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Mark D Berry - One of the best experts on this subject based on the ideXlab platform.
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membrane permeability of trace amines evidence for a regulated activity dependent nonexocytotic synaptic release
Synapse, 2013Co-Authors: Mark D Berry, Mithila R Shitut, Ahmed Almousa, Jane Alcorn, Bruno TomberliAbstract:Both pre- and post-synaptic effects of trace amines have been demonstrated. The putative intracellular location of Trace Amine-Associated Receptors necessitate that membrane transport processes be present in order for post-synaptic effects to occur. Here we examine the ability of trace amines to cross synthetic (Fluorosomes) and native (Synaptosomes) lipid bilayer membranes. Trace amines readily crossed Fluorosome membranes by simple diffusion, p-tyramine (P = 0.01) and tryptamine (P = 0.0004) showing significantly faster diffusion than dopamine and 5-HT, respectively, with diffusion half-lives of 13.5 ± 4.1 (p-tyramine) and 6.8 ± 0.7 seconds (tryptamine). Similarly, release of [3H]p-tyramine and [3H]2-phenylethylamine from pre-loaded Synaptosomes occurred significantly quicker than did [3H]dopamine (P = 0.0001), with half lives of 38.9 (p-tyramine), 7.8 (2-phenylethylamine) and 133.6 seconds (dopamine). This was, however, significantly slower than the diffusion mediated passage across Fluorosome membranes (P = 0.0001), suggesting a role for transporters in mediating trace amine release. Further, a pronounced shoulder region was observed in the Synaptosome [3H]p-tyramine release curve, suggesting that multiple processes regulate release. No such shoulder region was present for [3H]dopamine release. Surprisingly, both [3H]p-tyramine (P = 0.001) and [3H]2-phenylethylamine (P = 0.0001) release from Synaptosomes was significantly decreased under depolarizing conditions. As expected, depolarization significantly increased [3H]dopamine release. The data presented indicate that the release of p-tyramine and 2-phenylethylamine from neuronal terminals occurs by a different mechanism than dopamine, and does not involve classical exocytosis. The data are consistent with an initial release of trace amines by simple diffusion, followed by an activity-dependent regulation of synaptic levels via one or more transporter proteins. Synapse 67:656–667, 2013. © 2013 Wiley Periodicals, Inc.
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Membrane permeability of trace amines: Evidence for a regulated, activity‐dependent, nonexocytotic, synaptic release
Synapse (New York N.Y.), 2013Co-Authors: Mark D Berry, Mithila R Shitut, Ahmed Almousa, Jane Alcorn, Bruno TomberliAbstract:Both pre- and post-synaptic effects of trace amines have been demonstrated. The putative intracellular location of Trace Amine-Associated Receptors necessitate that membrane transport processes be present in order for post-synaptic effects to occur. Here we examine the ability of trace amines to cross synthetic (Fluorosomes) and native (Synaptosomes) lipid bilayer membranes. Trace amines readily crossed Fluorosome membranes by simple diffusion, p-tyramine (P = 0.01) and tryptamine (P = 0.0004) showing significantly faster diffusion than dopamine and 5-HT, respectively, with diffusion half-lives of 13.5 ± 4.1 (p-tyramine) and 6.8 ± 0.7 seconds (tryptamine). Similarly, release of [3H]p-tyramine and [3H]2-phenylethylamine from pre-loaded Synaptosomes occurred significantly quicker than did [3H]dopamine (P = 0.0001), with half lives of 38.9 (p-tyramine), 7.8 (2-phenylethylamine) and 133.6 seconds (dopamine). This was, however, significantly slower than the diffusion mediated passage across Fluorosome membranes (P = 0.0001), suggesting a role for transporters in mediating trace amine release. Further, a pronounced shoulder region was observed in the Synaptosome [3H]p-tyramine release curve, suggesting that multiple processes regulate release. No such shoulder region was present for [3H]dopamine release. Surprisingly, both [3H]p-tyramine (P = 0.001) and [3H]2-phenylethylamine (P = 0.0001) release from Synaptosomes was significantly decreased under depolarizing conditions. As expected, depolarization significantly increased [3H]dopamine release. The data presented indicate that the release of p-tyramine and 2-phenylethylamine from neuronal terminals occurs by a different mechanism than dopamine, and does not involve classical exocytosis. The data are consistent with an initial release of trace amines by simple diffusion, followed by an activity-dependent regulation of synaptic levels via one or more transporter proteins. Synapse 67:656–667, 2013. © 2013 Wiley Periodicals, Inc.
