The Experts below are selected from a list of 48 Experts worldwide ranked by ideXlab platform
Arne Schousboe - One of the best experts on this subject based on the ideXlab platform.
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depolarization by k and Glutamate activates different neurotransmitter release mechanisms in gabaergic neurons vesicular versus non vesicular release of gaba
Neuroscience, 1993Co-Authors: Bo Belhage, Gert H Hansen, Arne SchousboeAbstract:Abstract Neurotransmitter release and changes in the concentration of intracellular free calcium ([Ca ++ ] i ) were studied in cultured GABAergic cerebral cortical neurons, from mice, upon depolarization with either an unphysiologicaLly high Potassium concentration (55 mM) or the physiological excitatory neurotransmitter Glutamate (100 μM). Both depolarizing stimuli exerted prompt increases in the release of preloaded [ 3 H]GABA as well as in [Ca ++ ] i . However, the basic properties of transmitter release and the increase in [Ca ++ ] i , under a variety of conditions were different during stimulation with K + or Glutamate. Potassium-evoked release of [ 3 H]GABA consisted of two phases, a rapid, large and transient phase followed by a smaller, more persistent second phase. The rapid phase was inhibited (60%) by nocodazole which reduced the number of vesicles in the neuntes by 80%. This rapid phase of the GABA release was also reduced by organic (verapamil) and inorganic (Co ++ ) Ca ++ channel blockers but was insensitive to the GABA transport inhibitor SKF 89976A. In contrast, the second phase was less sensitive to nocodazole and Ca ++ channel antagonists but could be inhibited by SKF 89976A. The Glutamateinduced [ 3 H]GABA release, which was mainly mediated by N -methyl- d -aspartate receptors, consisted of a single, sustained phase. This was insensitive to nocodazole, partly inhibited by verapamil and could be blocked by Co ++ as well as SKF 89976A. The action of Co ++ could be attributed to a block of N -methyl- d -aspartate-associated ion channels. These findings strongly suggest that the majority of the K + -stimulated GABA release is dependent upon vesicles whereas the Glutamate induced release is non-vesicular and mediated by a depolarization-dependent reversal of the direction of high-affinity GABA transport. The basic differences in the mode of action of the two depolarizing stimuli were reflected in the properties of the increase in [Ca ++ ] i elicited by 55 mM K + and 100μM Glutamate, respectively. The K + -induced increase in [Ca ++ ] i was reduced by both verapamil and Ca ++ -free media whereas the corresponding Glutamate response was only sensitive to Ca ++ -free conditions. Exposure of the cells to nocodazole or SKF 89976A had no effect on the ability of K + or Glutamate to increase [Ca ++ ] i . Altogether, the results clearly demonstrate that K + -induced transmitter release from these GABAergic neurons is vesicular in nature whereas that induced by the neurotransmitter Glutamate is not.
Eric J Hill - One of the best experts on this subject based on the ideXlab platform.
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functional astrocyte neuron lactate shuttle in a human stem cell derived neuronal network
Journal of Cerebral Blood Flow and Metabolism, 2013Co-Authors: Marta A Tarczyluk, David A Nagel, John D Oneil, Rheinallt H Parri, Michael D Coleman, Eric J HillAbstract:The NT2.D1 cell line is one of the most well-documented embryocarcinoma cell lines, and can be differentiated into neurons and astrocytes. Great focus has also been placed on defining the electrophysiological properties of the neuronal cells, and more recently we have investigated the functional properties of their associated astrocytes. We now show for the first time that human stem cell-derived astrocytes produce glycogen and that co-cultures of these cells demonstrate a functional astrocyte-neuron lactate shuttle (ANLS). The ANLS hypothesis proposes that during neuronal activity, Glutamate released into the synaptic cleft is taken up by astrocytes and triggers glucose uptake, which is converted into lactate and released via monocarboxylate transporters for neuronal use. Using mixed cultures of NT2-derived neurons and astrocytes, we have shown that these cells modulate their glucose uptake in response to Glutamate. Additionally, we demonstrate that in response to increased neuronal activity and under hypoglycaemic conditions, co-cultures modulate glycogen turnover and increase lactate production. Similar results were also shown after treatment with Glutamate, Potassium, isoproterenol, and dbcAMP. Together, these results demonstrate for the first time a functional ANLS in a human stem cell-derived co-culture. © 2013 ISCBFM.
Bo Belhage - One of the best experts on this subject based on the ideXlab platform.
