bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of arachidonic acid on respiratory activities in isolated brain mitochondria
Authors: Hillered L. , Chan P. H. 
Published: January 2005

AbstractThe present investigation was designed to examine the effects of free arachidonic acid (20:4),in concentrations relevant to cerebral ischemia, on brain mitochondrial respiratory activities and the reversibility of these effects. Incubation of brain mitochondria with 20:4causeda dose‐department increasein substratesupported (state 4) respiration (i.e., uncoupling) and a concomitant inhibition of substrate‐, phosphate‐, and ADP‐supported (state (3) or dinitrophenol‐supported state (3u) respiration. The temperature dependence of the 20;4 effects on mitochondrial respiration was also studied. It was found that the uncoupling and the respiratory inhibition were at least as pronounced at physiological temperatures as at room temperature. Arrhenius plots of the state 3 respiratory rates suggested that 20:4 did not cause a significant change in membrane fuidity. Addition of bovine serum albumin to the reaction medium following preincubation with 20:4 reversed the inhibition of state 3 respiration. The results suggesat (1) that 20:4mayinhibit mitochondrial ATP production during conditions of incomplete cerebral ischemia and 2) that 20:4 may limit the postischemic recovery of mitochondrial function.
Development of the amino acid pools in chick embryo brain, heart, and eye: Taurine, valine, glutamine, and phosphoethanolamine
Authors: van Gelder N. M. , Bélanger F. 
Published: January 2005

AbstractThe redistribution of valine, from the nonrenewable yolk supply into excitable tissues, was studied during the first 15 days of chick embryogenesis. Valine levels in the extraembryonic circulation (the vitelline plexus) peak between days 7–9 (E7–9) and then decline steeply. In their first phase of differentiation (E2–E4), all embryonic tissues contain more valine than the blood plexus. From E4 to E7, the heart and brain exhibit initially a rapid fall in valine, but from day 7 on the decrease becomes more gradual. The eye during the same period reaches an equilibrium with circulating valine; as these levels fall from E9 to E15, the eye retains the valine that accumulated.Against this pattern of change, characteristic for an essential amino acid during embryogenesis, glutamine levels are at any time from two‐ to threefold higher than valine in all tissues. In the circulation, this ratio remains constant throughout the 15 days of embryonic development. Eye glutamine, higher on day 4, by E7 has entered into an equilibrium with glutamine in the plexus. A steady but two times higher glutamine level is maintained in the heart, although during the later stages of development it gradually tends to approach the plexus content. In sharp contrast, starting on E7 and accelerating on E9, a large increase of glutamine relative to valine or other essential amino acids is seen in developing brain tissue. This appears typical for most metabolic amino acids, suggesting that by days 9–10 the essential acid supply in the brain is being exhausted.Phosphoethanolamine, present in very low concentrations in the nutritional supply, is actively extracted by the plexus and other embryonic tissues. By day 4, tissue levels are five times higher than in the circulation. From then on, apparently sequestered pools of phosphoethanolamine in the heart and eye gradually diminish as the embryo matures. The brain continues to accumulate the metabolite until day 9.Taurine sequestration in the eye is saturated by day 4, and then appears to enter into an exchange equilibrium with the circulation. The heart steadily accumulates taurine during the entire embryonic period when levels are three to four times higher than in the plexus. Brain tissue is most active in taking up taurine, but the process has reached its limits by day 7. This limit is determined by the amount of taurine available in the yolk, since injections of taurine in the nutritional supply result on day 7 in a further increase in the brain. The heart, too, is able to sequester extra taurine but not before day 9 of embryogenesis. The eye, however, does not seem to develop a further capacity to sequester more taurine than is usually supplied by the circulation.
The effect of the experimental antitumor agent caracemide on brain choline acetyltransferase
Authors: Ho B. T. , Tansey L. W. , Feiffer R. , Newman R. A. , Farquhar D. , Field W. S. , Krakoff I. H. 
Published: January 2005