Bruno Tomberli - One of the best experts on this subject based on the ideXlab platform.
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membrane permeability of trace amines evidence for a regulated activity dependent nonexocytotic synaptic release
Synapse, 2013Co-Authors: Mark D Berry, Mithila R Shitut, Ahmed Almousa, Jane Alcorn, Bruno TomberliAbstract:Both pre- and post-synaptic effects of trace amines have been demonstrated. The putative intracellular location of Trace Amine-Associated Receptors necessitate that membrane transport processes be present in order for post-synaptic effects to occur. Here we examine the ability of trace amines to cross synthetic (Fluorosomes) and native (Synaptosomes) lipid bilayer membranes. Trace amines readily crossed Fluorosome membranes by simple diffusion, p-tyramine (P = 0.01) and tryptamine (P = 0.0004) showing significantly faster diffusion than dopamine and 5-HT, respectively, with diffusion half-lives of 13.5 ± 4.1 (p-tyramine) and 6.8 ± 0.7 seconds (tryptamine). Similarly, release of [3H]p-tyramine and [3H]2-phenylethylamine from pre-loaded Synaptosomes occurred significantly quicker than did [3H]dopamine (P = 0.0001), with half lives of 38.9 (p-tyramine), 7.8 (2-phenylethylamine) and 133.6 seconds (dopamine). This was, however, significantly slower than the diffusion mediated passage across Fluorosome membranes (P = 0.0001), suggesting a role for transporters in mediating trace amine release. Further, a pronounced shoulder region was observed in the Synaptosome [3H]p-tyramine release curve, suggesting that multiple processes regulate release. No such shoulder region was present for [3H]dopamine release. Surprisingly, both [3H]p-tyramine (P = 0.001) and [3H]2-phenylethylamine (P = 0.0001) release from Synaptosomes was significantly decreased under depolarizing conditions. As expected, depolarization significantly increased [3H]dopamine release. The data presented indicate that the release of p-tyramine and 2-phenylethylamine from neuronal terminals occurs by a different mechanism than dopamine, and does not involve classical exocytosis. The data are consistent with an initial release of trace amines by simple diffusion, followed by an activity-dependent regulation of synaptic levels via one or more transporter proteins. Synapse 67:656–667, 2013. © 2013 Wiley Periodicals, Inc.
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Membrane permeability of trace amines: Evidence for a regulated, activity‐dependent, nonexocytotic, synaptic release
Synapse (New York N.Y.), 2013Co-Authors: Mark D Berry, Mithila R Shitut, Ahmed Almousa, Jane Alcorn, Bruno TomberliAbstract:Both pre- and post-synaptic effects of trace amines have been demonstrated. The putative intracellular location of Trace Amine-Associated Receptors necessitate that membrane transport processes be present in order for post-synaptic effects to occur. Here we examine the ability of trace amines to cross synthetic (Fluorosomes) and native (Synaptosomes) lipid bilayer membranes. Trace amines readily crossed Fluorosome membranes by simple diffusion, p-tyramine (P = 0.01) and tryptamine (P = 0.0004) showing significantly faster diffusion than dopamine and 5-HT, respectively, with diffusion half-lives of 13.5 ± 4.1 (p-tyramine) and 6.8 ± 0.7 seconds (tryptamine). Similarly, release of [3H]p-tyramine and [3H]2-phenylethylamine from pre-loaded Synaptosomes occurred significantly quicker than did [3H]dopamine (P = 0.0001), with half lives of 38.9 (p-tyramine), 7.8 (2-phenylethylamine) and 133.6 seconds (dopamine). This was, however, significantly slower than the diffusion mediated passage across Fluorosome membranes (P = 0.0001), suggesting a role for transporters in mediating trace amine release. Further, a pronounced shoulder region was observed in the Synaptosome [3H]p-tyramine release curve, suggesting that multiple processes regulate release. No such shoulder region was present for [3H]dopamine release. Surprisingly, both [3H]p-tyramine (P = 0.001) and [3H]2-phenylethylamine (P = 0.0001) release from Synaptosomes was significantly decreased under depolarizing conditions. As expected, depolarization significantly increased [3H]dopamine release. The data presented indicate that the release of p-tyramine and 2-phenylethylamine from neuronal terminals occurs by a different mechanism than dopamine, and does not involve classical exocytosis. The data are consistent with an initial release of trace amines by simple diffusion, followed by an activity-dependent regulation of synaptic levels via one or more transporter proteins. Synapse 67:656–667, 2013. © 2013 Wiley Periodicals, Inc.
