that the species‐specific accumulation of neurofilaments that occurs in rabbit during aluminum intoxication is not a consequence of the primary structure of L.
Histamine effects on the 5‐HT1c receptor expressed in Xenopus oocytes
Authors: Shichijo S. , Payan D. G. , Harrowe G. , Mitsuhashi M. 
Published: January 2005

AbstractTo analyze the cross‐reactivity between serotonin (5‐HT) and histamine, the in vitro transcribed RNA for the 5‐HT1c receptor was functionally expressed in Xenopus oocytes. 5‐HT significantly increased 45Ca2+ efflux in RNA‐injected oocytes, but not in uninjected and water‐injected control oocytes. Furthermore, histamine and the H1 receptor agonists, but not the H2 and H3 agonists, significantly induced 45Ca2+ efflux in 5‐HT1c receptor RNA‐injected oocytes, but not in uninjected and water‐injected oocytes. However, the H1, H2, and H3 antagonists failed to inhibit histamine‐induced 45Ca2+ efflux at 10−6M. This finding suggests that the 5‐HT1c receptor can be activated by both 5‐HT and histamine, although the action of histamine is different from classic histamine pharmacology.
Changes in β‐adrenergic receptor distribution on immunocytes during differentiation: An analysis of T cells and macrpphages
Authors: Radojcic Tricia , Baird Stephen , Darko Denis , Smith Dennis , Bulloch Karen 
Published: January 2005

AbstractThe ability of cells of the immune system, immunocytes, to receive signals from the nervous as well as the endocrine system is dependent on the cells' expression of receptors for neurotransmitters and neurohormones. The number of receptors, especially beta adrenergic receptors (BARs), varies with the functional subset of immunocytes. However, little is known about how receptor number may vary during the life span (stem cell to mature activated immunocyte) of a given cell type. In this study, we have addressed this question by examining the affinities (Kd's) and the changes in receptor number (Bmax) on (1) clones of T cells and macrophages, (2) fresh thymocytes and splenocytes before and after activation with Concanavalin A (Con A) and phorbol myristate acetate (PMA)/ Ca+2 ionophore (A23187), and (3) the cloned human monocyte U937 and the murine thymic lymphoma cell BW5147, in the presence and absence of PMA and A23187 ionophore.Drug treatments of fresh and cloned immunocytes alter the number but not the affinity of β‐receptors. Con A increases the number of β‐adrenergic receptors per cell, whereas PMA/ionophore decreases it. Similar decreases in BAR number are induced by PMA on cell lines BW5147 and U937. These data indicate that changes in receptor number can be regulated with different states of cell maturation and function. Thus, the immunological status of a given cell can influence the expression of BARs, thereby modulating its ability to respond to signals from the nervous and endocrine systems.