bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlates between nuclear magnetic resonance spectroscopy, diffusion weighted imaging and CA1 morphometry following chronic brain ischemia
Authors: de la Torre J. C. , Butler K. , Kozlowski P. , Fortin T. , Saunders J. K. 
Published: January 2005

AbstractChronic brain ischemia (CBI) was induced in aging (13 month) rats by ligating the left subclavian artery and placing temporary occluders in each common carotid artery [three‐vessel occlusion (3‐VO)]. Carotid artery occluders were removed after 1, 2, or 3 weeks following brain ischemia or maintained for 9 weeks. Two rats were kept with their occluders in place for 25 weeks. On weeks 3 and 9 after CBI, 31 P‐/1H‐nuclear magnetic resonance (NMR) spectroscopy and high resolution diffusion weighted imaging were performed in vivo, non‐invasively for detection of hippocampal high energy phosphates, lactate, intracellular pH, N‐acetyl‐aspartate, choline, glutamate, creatine, and structural alterations of the brain following CBI. Brains were histologically processed for morphometry of glial fibrillary acidic protein (GFAP) and CA1 damaged neurons 9 weeks after CBI. 31P‐/1H‐NMR spectroscopy showed that high energy substrates remained normal in ischemic animals when compared to non‐ischemic controls except for an elevation of phosphomonoesters in the hippocampal region. Rats deoccluded 1 and 2 weeks after initiation of CBI had no NMR spectroscopic or imaging changes. Rats kept ischemic for 9 weeks showed high signal intensities in the parietal cortex detected by diffusion weighted imaging as well as CAI damage and increased GFAP density but no cortical atrophy or neuronal damage could be detected histologically. Rats kept ischemic for 25 weeks showed extensive cortical atrophy which corresponded to the high, signal intensity observed with diffusion weighted imaging in the group kept ischemic for 9 weeks. These findings indicate that NMR spectroscopy and difussion weighted imaging can be used to follow the progress of neuronal injury in vivo and non‐invasively. Moreover, diffusion weighted imaging may be an excellent predictor of cerebral damage and atrophy prior to histopatholog ical detection of such damage. Our present and previous findings using our 3‐VO model indicate that this aging rat model may be useful in screening potential therapy for neurodegenerative disorders associated with abnormal aging and memory impairment. © 1995 Wiley‐Liss, Inc.
Signal transduction alterations in peripheral nerves from streptozotocin‐induced diabetic rats
Authors: Goraya T. Y. , Wilkins P. , Douglas J. G. , Zhou J. , Berti‐Mattera L. N. 
Published: January 2005

AbstractWe have previously determined the presence of muscarinic receptors and the expression of several G proteins in homogenates and myelin fractions from ra sciatic nerves. In the present study we investigates whether changes in several signal transduction path ways in peripheral nerves might be responsible for some of the biochemical abnormalities (e.g., phosphoinositide metabolism) present in sciatic nerves from streptozotocin‐induced diabetic rats. Sciatic nerves from 5 week diabetic rats that were prelabelled with [3H]‐myo‐inositol displayed a significant increase in the basal release of inositol mono‐and bis‐phosphate, while carbamylcholine‐stimulated release was significantly smaller. Basal‐ and forskolinstimulated adenylyl cyclase activity was significantly decreased in sciatic nerve homogenates from diabetic animals. However, we were unable to detect any significant differences in the levels of cAMP in intact nerves or in nerve segments that were incubated in the presence or absence of forskolin. ADP‐ribosylation experiments showed that in sciatic nerves from experimentally diabetic rats there was a significant increase in the ADP‐ribosylation catalyzed by cholera and pertussis toxins. Measurements of the levels of a‐subunits of G proteins revealed that the expression of Gq/11α, Gsα, and Gi‐3α was increased by 30 to 50%. These results indicate that during the course of experimental diabetes, peripheral nerves exhibit an abnormal production of inositol phosphates and cAMP, together with an abnormal expression and/or function of G proteins. One of the consequences of such alterations is the diminished release of inositol phosphates triggered by muscarinic agonists in diabetic sciatic nerves. © 1995 Wiley‐Liss, Inc.
Neurons express ciliary neurotrophic factor mRNA in the early postnatal and adult rat brain
Authors: Seniuk‐Tatton N. A. , Henderson J. T. , Roder J. C. 
Published: January 2005

