The Experts below are selected from a list of 126 Experts worldwide ranked by ideXlab platform
Pirjo Saransaari - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of Glycine Release in Mouse Brain Stem Slices
Neurochemical Research, 2009Co-Authors: Pirjo SaransaariAbstract:In the brain stem glycine is associated with multiple sensory and visceral regulations, being involved in, for instance, cardiovascular, respiratory and auditory functions. We here studied the mechanisms of the release of preloaded [^3H]glycine from mouse brain stem slices in a superfusion system. A depolarizing concentration of K^+ ions (50 mM) evoked glycine release, but in the absence of Ca^2+ the effect was attenuated, indicating that a part of the evoked release represents Ca^2+-dependent exocytosis. The Ca^2+-independent release was enhanced by omission of Na^+ and Cl^−. The stimulatory effect of extracellular glycine confirmed the involvement of transporters functioning in a reverse direction. A part of the release is mediated by Na^+ and Cl^− channels, since it was inhibited by the Inhibitors of these, riluzole and 4-acetamido-4′-isothiocyanostilbene-2,2′-disulphonate, respectively. Glycine release was potentiated by the activation of protein kinase C and diminished by increasing cyclic guanosine monophosphate levels with a phosphodiesterase Inhibitor, zaprinast. The release was also modulated by the Phospholipase Inhibitor quinacrine and the tyrosine kinase Inhibitor genistein. Adenosine A_1 receptors likewise regulate glycine release, since it was enhanced by their agonist R(−)N^6-(2-phenylisopropyl)adenosine, which effect was blocked by the antagonist 8-cyclopentyl-1,3-dipropylxanthine. The ionotropic glutamate receptor agonists N -methyl- d -aspartate, kainate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate failed to have any effects contrary to their effects in higher brain regions, e.g., in the hippocampus. The group I and III metabotropic glutamate receptor agonists (S)-3,5-dihydroxyphenylglycine and O-phospho- l -serine, respectively, increased the release in a receptor-mediated manner. Glycine release in the brain stem was also markedly enhanced by cell-damaging conditions, including hypoxia, hypoglycemia and ischemia.
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Modulation of GABA Release by Second Messenger Substances and NO in Mouse Brain Stem Slices Under Normal and Ischemic Conditions
Neurochemical Research, 2006Co-Authors: Pirjo SaransaariAbstract:GABA is the Inhibitory neurotransmitter in most brain stem nuclei. The properties of release of preloaded [^3H]GABA were now investigated with slices from the mouse brain stem under normal and ischemic (oxygen and glucose deprivation) conditions, using a superfusion system. The ischemic GABA release increased about fourfold in comparison with normal conditions. The tyrosine kinase Inhibitor genistein had no effect on GABA release, while the Phospholipase Inhibitor quinacrine reduced both the basal and K^+-evoked release in normoxia and ischemia. The activator of protein kinase C (PKC) 4β-phorbol 12-myristate 13-acetate had no effects on the releases, whereas the PKC Inhibitor chelerythrine reduced the basal release in ischemia. When the cyclic guanosine monophosphate (cGMP) levels were increased by superfusion with zaprinast and other phosphodiesterase Inhibitors, GABA release was reduced under normal conditions. The NO donors S -nitroso- N -acetylpenicillamine (SNAP) and hydroxylamine (HA) enhanced the basal and K^+-stimulated release by acting directly on presynaptic terminals. Under ischemic conditions GABA release was enhanced when cGMP levels were increased by zaprinast. This effect was confirmed by inhibition of the release by the guanylate cyclase Inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). The NO-producing agents SNAP, HA, and sodium nitroprusside potentiated GABA release in ischemia. These effects were reduced by the NO synthase Inhibitor N^G-nitro- l -arginine, but not by ODQ. The results show that particularly NO and cGMP regulate both normal and ischemic GABA release in the brain stem. Their effects are however complex.
Sabine Chapuyregaud - One of the best experts on this subject based on the ideXlab platform.
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progesterone and a Phospholipase Inhibitor increase the endosomal bis monoacylglycero phosphate content and block hiv viral particle intercellular transmission
Biochimie, 2013Co-Authors: Sabine Chapuyregaud, Caroline Subra, Mary Requena, Philippe De Medina, Sawsan Amara, Isabelle DeltonvandenbrouckeAbstract:Abstract Progesterone, the cationic amphiphile U18666A and a Phospholipase Inhibitor (Methyl Arachidonyl Fluoro Phosphonate, MAFP) inhibited by 70%–90% HIV production in viral reservoir cells, i.e. human THP-1 monocytes and monocyte-derived macrophages (MDM). These compounds triggered an inhibition of fluid phase endocytosis (macropinocytosis) and modified cellular lipid homeostasis since endosomes accumulated filipin-stained sterols and Bis(Monoacylglycero)Phosphate (BMP). BMP was quantified using a new cytometry procedure and was increased by 1.25 times with MAFP, 1.7 times with U18666A and 2.5 times with progesterone. MAFP but not progesterone or U18666A inhibited the hydrolysis of BMP by the Pancreatic Lipase Related Protein 2 (PLRP2) as shown by in-vitro experiments. The possible role of sterol transporters in steroid-mediated BMP increase is discussed. Electron microscopy showed the accumulation of viral particles either into large intracellular viral-containing compartments or outside the cells, indicating that endosomal accumulation of BMP could block intracellular biogenesis of viral particles while inhibition of macropinocytosis would prevent viral particle uptake. This is the first report linking BMP metabolism with a natural steroid such as progesterone or with involvement of a Phospholipase A1 activity. BMP cellular content could be used as a biomarker for efficient anti-viral drugs.
Marzia Malcangio - One of the best experts on this subject based on the ideXlab platform.