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depolarization by k and Glutamate activates different neurotransmitter release mechanisms in gabaergic neurons vesicular versus non vesicular release of gaba
Neuroscience, 1993Co-Authors: Bo Belhage, Gert H Hansen, Arne SchousboeAbstract:Abstract Neurotransmitter release and changes in the concentration of intracellular free calcium ([Ca ++ ] i ) were studied in cultured GABAergic cerebral cortical neurons, from mice, upon depolarization with either an unphysiologicaLly high Potassium concentration (55 mM) or the physiological excitatory neurotransmitter Glutamate (100 μM). Both depolarizing stimuli exerted prompt increases in the release of preloaded [ 3 H]GABA as well as in [Ca ++ ] i . However, the basic properties of transmitter release and the increase in [Ca ++ ] i , under a variety of conditions were different during stimulation with K + or Glutamate. Potassium-evoked release of [ 3 H]GABA consisted of two phases, a rapid, large and transient phase followed by a smaller, more persistent second phase. The rapid phase was inhibited (60%) by nocodazole which reduced the number of vesicles in the neuntes by 80%. This rapid phase of the GABA release was also reduced by organic (verapamil) and inorganic (Co ++ ) Ca ++ channel blockers but was insensitive to the GABA transport inhibitor SKF 89976A. In contrast, the second phase was less sensitive to nocodazole and Ca ++ channel antagonists but could be inhibited by SKF 89976A. The Glutamateinduced [ 3 H]GABA release, which was mainly mediated by N -methyl- d -aspartate receptors, consisted of a single, sustained phase. This was insensitive to nocodazole, partly inhibited by verapamil and could be blocked by Co ++ as well as SKF 89976A. The action of Co ++ could be attributed to a block of N -methyl- d -aspartate-associated ion channels. These findings strongly suggest that the majority of the K + -stimulated GABA release is dependent upon vesicles whereas the Glutamate induced release is non-vesicular and mediated by a depolarization-dependent reversal of the direction of high-affinity GABA transport. The basic differences in the mode of action of the two depolarizing stimuli were reflected in the properties of the increase in [Ca ++ ] i elicited by 55 mM K + and 100μM Glutamate, respectively. The K + -induced increase in [Ca ++ ] i was reduced by both verapamil and Ca ++ -free media whereas the corresponding Glutamate response was only sensitive to Ca ++ -free conditions. Exposure of the cells to nocodazole or SKF 89976A had no effect on the ability of K + or Glutamate to increase [Ca ++ ] i . Altogether, the results clearly demonstrate that K + -induced transmitter release from these GABAergic neurons is vesicular in nature whereas that induced by the neurotransmitter Glutamate is not.
Marta A Tarczyluk - One of the best experts on this subject based on the ideXlab platform.
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functional astrocyte neuron lactate shuttle in a human stem cell derived neuronal network
Journal of Cerebral Blood Flow and Metabolism, 2013Co-Authors: Marta A Tarczyluk, David A Nagel, John D Oneil, Rheinallt H Parri, Michael D Coleman, Eric J HillAbstract:The NT2.D1 cell line is one of the most well-documented embryocarcinoma cell lines, and can be differentiated into neurons and astrocytes. Great focus has also been placed on defining the electrophysiological properties of the neuronal cells, and more recently we have investigated the functional properties of their associated astrocytes. We now show for the first time that human stem cell-derived astrocytes produce glycogen and that co-cultures of these cells demonstrate a functional astrocyte-neuron lactate shuttle (ANLS). The ANLS hypothesis proposes that during neuronal activity, Glutamate released into the synaptic cleft is taken up by astrocytes and triggers glucose uptake, which is converted into lactate and released via monocarboxylate transporters for neuronal use. Using mixed cultures of NT2-derived neurons and astrocytes, we have shown that these cells modulate their glucose uptake in response to Glutamate. Additionally, we demonstrate that in response to increased neuronal activity and under hypoglycaemic conditions, co-cultures modulate glycogen turnover and increase lactate production. Similar results were also shown after treatment with Glutamate, Potassium, isoproterenol, and dbcAMP. Together, these results demonstrate for the first time a functional ANLS in a human stem cell-derived co-culture. © 2013 ISCBFM.
Robert P. Erickson - One of the best experts on this subject based on the ideXlab platform.
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Taste of Glutamate salts in young and elderly subjects: role of inosine 5'-monophosphate and ions.
Physiology & behavior, 1991Co-Authors: Susan S. Schiffman, Amy E. Frey, J.a. Luboski, M.a. Foster, Robert P. EricksonAbstract:Taste sensitivity to five Glutamate salts (sodium Glutamate, Potassium Glutamate, ammonium Glutamate, calcium diGlutamate, and magnesium diGlutamate) were determined in sixteen young (mean age 25.58 years) and eighteen elderly (mean age 86.89 years) subjects. The effect of inosine 5'-monophosphate (IMP) and ions on taste perception of Glutamate compounds was also investigated. The detection thresholds for Glutamate salts were 5.04 times higher in elderly subjects than in young subjects; the recognition thresholds were 3.84 times higher. For young subjects, 0.1 mM IMP lowered detection and recognition thresholds for all 5 salts. A stronger concentration of IMP (1 mM) had this effect in both young and elderly groups. Elderly subjects perceived suprathreshold concentrations as less intense than young subjects. Chloride and acetate salts of sodium, Potassium, and calcium reduced the detection and recognition thresholds of L-glutamic acid but had no effect sodium Glutamate thresholds.