AbstractThe regional and subcellular localization in the central nervous system (CNS) of postnatal day 5, day 15, and adult rats of ciliary neurotrophic factor (CNTF) mRNA was examined by in situ hybridization with biotinylated riboprobes. Probe specificity was determined by Northern blot analysis of poly(A) + RNA extracted from adult rat brain using digoxigenin labeled riboprobes and chemiluminescent detection. Both a 4 kb and a 1.2 kb transcript were detected in the cortex and brainstem. In situ hybridization revealed that CNTF mRNA was widely distributed in neurons and glia throughout the CNS at each of the developmental time points. The density of the neuronal hybridization signal was found to be greater in neuronal nuclei than in their cytoplasm. In the nucleus of most neurons, CNTF mRNA distribution was concentrated in a perinucleolar fashion. Alternate sections from the same animals, which were incubated with a specific polyclonal antibody against a CNTF peptide fragment, revealed that both neurons and glia in postnatal day 5, day 15, and adult rat brain were immunoreactive for CNTF. © 1995 Wiley‐Liss, Inc.
Identication of glial cell types involved in mediating epidermal growth factor's effects on septal cholinergic neurons
Authors: Kenigsberg R. L. , Mazzoni I. E. 
Published: January 2005

AbstractWe found previously that epidermal growth factor (EGF) decreases choline acetyltransferase (ChAT) activity in forebrain cholinergic neurons in vitro indirectly via glia (Kenigsberg et al.: Neuroscience 50:85–97, 1992). However, which glial type(s) are implicated in this response remained to be determined. Here we report that in primary cultures from the fetal rat medial septal area the complete elimination of oligodendrocytes or partial elimination of microglia from these cultures does not change the cholinergic cell response to EGF. However, the elimination of astroglia in our cultures by α‐aminoadipic acid treatment blocks EGF's effects on the chofinergic neurons. Co‐culture experiments using pure neuronal and purified glial cells from the medial septum further demonstrate that the cholinergic cell response to EGF can be maintained in the presence of astroglia only. In addition, it appears that EGF regulates the release of soluble factors from pure astroglial cultures following their peak mitotic response to EGF that decreases ChAT enzymatic activity. This soluble cholinergic neuromodulatory activity found in conditioned media from EGF‐treated astrocytes has a molecular weight greater than or equal to 10 kD and loses potency following multiple freeze‐thaw cycles.These results suggest that a direct glial cell response to a specific glial growth factor like EGF may have an important impact on the expression of local neurons, like the cholinergic in the forebrain. © 1995 Wiley‐Liss, Inc.
Coincidence of L‐glutamate/L‐aspartate transporter (GLAST) and glutamine synthetase (GS) immunoreactions in retinal glia: Evidence for coupling of GLAST and GS in transmitter clearance
Authors: Derouiche A. , Rauen T. 
Published: January 2005

AbstractOur aim was to identify proteins that mediate the uptake and degradation of synaptically released glutamate, focusing on the rat retina with its well‐defined glutamatergic pathways. Immunoreactivity against the L‐glutamate/L‐aspartate transporter (GLAST) is present in Müller cells. Ultrastructurally, even the finest glial processes, particularly those ensheathing identified structures of glutamatergic transmission (rod spherules), are immunoreactive for GLAST. Further light and electron microscopic observations revealed that also retinal astrocytes and pigment epithelial cells are immunoreactive for GLAST. No neuronal or microglial staining was observed. This is in line with uptake of exogenous [3H]glutamate previously localized specifically in Müller cells and pigment epithelium (Ehinger and Falck: Brain Res 33:157‐172, 1971). Since endogenous glutamate can only be demonstrated in Muller cells if glutamine synthetase (GS) is inhibited (Pow and Robinson: Neuroscience 60:355‐366, 1994), the immunocytochemical localization of GS was determined. GS immunoreactivity was found in all but only those cell types immunoreactive for GLAST. The light and electron microscopic patterns of immunoreactivity were very similar, particularly in the outer plexiform layer: The three cell types containing both GS and GLAST (Müller cells, astrocytes, and retinal pigment epithelium) are related developmentally. In the light of the two references quoted the present data indicate that the proteins mediating retinal uptake and degradation of synaptically released glutamate may be GLAST and GS, respectively, and that they may operate in concert to terminate the neurotransmitter action of glutamate. © 1995 Wiley‐Liss, Inc.
Growth related changes in sugar determinants on the surface of C6 glioma cells in culture: A cytochemical lectin‐binding study
Authors: Berezovskaya O. L. , Mares V. , Skibo G. G. 
Published: January 2005

