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Mario Patrizio - One of the best experts on this subject based on the ideXlab platform.
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Astrocyte heterogeneity endogenous amino acid levels and release evoked by non n methyl d aspartate receptor agonists and by potassium induced swelling in Type 1 and Type 2 Astrocytes
Journal of Neurochemistry, 1992Co-Authors: Giulio Levi, Mario PatrizioAbstract:: The aim of the present study was to determine whether endogenous amino acids are released from Type-1 and Type-2 Astrocytes following non-N-methyl-D-aspartate (NMDA) receptor activation and whether such release is related to cell swelling. Amino acid levels and release were measured by HPLC in secondary cultures from neonatal rat cortex, highly enriched in Type-1 or Type-2 Astrocytes. The following observations were made. (a) The endogenous level of several amino acids (glutamate, alanine, glutamine, asparagine, taurine, serine, and threonine) was substantially higher in Type-1 than in Type-2 Astrocytes. (b) The spontaneous release of glutamine and taurine was higher in Type-1 than in Type-2 Astrocytes; that of other amino acids was similar. (c) Exposure of Type-2 Astrocyte cultures to 50 microM kainate or quisqualate doubled the release of glutamate and caused a lower, but significant increase in that of aspartate, glycine, taurine, alanine, serine (only in the case of kainate), and glutamine (only in the case of quisqualate). These effects were reversed by the antagonist CNQX. (d) Exposure of Type-1 Astrocyte cultures to 50-200 microM kainate or 50 microM quisqualate did not affect endogenous amino acid release, even after treating the cultures with dibutyryl cyclic AMP. (e) Exposure of Type-1 or Type-2 Astrocyte cultures to 50 mM KCl (replacing an equimolar concentration of NaCl) enhanced the release of taurine greater than glutamate greater than aspartate. The effect was somewhat more pronounced in Type-2 than in Type-1 Astrocytes. Veratridine (50 microM) did not cause any increase in amino acid release. (f) The release of amino acids induced by high [K+] appeared to be related to cell swelling, in both Type-1 and Type-2 Astrocytes. Swelling and K(+)-induced release were somewhat higher in Type-2 than in Type-1 Astrocytes. In contrast, neither kainate nor quisqualate caused any appreciable increase in cell volume. It is concluded that non-NMDA receptor agonists stimulate the release of several endogenous amino acids (some of which are neuroactive) from Type-2 but not from Type-1 Astrocytes. The effect does not seem to be related to cell swelling, which causes a different release profile in both Type-1 and Type-2 Astrocytes. The absence of kainate- and quisqualate-evoked release in Type-1 Astrocytes suggests that the density of non-NMDA receptors in this cell Type is very low.
Synthia H Sun - One of the best experts on this subject based on the ideXlab platform.
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endothelin 1 stimulated capacitative ca2 entry through eta receptors of a rat brain derived Type 1 Astrocyte cell line ia 1g1
Cellular Signalling, 2003Co-Authors: Chiamei Wang, Amos C Hung, Hungjung Lin, Synthia H SunAbstract:Abstract The present study demonstrated that endotheline-1 (ET-1) stimulated a biphasic (transient and sustained) increase in [Ca 2+ ] i and signaling was blocked by BQ123 and inhibited by BQ788. RT-PCR analysis revealed that ET A was expressed more than ET B mRNA—suggesting that ET A is the major receptor. Simply reintroducing Ca 2+ in the buffer stimulated a sustained increase in [Ca 2+ ] i and the effect was inhibited by U73122, thapsigargin (TG), miconazole and SKF96365. When measured in Ca 2+ -free buffer, the ET-1-stimulated Ca 2+ transient decreased by 73% and the reintroduction of Ca 2+ induced a large sustained increase in [Ca 2+ ] i . These effects were not affected by nifedipine, but were inhibited by miconazole and SKF96365—indicating that the sustained increase in [Ca 2+ ] i mediated by ET-1 was mostly due to capacitative Ca 2+ entry (CCE). The ET-1-induced CCE was inhibited by phorbol ester (PMA) but was enhanced by GF109203X; it was also enhanced by 8-bromo-cyclic AMP (8-Br-cAMP) but was inhibited by H89. Thus, protein kinase C (PKC) negatively regulated and cAMP-dependent protein kinase (PKA) positively regulated the ET-1-mediated CCE in these cells.
Giulio Levi - One of the best experts on this subject based on the ideXlab platform.