AbstractCaracemide was found to inhibit choline acetyltransferase (CAT) from rat brain. A concentration of 0.5 mM caracemide inhibited the enzyme by 93%, whereas a degradation product from caracemide, N‐(methycarbamoyloxy)acetamide, produced only a 50% inhibition. Two other degration products, N(methyl‐carbamoyloxy)‐N′‐methylurea and N‐hydroxy‐N′‐methlurea, lacked any inhibitory activity. With bovine brain CAT, caracemide showed noncompetitive inhibitio with the substrate choline, Km337 μM, KiμM, Vmax2.83 nmol acetylcholine fromed/ mg/mg protein and mixed inhibition with the substrate acetyl‐CoA, Km21 μM, Ki146 μM, Vmax3.85 noml acetylcholine formed/min/mg porotein.
Neuroimmune intercommunication, central opioids, and the immune response to bacterial endotoxin
Authors: Dougherty P. M. , Dafny N. 
Published: January 2005

AbstractMuramul dipeptide is the smallest biologically active fragment of the lipoplyasccharide (LPS) moiety of gram‐negative cell walls. The present report demonstrates that this product, associated with the immune response to bacterial infection, can modify CNS activity. Specifically, it is demonstrated that 6‐0‐stearoyl‐muramyl depeptide (MDP) can attenuate opiate withdrawal severity in a dose‐dependent fashion when injected into areas of the brain essential for this phenomenon. In additiion, MDP alters both baseline and postnarcotic electrophysiologic responses of four brain areas essential for various opioid activities. Similar findings have been reproted for interferon‐alpha (IFN‐α), a peptide associated with the immune response to virus. Yet, even though MDP and IFN are shown to exert similar effects on opioid activity, there are also some very distinct differences in the actions of both of these immune response products. These observations suggest that central opioid systems may provide targets for the perception as well as the differentiation of afferent immunologic sensory input to the brain.
The influence of laminin on the initial differentiation of cultured neural tube neurons
Authors: Heaton M. B. , Swanson D. J. 
Published: January 2005

AbstractPortions of the metencephalic neural tube containing the trigeminal (V) motor nucleus from 40‐hr chick embryos were excised and held freely floating in culture medium for 36–40 hr, so that neuronal generation within motor V could be completed, but precluding neuronal differentiation. The explants were then dissocited and plated either on (1) glass coverslips that had been coated with the extracellular matrix (ECM) glycoprotein, laminin, and subsequently irradiated to produce a grid pattern; or (2) coverslips, one‐half of which had been coated with laminin, and the other one‐half with collagen, another component of the ECM. The purpose of these studies was to assess possible laminin influences on neuronal adhesion and nerve fiber expression and extension during these periods of initial neuronal differentiation. The early neural tube neurons selectively adhered to the established laminin grid pattern; neuronal survival, elaboration of neurites, and extent of neurites were significantly enhanced on the laminin side of the laminin/collagen preparations. These latter effects were specifically blocked by the application of anti‐laminin. In demonstrating these influences during stages of initial neuronal differentiation, the results support the hypothesis that laminin may play a role in normal neurogenesis, presumably by providing an adhesive surface for outgrowing growth cones.
Regulation of the number of α‐bungarotoxin binding sites in cultured chick myotubes by a 1,4 dihydropyridine calcium channel antagonist
Authors: Smilowitz H. , Smart E. , Bowik C. , Chang R.‐J. 
Published: January 2005

AbstractCalcium has been suggested as the second messenger link between skeletal muscle activity and AchR gene expression and synthesis. We have compared the concentrations of the Ca2+ channel antagonists D600 and nisoldipine needed both to block Ca2+ uptake into cultured myotubes and to increase AchR expression. The good correspondence between these two measurements and the use of the highly specific Ca2+ channel antagonist nisoldipine strengthens the hypothesis that antagonist nisoldipine strengthens the hypothesis that AchR expression is regulated by levels of intracellular Ca2+.
Heterosis for myelin content is limited to the central nervous system
Authors: Miskimins R. , Yu R. K. 
Published: January 2005

AbstractWe have recently described a murine model for studying aspects of myelination (Seyfried and Yu, 1980; Ebato et al., 1983; Miskimins et al., 1986). This mouse shows hypermyelination during the period of most active synthesis of myelin, 9 to 21 days post‐natal. The myelin parameters showing an increase were all measured in the central nervous system. We investigated here whether this effect extends into the peripheral nervous system. Our results indicate that the hypermyelination is limited to the central nervous system.
Effects of insulin and‐like growth factor (IGF‐I)on oligodendrocyte‐enriched glial culture
Authors: van der Pal R. H. M , Koper J. W. , van Golde L. M. G. , Lopes‐Cardozo M. 
Published: January 2005