AbstractThe cell surface sugar determinants (CSSD) were examined in C6 glioma cells in cultures at different conditions of growth by peroxidase conjugates of the lectins: peanut agglutinin (PNA), Ricinus communis agglutinin (RCA), Helix pomatia agglutinin (HPA), wheat germ agglutinin (WGA), lentil agglutinin (LCA), laburnum bork agglutinin (LABA), and lotus agglutinin (TPA). It was found that the cells bound more intensively WGA, LCA, and RCA compared to PNA, HPA; the weakest staining was provided by LABA and TPA. Binding intensity for PNA significantly increased after pretreatment of the cells with neuraminidase. This indicates that a part of the β‐D‐galactose residues on the surface membrane of C6 glioma cells is covered by sialic acid. The process of sialization was increased during the culturing of C6 glioma cells. Addition of cis‐DDP or dBcAMP to cultures growing in medium with 10% of CS increased the number of Gal residues which are not covered by sialic acid.The expression of β‐D‐galactose (Gal), N‐acetyl‐Dgalactosamine (NAcDGal), and fucose (Fuc) residues appeared to be most responsive to changes in growth conditions and degree of cell differentiation. The expressions of N‐acetyl‐D‐glucosamine (NAcDGIc) and mannose (Man) residues were high and seems did not depend on changing of the conditions of culturing.In C6 glioma cells cultures in which the rate of cell division, formation of the cell processes, and adhesiveness of the cells to the substratum were reduced by growing cells in MEM +, expression of β‐Gal, NAcDGa1, and Fuc was considerably reduced. The decrease of expression of R‐Gal, NAcDGaI, and Fuc on the surface of cell membrane was more pronounced in MEM + with 1% of CS than in MEM + with 10% of CS. In DbcAMP and cis‐DDP treated cultures, grown in medium with 1% serum, in which cell division was inhibited without obvious changes in cell adhesiveness to the substratum, binding of PNA and HPA was increased due to higher expression of β‐Gal and NAcDGaI. From these observations it was concluded that the pattern of expression of sugar residues on the cell surface varies according to the biological state of the cells and are easily affected by tissue culture conditions. © 1995 Wiley‐Liss, Inc.
Activation of the hypothalamo‐anterior pituitary corticotropin‐releasing hormone, adrenocorticotropin hormone and β‐endorphin systems during the estradiol 17β‐induced plasma LH surge in the ovariectomized monkey
Authors: Kerdelhué B. , Jones G. S. , Gordon K. , Seltman H. , Lenoir V. , Parsadaniantz S. Mélik , Williams R. F. , Hodgen G. D. 
Published: January 2005

AbstractThe present work describes time‐dependent changes in the content of corticotropin‐releasing hormone (CRH), adrenocorticotropin (ACTH), and β‐endorphin (β ‐EP) in the hypothalamus (HT) and anterior pituitary (AP) and in the concentration of ACTH and β‐EP in the plasma during the 17β estradiol (E2) benzoate (E2B)‐induced luteinizing hormone (LH) surge in ovariectomized cynomolgus monkeys. Monkeys were euthanized at 0, 30, 48, 72, and 96 hr post‐E2B. HT and AP were rapidly dissected, extracted in 2 N acetic acid containing 1 mM phenylmethane sulfonyl fluoride at 4°C, and centrifuged at 18,000g for 30 min. Peptide concentrations were measured in the supernatant by specific radioimmunoassays (RIAs). In the HT, there were significant (P < 0.05) decreases in ACTH and β ‐EP content by 30 hr post‐E2B and a significant (P < 0.05) decrease in HT CRH content 48 hr post‐E2B. Thereafter, CRH, ACTH, and β‐EP content increased up to 72 hr post‐E2B. In the AP, there was an almost linear decrease in the CRH content through 48 hr post‐E2B followed by a marked 20‐fold (P< 0.01) increase in the AP CRH content at 72 hr post‐E2B, which corresponds to the time of the descending arm of the LH surge. The patterns of ACTH and β‐EP content were very similar in the AP, while that of CRH differed markedly. In contrast, in the HT CRH, ACTH, and β‐EP profiles were very similar. Significant (P< 0.05) increases in circulating levels of ACTH, β‐EP, and cortisol were evident at 30 hr (all 3 hormones), 48 hr (β‐EP and cortisol), and 72 hr (cortisol) post‐E2B, which corresponds with the time of decreased hypothalamic content of CR1I, ACTH, and β‐EP. These results suggest that there may be a marked activation of the hypothalamo‐anterior pituitary‐adrenal axis during the negative and positive feedback phases of the E2B‐induced LH surge in the ovariectomized monkey. © 1995 Wiley‐Liss, Inc.
Transmitter release by non‐receptor activation of the α‐subunit of guanine nucleotide regulatory protein in rat striatal slices
Authors: Zelles T. , Chernaeva L. , Baranyi M. , Déri Z. , Adam‐Vizi V. , Vizi E. S. 
Published: January 2005