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Mechanism by which brain-derived neurotrophic factor increases dopamine release from the rabbit retina
Investigative Ophthalmology and Visual Science, 2003Co-Authors: Michael Neal, Joanna Cunningham, Isobel Lever, Sophie Pezet, Marzia MalcangioAbstract:PURPOSE: To determine whether BDNF modulates the release of dopamine from amacrine cells in the rabbit retina. METHODS: Isolated retinas from rabbits killed with pentobarbital were incubated in Krebs bicarbonate medium containing pargyline, nomifensine, and bovine serum albumin. The medium was changed at 10-minute intervals, and the dopamine in the resultant samples measured by HPLC. Five samples were collected to establish the spontaneous resting release of dopamine, and then the retina was exposed to BDNF for a further two collection periods. Double-label immunohistochemistry was used to identify tyrosine hydroxylase containing neurons and to localize TrkB (BDNF) receptors. RESULTS: Exposure of the retina to BDNF (70-150 ng/mL) caused a concentration-dependent increase in the release of dopamine. The maximum effect was produced by 150 ng/mL BDNF, which almost doubled the release. The BDNF-evoked release was abolished in low-calcium/high-magnesium medium. It was also prevented by the tyrosine kinase Inhibitors k252a and genistein, the Phospholipase Inhibitor U73122, and the sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) Inhibitors thapsigargin and cyclopiazonic acid. Antagonists of gamma-aminobutyric acid (GABA) and glutamate did not affect the BDNF-evoked release of dopamine. ELISA assay confirmed the presence of BDNF in the retina, and immunohistochemistry revealed that some tyrosine hydroxylase-containing neurons possessed TrkB receptors. CONCLUSIONS: BDNF quickly (within minutes) increases the release of dopamine from amacrine cells in the rabbit retina by an action that is likely to involve TrkB receptors. The mechanism linking TrkB receptor activation to the release of dopamine involves activation of Phospholipase-Cgamma, with the subsequent production of IP(3) and calcium release from the endoplasmic reticulum. The resultant capacitative entry of calcium seems to be the actual trigger for BDNF-induced release of dopamine.
Isabelle Deltonvandenbroucke - One of the best experts on this subject based on the ideXlab platform.
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progesterone and a Phospholipase Inhibitor increase the endosomal bis monoacylglycero phosphate content and block hiv viral particle intercellular transmission
Biochimie, 2013Co-Authors: Sabine Chapuyregaud, Caroline Subra, Mary Requena, Philippe De Medina, Sawsan Amara, Isabelle DeltonvandenbrouckeAbstract:Abstract Progesterone, the cationic amphiphile U18666A and a Phospholipase Inhibitor (Methyl Arachidonyl Fluoro Phosphonate, MAFP) inhibited by 70%–90% HIV production in viral reservoir cells, i.e. human THP-1 monocytes and monocyte-derived macrophages (MDM). These compounds triggered an inhibition of fluid phase endocytosis (macropinocytosis) and modified cellular lipid homeostasis since endosomes accumulated filipin-stained sterols and Bis(Monoacylglycero)Phosphate (BMP). BMP was quantified using a new cytometry procedure and was increased by 1.25 times with MAFP, 1.7 times with U18666A and 2.5 times with progesterone. MAFP but not progesterone or U18666A inhibited the hydrolysis of BMP by the Pancreatic Lipase Related Protein 2 (PLRP2) as shown by in-vitro experiments. The possible role of sterol transporters in steroid-mediated BMP increase is discussed. Electron microscopy showed the accumulation of viral particles either into large intracellular viral-containing compartments or outside the cells, indicating that endosomal accumulation of BMP could block intracellular biogenesis of viral particles while inhibition of macropinocytosis would prevent viral particle uptake. This is the first report linking BMP metabolism with a natural steroid such as progesterone or with involvement of a Phospholipase A1 activity. BMP cellular content could be used as a biomarker for efficient anti-viral drugs.
Philippe De Medina - One of the best experts on this subject based on the ideXlab platform.
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progesterone and a Phospholipase Inhibitor increase the endosomal bis monoacylglycero phosphate content and block hiv viral particle intercellular transmission
Biochimie, 2013Co-Authors: Sabine Chapuyregaud, Caroline Subra, Mary Requena, Philippe De Medina, Sawsan Amara, Isabelle DeltonvandenbrouckeAbstract:Abstract Progesterone, the cationic amphiphile U18666A and a Phospholipase Inhibitor (Methyl Arachidonyl Fluoro Phosphonate, MAFP) inhibited by 70%–90% HIV production in viral reservoir cells, i.e. human THP-1 monocytes and monocyte-derived macrophages (MDM). These compounds triggered an inhibition of fluid phase endocytosis (macropinocytosis) and modified cellular lipid homeostasis since endosomes accumulated filipin-stained sterols and Bis(Monoacylglycero)Phosphate (BMP). BMP was quantified using a new cytometry procedure and was increased by 1.25 times with MAFP, 1.7 times with U18666A and 2.5 times with progesterone. MAFP but not progesterone or U18666A inhibited the hydrolysis of BMP by the Pancreatic Lipase Related Protein 2 (PLRP2) as shown by in-vitro experiments. The possible role of sterol transporters in steroid-mediated BMP increase is discussed. Electron microscopy showed the accumulation of viral particles either into large intracellular viral-containing compartments or outside the cells, indicating that endosomal accumulation of BMP could block intracellular biogenesis of viral particles while inhibition of macropinocytosis would prevent viral particle uptake. This is the first report linking BMP metabolism with a natural steroid such as progesterone or with involvement of a Phospholipase A1 activity. BMP cellular content could be used as a biomarker for efficient anti-viral drugs.