AbstractThe brains from 1‐week‐old rat pups were used to prepare cultures of glial cells. After 24 hr in culture the cells were changed to a chemically defined serum‐free medium (CDM). We have used antibodies against gangliosides (monoclonals A2B5 and LB1) and against galactocerebrosides to monitor the influence of insulin on the development of oligodenrocytes from precursor cells. In these oligodendrocyte‐enriched cultures we investigated the influence of insulin and IGF‐I on the activity of the marker enzymes 2′,3′‐cyclic‐nucleotide 3′‐phosphodiesterase (CNPase) and glycerol‐3‐phosphate dehydrogenase (G3PDH), and on lipid metabolism.

Incorporation of [35S] sulfate into sulfolipids was stimulated by insulin (optimal concentration 100 nM). A sharp peak in sulfolipid synthesis was seen at day 5–6in culture.
Insulin stimulated the expression of CNPase and G3PDH in culture.
The stimulating effect of insulin on sulfolipid synthesis, CNPase, and G3PDH activity was mimcked by IGF‐I (13 nM).
The incorporation of [35S] into sulfolipids and [2‐3H] acetate into fatty acids and cholesterol was reversibly reduced by temporary omission of insulin from the medium.
These results indicate that insulin and IGF‐I stimulate the development of oligodendroctes in our culture system and that insulin has a general anabolic effect on the lipid metabolism of the cells.
Rapid shrinkage of rat striatal extracellular space after local kainate application and ischemia as recorded by impedance
Authors: Korf J. , Postema F. 
Published: January 2005

AbstractEarly changes in tissue extracellur space following exposure to the excitotoxin kainate in the striatum were compared to those following cardiac arrest of rats anesthetized by chloral hydrate. Tissue extracellular space was monitored by impedance measurements. The possible role of voltage‐sensitive Na channels and energy metabolism was studied by local and systemic application of tetrodotoxine (TTX) and glucose, respectively.After both kainate intoxication and cardiac arrest the extracellular space (normally about 20%) became less than one‐half within 15 min. TTX caused a delay in the effect of cardiac arrest, and a slight attenuation of that of kainate. Glucose was inffective in both preparation. Parallel to a decrease in the extracellular space whole tissue Na/K ratio increased.These experiment show that excitotoxins and cardiac arrest cause similar (and not additive) change in the extracellular space and that these change are not mediated by na channel. In cardiac arrest oneset of the extracellular space alteration is triggered by Na+ influx, thus presumably by neurotransmitter release. It is suggested that most (if not at all) currently described protective measures against ischemic, hypoxic, or hypoglycemic brain damage are based on a prolongation of the time of onset leading to cell depolarization, rather than suppressing damaging processes during depolarization.
Activators of protein kinase C enhance cyclic AMP accumulation in cerebral cortical and diencephalic neurons in primary culture
Authors: Tapia‐Arancibia L. , Veriac S. , Pares‐Herbute N. , Astier H. 
Published: January 2005

AbstractThe effects of the active phorbol ester 12‐myristate, 13‐acetate (PMA), the inactive ester 4 α‐phorbol 12,13‐didecanoate (4 α‐PDD), and the synthetic diacylglycerol 1‐oleoyl‐2‐acetyl‐glycerol (OAG) on cyclic AMP production were examined in rat cerebral cortical and diencephalic cells. With the aid of a prelabeling technique for measuring cyclic AMP accumulation in the cells, it was found that neither PMA nor OAG significantly increased cyclic AMP formation in either type of cell. In contrast, PMA enhanced the cyclic AMP response to vasoactive intestinal peptide (VIP) and forskolin in cerebral cortical and diencephalic cells, whereas 4 α‐PDD was inactive. A 15‐min preincubation was used to obtain maximal enhancement. The concentration dependence of PMA on VIP‐stimulated cyclic AMP accumulation was determined in cortical cells (EC50 = 6.2 × 10−8M).OAG was also able to potentiate VIP‐induced cyclic AMP formation in cortical and diencephalic cells. However, its potentiating effect was weaker than that observed with PMA treatment. The data show, at an early stage of development (primary cultures, 8–10 days), a modulation of VIP‐ or forskolin‐cyclic AMP response by the activators of protein kinase C, i.e., PMA and OAG, in two different structures of the central nervous system: the cerebral cortex and the diencephalon. To our knowledge, this is the first demonstration of such a potentiation within the diencephalon.
CNS neuronal cell line‐derived factors regulate gliogenesis in neonatal rat brain cultures
Authors: Bottenstein Jane E. , Hunter S. F. , Seidel M. 
Published: January 2005