Bhanu P Jena - One of the best experts on this subject based on the ideXlab platform.
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unique lipid chemistry of synaptic vesicle and Synaptosome membrane revealed using mass spectrometry
ACS Chemical Neuroscience, 2017Co-Authors: Kenneth T Lewis, Krishna Rao Maddipati, Akshata R Naik, Bhanu P JenaAbstract:Synaptic vesicles measuring 30–50 nm in diameter containing neurotransmitters either completely collapse at the presynaptic membrane or dock and transiently fuse at the base of specialized 15 nm cup-shaped lipoprotein structures called porosomes at the presynaptic membrane of Synaptosomes to release neurotransmitters. Recent study reports the unique composition of major lipids associated with neuronal porosomes. Given that lipids greatly influence the association and functions of membrane proteins, differences in lipid composition of synaptic vesicle and the Synaptosome membrane was hypothesized. To test this hypothesis, the lipidome of isolated Synaptosome, Synaptosome membrane, and synaptic vesicle preparation were determined by using mass spectrometry in the current study. Results from the study demonstrate the enriched presence of triacyl glycerols and sphingomyelins in synaptic vesicles, as opposed to the enriched presence of phospholipids in the Synaptosome membrane fraction, reflecting on the tight...
Carlos Gutiérrez-merino - One of the best experts on this subject based on the ideXlab platform.
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INACTIVATION OF ECTO-ATPASE ACTIVITY OF RAT BRAIN SynaptosomeS
Biochimica et Biophysica Acta, 1996Co-Authors: Francisco Javier Martin-romero, Elena García-martín, Carlos Gutiérrez-merinoAbstract:Abstract The ecto-ATPase activity of Synaptosomes plasma membrane decays exponentially as a function of time from 0.35 ± 0.05 to 0.08 ± 0.02 μmol ATP hydrolyzed per min per mg Synaptosome protein. The first-order rate constant of inactivation is dependent on the Mg-ATP concentration varying from 0.042 ± 0.001 min−1 with 30 μM ATP up to 0.216 ± 0.003 min−1 with 2 mM ATP. The non-hydrolyzable ATP analogue, β-γ-methyleneadenosine 5′-triphosphate, did not produce inactivation of the ecto-ATPase activity. Thus, the inactivation of the ecto-ATPase activity requires hydrolysis of ATP. Product inhibition can be excluded because ADP, AMP, adenosine and inorganic phosphate up to 1 mM had no effect on the inactivation of the ecto-ATPase. Concanavalin A partially protected against the ATP-dependent inactivation. The ecto-ATPase inactivation produced by Mg-ATP is partially reverted by centrifugation, removal of the supernatant and resuspension of Synaptosomes in a fresh medium. This partial reversion occurs in parallel to the release to the suparnatant of phosphorylated protein(s) of 90–95 kDa. Alkaline phosphatase treatment fully reverts the ecto-ATPase inactivation. We conclude that the ATP-induced inactivation is mediated, at least partially, by phosphorylation of membrane proteins.
Ahmed Almousa - One of the best experts on this subject based on the ideXlab platform.