AbstractThe effects of 5 mM NaF + 10 μM AIC13, a direct activator of guanine nucleotide‐binding proteins (G proteins), on the release of [3H]dopamine ([3H]DA), [3H]gamma‐aminobutyric acid ([3H]GABA), and [3H]acethylcholine ([3H]ACh) were investigated in slices of rat striatum. When the tissue was exposed to NaF + AIC13 the release of [3H]DA, [3H]GABA, and [3H]ACh was enhanced significantly. In a calcium free solution the release of [3H]GABA and [3H]DA was increased by NaF + A1C13 much more than in the presence of [Ca2+]. In slice preparations taken from reserpinized animals, in which the vesicular storage of [3H]DA was therefore prevented, NaF + AIC13 had no effect on [3H]DA release. HPLC analysis of the radioactivity of the perfusate showed that, in the presence of NaF + AICI3, the content of dihydroxyphenylacetic acid (DOPAC) in perfusate samples increased significantly, while in pargyliue‐treated animals only the DA content was increased. Inhibition of DA carriers by nomifensine or low temperature prevented the effect of NaF + AIC13. N‐ethylmaleimide (NEM) preincubation did not modify the effect of NaF + AICl3 on [3H]DA release. Neomycin (0.1 mM), a phospholipase C (PLC) inhibitor, significantly decreased the effect of NaF + AlC13 on [3H]DA and [3H]GABA release. The internal concentration of Ca2+ in synaptosomes was enhanced by NaF + AIC13 in normal solution. However, [Ca2+]i was not influenced by NaF + AIC13 in Ca2+ ‐free medium. It is concluded that a non‐receptor‐mediated activation, by NaF + AICl3, of the a‐subunit of a G protein, results in a [Ca2+]o,‐independent release of DA and GABA, but not that of ACh. © 1995 Wiley‐Liss, Inc.
A 110‐kD nuclear shuttling protein, nucleolin, binds to the neurite‐promoting IKVAV site of laminin‐1
Authors: Kibbey M. C. , Johnson B. , Petryshyn R. , Jucker M. , Kleinman H. K. 
Published: January 2005

AbstractThe basement membrane protein laminin and the IKVAV‐containing sequence from the laminin αl chain have been found to promote the differentiation of primary neurons and a variety of neural cell lines. We previously reported that a 110‐kd IKVAV‐binding protein (LBP110) isolated from brain appears to be a member of the β‐amyloid precursor protein (APP) family by immunologic and functional studies, which showed that LBP110/APP is also important in neurite outgrowth (Kibbey et al.: Proc Natl Acad Sci USA 90:10150‐10153, 1993). In the preparation of this binding protein, a contaminating IKVAV‐binding protein of identical molecular weight, nucleolin, was also identified. Here we have studied the relationship between these binding proteins. We find that nucleolin binds specifically to the IKVAV sequence independently of LBP110/APP. We have also demonstrated significant levels of nucleolin in mature brain and in differentiating neural cells, suggesting that nucleolin functions not only in cell proliferation and in ribosome biogenesis as was previously reported, but also in the differentiation and maintenance of neural tissue. Our identification of cytoplasmic and cell‐surface nucleolin, an IKVAV‐binding protein, suggests that this protein may function in signalling by extracellular matrix. © 1995 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Fever induced in rats by intrahypothalamic macrophage inflammatory protein (MIP)‐1β: Role of protein synthesis
Authors: Fernández‐Alonso A. , Miñano F. J. , Myers R. D. 
Published: January 2005