AbstractRecent studies suggest that heterotypic cell‐cell interactions influence gliogenesis in the developing rat central nervous system. CNS neuron‐derived factors have been hypothesized to exist, and several have been identified and partially characterized which affect the number of oligodendrocytes in vitro. In order to study further the role of neurons in gliogenesis, we have used serumfree culture conditions, the B104 CNS neuronal cell line as a source of soluble factors, and dissociated neonatal rat brain cells as a source of glial cells. We have analyzed the response of the glial cells to serum‐free B104 conditioned medium using morphological, immunocytochemical, autoradiographic, and enzymatic methods. Dose‐dependent increases in the number of morphologically identified oligodendrocytes occur in response to this conditioned medium. Galactocerebroside (GalC) is a specific marker for oligodendrocytes, and the A2B5 antigen marks bipotential glial progenitor cells and their progeny: immature oligodendrocytes and type 2 astrocytes. In the presence of conditioned medium, the number of cells expressing GalC and/or A2B5 antigen increases over time when measured at 4, 8, and 12 days in vitro. A significantly weaker effect is seen if serum is also present. Since the vast majority of A2B5‐positive cells in conditioned medium treated cultures lack glial fibrillary acidic protein (GFA), indicative of type 2 astrocytes, they represent glial progenitors and immature oligodendrocytes. Double immunostaining combined with autoradiography suggests that the latter cell types are the target cells for the oligodendrocyte‐promoting activity. In addition, the conditioned medium markedly increases 2′,3′ cyclic nucleotide 3′‐phosphodiesterase (an oligodendrocyte marker) and to a lesser extent enhances glutamine synthetase activity (an astrocyte marker). Type 1 astrocytes are also more morphologically differentiated in this condition, and their percentage is decreased simulataneously. Conditioned medium from other donor neural cells either has no activity or is much less effective than B104 conditioned medium. The active factors are soluble, sensitive to both trypsin and 100°C treatment for 20 min, and appear to be 30–100 kilodaltons by stirred cell ultrafiltration. In summary, we have identified a potent source of growith‐stimulating factors that produce increased numbers of glial progenitor cells and oligodendrocytes; the same conditioned medium also appears to inhibit type 1 astrocyte proliferation.
Molecular modelling of the immunoglobulin‐like domains of the neural cell adhesion molecule (NCAM): Implications for the positioning of functionally important sugar side chains
Authors: Santoni M.‐J. , Goridis C. , Fontecilla‐Camps J. C. 
Published: January 2005

AbstractThe neural cell adhesion molecule (NCAM) is thought to mediate cell–cell adhesion by a homophilic mechanism involving binding sites located in the N‐terminal region of the protein. This region of the molecule consists of five domains that are homologous to each other and share conserved residues with immunoglobulin domains. We report here secondary structure predictions for the five NCAM domains and three‐dimensional models for two of them. The results are entirely consistent with an immunoglobulin‐like folding of the NCAM domains into seven strands forming two b̃‐sheets. NCAM–NCAM binding may thus be analogous to the pairwise associations of immunoglobulin constant domains, which are involved in dimer formation. Insertions and deletions are located mostly in b̃‐turn regions. Two α‐helical regions in the third and fourth domain are predicted with high probability. NCAM bears two kinds of functionally important sugar side chains, sialic acid polymers in the fifth domain, which modulate NCAM binding, and the L2 moiety, which is involved in cell adhesion and can be assigned to the third domain. Three‐dimensional modelling of the corresponding domains indicates that two of the three sites for N‐linked glycosylation in the fifth and the single site in the third domain are located on he face of the domain, which in immunoglobulin contant regions engages in intermolecular interactions.
Expression of monoclonal antibody Q113 immunoreactivity in the rat cerebral cortex: Unique differential sublayering of layer I. Staining of radial glia
Authors: Plioplys A. V. , Hawkes R. 
Published: January 2005