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membrane permeability of trace amines evidence for a regulated activity dependent nonexocytotic synaptic release
Synapse, 2013Co-Authors: Mark D Berry, Mithila R Shitut, Ahmed Almousa, Jane Alcorn, Bruno TomberliAbstract:Both pre- and post-synaptic effects of trace amines have been demonstrated. The putative intracellular location of Trace Amine-Associated Receptors necessitate that membrane transport processes be present in order for post-synaptic effects to occur. Here we examine the ability of trace amines to cross synthetic (Fluorosomes) and native (Synaptosomes) lipid bilayer membranes. Trace amines readily crossed Fluorosome membranes by simple diffusion, p-tyramine (P = 0.01) and tryptamine (P = 0.0004) showing significantly faster diffusion than dopamine and 5-HT, respectively, with diffusion half-lives of 13.5 ± 4.1 (p-tyramine) and 6.8 ± 0.7 seconds (tryptamine). Similarly, release of [3H]p-tyramine and [3H]2-phenylethylamine from pre-loaded Synaptosomes occurred significantly quicker than did [3H]dopamine (P = 0.0001), with half lives of 38.9 (p-tyramine), 7.8 (2-phenylethylamine) and 133.6 seconds (dopamine). This was, however, significantly slower than the diffusion mediated passage across Fluorosome membranes (P = 0.0001), suggesting a role for transporters in mediating trace amine release. Further, a pronounced shoulder region was observed in the Synaptosome [3H]p-tyramine release curve, suggesting that multiple processes regulate release. No such shoulder region was present for [3H]dopamine release. Surprisingly, both [3H]p-tyramine (P = 0.001) and [3H]2-phenylethylamine (P = 0.0001) release from Synaptosomes was significantly decreased under depolarizing conditions. As expected, depolarization significantly increased [3H]dopamine release. The data presented indicate that the release of p-tyramine and 2-phenylethylamine from neuronal terminals occurs by a different mechanism than dopamine, and does not involve classical exocytosis. The data are consistent with an initial release of trace amines by simple diffusion, followed by an activity-dependent regulation of synaptic levels via one or more transporter proteins. Synapse 67:656–667, 2013. © 2013 Wiley Periodicals, Inc.
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Membrane permeability of trace amines: Evidence for a regulated, activity‐dependent, nonexocytotic, synaptic release
Synapse (New York N.Y.), 2013Co-Authors: Mark D Berry, Mithila R Shitut, Ahmed Almousa, Jane Alcorn, Bruno TomberliAbstract:Both pre- and post-synaptic effects of trace amines have been demonstrated. The putative intracellular location of Trace Amine-Associated Receptors necessitate that membrane transport processes be present in order for post-synaptic effects to occur. Here we examine the ability of trace amines to cross synthetic (Fluorosomes) and native (Synaptosomes) lipid bilayer membranes. Trace amines readily crossed Fluorosome membranes by simple diffusion, p-tyramine (P = 0.01) and tryptamine (P = 0.0004) showing significantly faster diffusion than dopamine and 5-HT, respectively, with diffusion half-lives of 13.5 ± 4.1 (p-tyramine) and 6.8 ± 0.7 seconds (tryptamine). Similarly, release of [3H]p-tyramine and [3H]2-phenylethylamine from pre-loaded Synaptosomes occurred significantly quicker than did [3H]dopamine (P = 0.0001), with half lives of 38.9 (p-tyramine), 7.8 (2-phenylethylamine) and 133.6 seconds (dopamine). This was, however, significantly slower than the diffusion mediated passage across Fluorosome membranes (P = 0.0001), suggesting a role for transporters in mediating trace amine release. Further, a pronounced shoulder region was observed in the Synaptosome [3H]p-tyramine release curve, suggesting that multiple processes regulate release. No such shoulder region was present for [3H]dopamine release. Surprisingly, both [3H]p-tyramine (P = 0.001) and [3H]2-phenylethylamine (P = 0.0001) release from Synaptosomes was significantly decreased under depolarizing conditions. As expected, depolarization significantly increased [3H]dopamine release. The data presented indicate that the release of p-tyramine and 2-phenylethylamine from neuronal terminals occurs by a different mechanism than dopamine, and does not involve classical exocytosis. The data are consistent with an initial release of trace amines by simple diffusion, followed by an activity-dependent regulation of synaptic levels via one or more transporter proteins. Synapse 67:656–667, 2013. © 2013 Wiley Periodicals, Inc.