AbstractThe effect of macrophage inflammatory protein‐β (MIP‐1β) on body temperature, following its injection into the anterior hypothalamic pre‐optic area (AH/POA), was examined by a radiotelemetry system in the freely moving rat. The purpose of this study was to examine the action of an inhibitor of protein synthesis, anisomycin, on the pyrexia which follows intrahypothalamic injection of MIP‐1β. The microinjection of 10 to 20 pg MIP‐1β into the AH/POA induced a. dose‐dependent monophasic increase in body temperature, whereas a higher dose of 25 pg of the cytokine caused a biphasic febrile response. When MIP‐β was heated at 70°C for 30 min prior to its administration, the pyrogenic response was abolished. Pretreatment of the micro‐injection site in the AH/POA with 10 αg anisomycin did not alter the febrile response to 25 pg MIP‐1β given at the same site in the AH/POA. When 10 mg/kg anisomycin was administered subcutaneously, the febrile response to 25 pg MIP‐1β injected in the AH/POA was significantly suppressed. The present results suggest that fever caused by MIP‐β within the cells of the AH/ POA may not require the synthesis of a new protein factor; however, the de novo synthesis of a protein outside of the AH/POA presumably plays a functional role, at least in part, in the intense fever produced by this cytokine in the hypothalamus. © 1995 Wiley‐Liss, Inc.
Effects of ethanol on neuroblastoma cells in culture: Role of gangliosides in neuritogenesis and substrate adhesion
Authors: Leskawa K. C. , Maddox T. , Webster K. A. 
Published: January 2005

AbstractMurine Neuro‐2A neuroblastoma cells were exposed to ethanol in culture under two experimental paradigms: (1) short‐term (24 hr or less) and low concentrations (0.05 to 0.5%; 8.5 to 86 mM) and (2) longterm (48 hr at 0.5%; 86 mM). Long‐term ethanol exposure did not affect Neuro‐2A viability, determined by DNA synthesis or the ability to exclude Trypan Blue. Similarly, long‐term ethanol treatment did not inhibit differentiation, exhibited by the extension of neurites, promoted by either dibutyryl‐cyclic‐AMP or by incubation with exogenous ganglioside GMI. The incorporation of exogenous ganglioside GM1 into plasma membranes was not influenced by varying concentrations of ethanol (up to 1.2%; 204 mM). In contrast, ethanol did influence Neuro‐2A cell attachment to collagen in a dualistic manner. During short‐term ethanol exposure, cell attachment was enhanced. However, when cells were initially exposed to ethanol for 48 hr a marked inhibition of subsequent attachment was observed. Long‐term ethanol exposure also inhibited attachment to other substrata, including laminin, fibronectin and vitronectin. Incubation of Neuro‐2A cells with either exogenous ganglioside Gull or a mixture of brain gangliosides partially reversed the inhibition of attachment to collagen. This reversal did not appear to be due to any one particular ganglioside structure, however. Mixed brain gangliosides were fractionated into three fractions, according to the number of sialic acid residues. Each of the three fractions were equally effective in partially restoring Neuro‐2A cell attachment to collagen after long‐term ethanol treatment. The results suggest that the mechanism by which these effects occur is at the level of plasma membrane fluidity, because both ethanol and glycosphingolipid content are known to influence membrane lateral mobility, although other mechanisms, such as changes in headgroup hydration, are possible. © 1995 Wiley‐Liss, Inc.
Perinatal morphine I: Effects on synapsin and neurotransmitter systems in the brain
Authors: Di Giulio A. M. , Tenconi B. , Malosio M. L. , Vergani L. , Bertelli A. , Gorio A. 
Published: January 2005

AbstractWe have previously shown that rat perinatal exposure to morphine causes dopaminergic and met‐enkephalin (ME) and substance P (SP) changes in the striatum during the early postnatal period (Tenconi et al.: Int J Dev Neurosci 10:517‐526, 1992); in addition it increases the susceptibility to neurotoxic lesions and impairs regenerative capacity of the serotoninergic system (Gorio et al.: J Neurosci Res 34: 462‐471, 1993). Our study shows that ME and SP levels increase postnatally in several areas of the rat brain, reaching the highest values between 30 and 60 days, after which the peptide content subsides to lower levels. Perinatal exposure to morphine increases such ME and SP levels during the early stages of postnatal life. No effect of morphine on 5‐HT and NE is observed, while the dopaminergic system is mainly affected in the mesencephalon. The pre‐ and postnatal brain expression of synapsin I mRNA is gradually and progressively localized in discrete areas of the brain. In the brain of rats perinatally exposed to morphine, the abundance of synapsin I mRNA expression is markedly reduced. Therefore, perinatal exposure to morphine affects early postnatal synaptic development in the brain as shown by the altered peptidergic and monoaminergic content and by the reduced synapsin I mRNA expression. © 1995 Wiley‐Liss, Inc.