AbstractMonoclonal antibody mabQ113 recognizes a 120‐kilodalton polypeptide which, in the cerebellar cortex, is confined exclusively to a subset of Purkinje cells which are organized in parasagittal bands (Hawkes et al.: Brain Research 333:359–365, 1985). In all other areas of the adult rat brain examined the localization of the mabQ113 epitope was marked by regional neuronal and glial coexpression (Plioplys and Hawkes: Brain Research 375:1–12, 1986).Similar neuronal‐glial co‐expression was characteristic of the adult rat cerebral cortex. Intriguingly, mabQ113 revealed a unique differential sublamination of layer I. In the neocortex, layer I was split into two sublayers, with the more superficial sublayer weakly stained and the deeper sublayer stained more intensely, whereas in the pyriform cortex, layer I was split into three. These sublaminations do not correspond to previously described subdivisions of layer I.In the developing cortex, the mabQ113 epitope is found in radial glial fibers. Stained radial fibers are first seen beginning at E17, reach a maximum at P4 and finally disappear between P12 and P14. The laminar distribution of mabQ113‐immunoreactivity emerges earlier in the pyriform cortex than the neocortex: the sublamination of layer I is seen at P4 in the pyriform cortex but not until P8 in the neocortex.The significance of these observations is discussed.
Macrophage‐like cells from explant cultures of rat sciatic nerve produce apolipoprotein E
Authors: Goodrum J. F. , Novicki D. L. 
Published: January 2005

AbstractApolipoprotein E is synthesized and secreted by degenerating peripheral nerve, but the role of resident endoneurial cells in this process is not clear. To exclude the involvement of nonresident cells, we examined the cellular source of endoneurial apolipoprotein E in explant cultures of rat sciatic nerve. The cellular outgrowth from these explant cultures released apolipoprotein E into the culture medium. The cellular outgrowth contained fibroblasts, Schwann cells, and a population of cells with many phenotypic characteristics of macrophages, including the production of apolipoprotein E. No other cell type in the cultures appeared to contribute to this production. These data suggest that apolipoprotein E is produced by resident endoneurial cells in explant cultures and that these cells are macrophages.
Nerve growth factor binding in aged rat central nervous system: Effect of acetyl‐l‐carnitine
Authors: Angelucci L. , Ramacci M. T. , Taglialatela G. , Hulsebosch C. , Morgan B. , Werrbach‐Perez K. , Perez‐Polo J. R. 
Published: January 2005

AbstractThe nerve growth factor protein (NGF) has been demonstrated to affect neuronal development and maintenance of the differentiated state in certain neurons of the peripheral and central nervous system (CNS) of mammals. In the CNS, NGF has sparing effects on cholinergic neurons of the rodent basal forebrain (BF) following lesions where it selectively induces choline acetyltransferase (ChAT). NGF also induces ChAT in the areas to which BF provides afferents. In aged rats, there is a reduction in the NGF‐binding capacity of sympathetic ganglia. Here, we wish to report that there is a decrrease in the NGF‐binding capacity of the hippocampus and basal forebrain of aged (26‐month‐old) rats as compared to 4‐month‐old controls but no change in NGF binding in cerebellum. In all instances, equilibrium binding dissociation constants did not differ significantly. Treatment of rats with acetyl‐L‐carnitine, reported to improve cognitive performance of aged rats, ameliorates these age‐related deficits.
Axotomy of the rat facial nerve leads to increased CR3 complement receptor expression by activated microglial cells
Authors: Graeber M. B. , Streit W. J. , Kreutzberg G. W. 
Published: January 2005

AbstractAxotomy of the rat facial nerve leads to mitotic divisions of microglial cells without developing into phagocytes. In order to study the functional characteristics of those activated, i.e., proliferating but nonphagocytic, microglia we investigated the expression of monocyte/macrophage antigens by these cells. Our results show that activated microglia lack monocyte/macrophage antigens recognized by the monoclonal antibodies Ox‐41, ED1, ED2, and Ki‐M2R but express high levels of CR3 complement receptors in situ.