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Astrocyte heterogeneity endogenous amino acid levels and release evoked by non n methyl d aspartate receptor agonists and by potassium induced swelling in Type 1 and Type 2 Astrocytes
Journal of Neurochemistry, 1992Co-Authors: Giulio Levi, Mario PatrizioAbstract:: The aim of the present study was to determine whether endogenous amino acids are released from Type-1 and Type-2 Astrocytes following non-N-methyl-D-aspartate (NMDA) receptor activation and whether such release is related to cell swelling. Amino acid levels and release were measured by HPLC in secondary cultures from neonatal rat cortex, highly enriched in Type-1 or Type-2 Astrocytes. The following observations were made. (a) The endogenous level of several amino acids (glutamate, alanine, glutamine, asparagine, taurine, serine, and threonine) was substantially higher in Type-1 than in Type-2 Astrocytes. (b) The spontaneous release of glutamine and taurine was higher in Type-1 than in Type-2 Astrocytes; that of other amino acids was similar. (c) Exposure of Type-2 Astrocyte cultures to 50 microM kainate or quisqualate doubled the release of glutamate and caused a lower, but significant increase in that of aspartate, glycine, taurine, alanine, serine (only in the case of kainate), and glutamine (only in the case of quisqualate). These effects were reversed by the antagonist CNQX. (d) Exposure of Type-1 Astrocyte cultures to 50-200 microM kainate or 50 microM quisqualate did not affect endogenous amino acid release, even after treating the cultures with dibutyryl cyclic AMP. (e) Exposure of Type-1 or Type-2 Astrocyte cultures to 50 mM KCl (replacing an equimolar concentration of NaCl) enhanced the release of taurine greater than glutamate greater than aspartate. The effect was somewhat more pronounced in Type-2 than in Type-1 Astrocytes. Veratridine (50 microM) did not cause any increase in amino acid release. (f) The release of amino acids induced by high [K+] appeared to be related to cell swelling, in both Type-1 and Type-2 Astrocytes. Swelling and K(+)-induced release were somewhat higher in Type-2 than in Type-1 Astrocytes. In contrast, neither kainate nor quisqualate caused any appreciable increase in cell volume. It is concluded that non-NMDA receptor agonists stimulate the release of several endogenous amino acids (some of which are neuroactive) from Type-2 but not from Type-1 Astrocytes. The effect does not seem to be related to cell swelling, which causes a different release profile in both Type-1 and Type-2 Astrocytes. The absence of kainate- and quisqualate-evoked release in Type-1 Astrocytes suggests that the density of non-NMDA receptors in this cell Type is very low.
James A Weyhenmeyer - One of the best experts on this subject based on the ideXlab platform.
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isolation cloning and characterization of a putative Type 1 Astrocyte cell line
Brain Research, 1997Co-Authors: Kimberly J N Seidman, Andelle L Teng, Robin Rosenkopf, Paul Spilotro, James A WeyhenmeyerAbstract:We have established a permanent cell line (1H91) of putative Type-1 Astrocyte precursor cells that were clonally derived from a single cell isolated from E16 mouse cerebellum. Epidermal growth factor (EGF) and transforming growth factor (TGFα) are strong mitogens for 1H91 cells (ED50 of 9.02+1.74 ng/ml and 15.98±2.34 ng/ml, respectively), while basic fibroblast growth factor (bFGF) is only weakly mitogenic and platelet derived growth factor (PDGF) has no mitogenic activity. In the proliferative state, the 1H91 cells are immunohistochemically positive for nestin and vimentin, and negative for A2B5, CNPase, neurofilament (NF), and neuron specific enolase (NSE). The majority of EGF-treated 1H91 cells are not immunoreactive for glial acid fibrillary protein (GFAP). In the presence of 5 ng/ml bFGF, 1H91 cells become non-mitotic and develop a morphology consistent with a fibrous Astrocyte. In contrast to the proliferating cultures, the bFGF treated cultures were strongly immunoreactive for GFAP, only mildly immunoreactive for nestin and vimentin, and negative for A2B5, CNPase, NF, and NSE. Type-1 Astrocytes are known to proliferate in response to EGF, and are immunohistochemically GFAP positive, A2B5 negative, and CNPase negative [38]. However, Type-1 Astrocytes only develop a fibrous morphology during the process of reactive gliosis [31]. Since EGF is a strong mitogen for 1H91 cells, and these cells may be differentiated into GFAP positive, A2B5 negative, CNPase negative Astrocytes, we conclude that 1H91 cells conform to a Type-1 Astrocyte precursor phenoType. In addition, the fibrous morphology of the bFGF treated 1H91 cells suggests that these cells follow the process of reactive gliosis. Therefore, the 1H91 clonal cell line may provide an in vitro model for studying the underlying cellular mechanisms of the Type-1 Astrocyte in reactive gliosis.
Fang Liu - One of the best experts on this subject based on the ideXlab platform.
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neuroligand evoked calcium dependent release of excitatory amino acids from cultured Astrocytes
Journal of Neurochemistry, 2002Co-Authors: Srdija Jeftinija, Ksenija Jeftinija, Gordana Stefanovic, Fang LiuAbstract:The release of excitatory amino acids (EAAs) from neuron-free cultures of neocortical Astrocytes was monitored using HPLC. The neuroligand bradykinin caused a dose-dependent receptor-mediated increase in release of the EAAs glutamate and aspartate from Type 1 Astrocyte cell cultures obtained from rat cerebral cortex. Removal of calcium from the extracellular fluid prevented the bradykinin-induced release of EAAs from Astrocytes. The addition of the calcium ionophore ionomycin caused a calcium-dependent release of EAAs. Inhibitors of the glutamate transporters p-chloromercuriphenylsulfonic acid, L-trans-pyrrolidine-2,4-dicarboxylate, and dihydrokainate failed to impair the ability of bradykinin to stimulate glutamate release from Astrocytes. alpha-Latrotoxin, an active compound of black widow spider venom, caused a significant increase of the release of glutamate in calcium-containing saline. In calcium-depleted saline, alpha-latrotoxin produced an initial increase in the concentration of glutamate followed by a decline in the concentration of glutamate indicating stimulation of exocytosis coupled with low calcium-induced inhibition of endocytosis. Taken together, these data suggest that Astrocytes may release neurotransmitter through a mechanism that is similar to the neuronal secretory process. Given the important role of glutamate in the induction of long-term potentiation, learning, memory, and excitotoxicity, it will be important to determine external signals that control both the uptake and release of glutamate by Astrocytes.
