The Experts below are selected from a list of 49431 Experts worldwide ranked by ideXlab platform
Francis Chaouloff - One of the best experts on this subject based on the ideXlab platform.
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The Stress Hormone corticosterone conditions AMPAR surface trafficking and synaptic potentiation
Nature Neuroscience, 2008Co-Authors: Laurent Groc, Daniel Choquet, Francis ChaouloffAbstract:Corticosterone triggers increased AMPA receptor membrane mobility and surface expression, according to a new study by Groc and colleagues. This mechanism helps to explain the observed modulation of synaptic plasticity and strength induced by this Stress Hormone. Corticosterone facilitates hippocampal glutamate transmission, but the cellular pathways by which AMPA receptor (AMPAR) signaling is adjusted remain elusive. Single quantum-dot imaging in live rat hippocampal neurons revealed that corticosterone triggers, via distinct corticosteroid receptors, time-dependent increases in GluR2-AMPAR surface mobility and synaptic surface GluR2 content. Furthermore, corticosterone potentiates the increase of synaptic surface GluR2 contents by a chemical long-term potentiation stimulus, revealing the influence that corticosterone has on AMPAR trafficking.
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The Stress Hormone corticosterone conditions AMPAR surface trafficking and synaptic potentiation.
Nature neuroscience, 2008Co-Authors: Laurent Groc, Daniel Choquet, Francis ChaouloffAbstract:Corticosterone facilitates hippocampal glutamate transmission, but the cellular pathways by which AMPA receptor (AMPAR) signaling is adjusted remain elusive. Single quantum-dot imaging in live rat hippocampal neurons revealed that corticosterone triggers, via distinct corticosteroid receptors, time-dependent increases in GluR2-AMPAR surface mobility and synaptic surface GluR2 content. Furthermore, corticosterone potentiates the increase of synaptic surface GluR2 contents by a chemical long-term potentiation stimulus, revealing the influence that corticosterone has on AMPAR trafficking.
Laurent Groc - One of the best experts on this subject based on the ideXlab platform.
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The Stress Hormone corticosterone conditions AMPAR surface trafficking and synaptic potentiation
Nature Neuroscience, 2008Co-Authors: Laurent Groc, Daniel Choquet, Francis ChaouloffAbstract:Corticosterone triggers increased AMPA receptor membrane mobility and surface expression, according to a new study by Groc and colleagues. This mechanism helps to explain the observed modulation of synaptic plasticity and strength induced by this Stress Hormone. Corticosterone facilitates hippocampal glutamate transmission, but the cellular pathways by which AMPA receptor (AMPAR) signaling is adjusted remain elusive. Single quantum-dot imaging in live rat hippocampal neurons revealed that corticosterone triggers, via distinct corticosteroid receptors, time-dependent increases in GluR2-AMPAR surface mobility and synaptic surface GluR2 content. Furthermore, corticosterone potentiates the increase of synaptic surface GluR2 contents by a chemical long-term potentiation stimulus, revealing the influence that corticosterone has on AMPAR trafficking.
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The Stress Hormone corticosterone conditions AMPAR surface trafficking and synaptic potentiation.
Nature neuroscience, 2008Co-Authors: Laurent Groc, Daniel Choquet, Francis ChaouloffAbstract:Corticosterone facilitates hippocampal glutamate transmission, but the cellular pathways by which AMPA receptor (AMPAR) signaling is adjusted remain elusive. Single quantum-dot imaging in live rat hippocampal neurons revealed that corticosterone triggers, via distinct corticosteroid receptors, time-dependent increases in GluR2-AMPAR surface mobility and synaptic surface GluR2 content. Furthermore, corticosterone potentiates the increase of synaptic surface GluR2 contents by a chemical long-term potentiation stimulus, revealing the influence that corticosterone has on AMPAR trafficking.
Alan D. Cherrington - One of the best experts on this subject based on the ideXlab platform.
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Role of epinephrine and norepinephrine in the metabolic response to Stress Hormone infusion in the conscious dog
The American journal of physiology, 1997Co-Authors: Owen P. Mcguinness, Vickie Shau, Eric M. Benson, Mike Lewis, Robert T. Snowden, James E. Greene, Doss W. Neal, Alan D. CherringtonAbstract:The role of epinephrine and norepinephrine in contributing to the alterations in hepatic glucose metabolism during a 70-h Stress Hormone infusion (SHI) was investigated in four groups of chronicall...
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Role of cortisol in the metabolic response to Stress Hormone infusion in the conscious dog
Metabolism: clinical and experimental, 1996Co-Authors: Fujiwara Toshihiko, Alan D. Cherrington, Doss Neal, Owen P. McguinnessAbstract:Abstract The role of cortisol in directing the metabolic response to a combined infusion of glucagon, epinephrine, norepinephrine, and cortisol (Stress Hormones) was investigated. Chronically catheterized, conscious fasted dogs were studied before Hormone infusion and after a 70-hour Stress Hormone infusion containing glucagon, epinephrine, norepinephrine, and cortisol (n = 11) or containing all these Hormones except cortisol (n = 5). Combined Stress Hormone infusion increased arterial plasma glucagon, cortisol, epinephrine, and norepinephrine approximately sixfold. Whole-body glucose production (R a ), glycogenolysis, and gluconeogenesis were assessed using tracer and arteriovenous-difference techniques. The absence of an increase in cortisol during Stress Hormone infusion attenuated the increase in arterial plasma glucose concentration and R a (Δ 81 ± 16 v 24 ± 3 mg/dL and 1.7 ± 0.3 v 0.8 ± 0.4 mg/kg/min, respectively). However, it did not alter the increase in net hepatic glucose output (Δ 0.7 ± 0.3 v 0.8 ± 0.4 mg / kg / min ). When the increase in cortisol was absent, the increase in net hepatic gluconeogenic precursor uptake was attenuated (Δ 0.7 ± 0.3 v 0.1 ± 0.3 mg glucose/kg/min) due to a decrease in gluconeogenic precursor levels. The efficiency of gluconeogenesis increased to a greater extent (Δ 0.19 ± 0.07 v 0.31 ± 0.11) when cortisol was not infused. The absence of an increase in cortisol also led to marked glycogen depletion in the liver (10 ± 4 v 55 ± 10 mg/g liver). Cortisol thus plays a pivotal role in the metabolic response to Stress Hormone infusion by sustaining gluconeogenesis through a stimulatory effect on hepatic gluconeogenic precursor supply and by maintaining hepatic glycogen availability.
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Role of glucagon in the metabolic response to Stress Hormone infusion in the conscious dog
American Journal of Physiology-Endocrinology and Metabolism, 1994Co-Authors: Owen P. Mcguinness, K. Burgin, Christopher Moran, Deanna P. Bracy, Alan D. CherringtonAbstract:The impact of the absence of an increase in glucagon on the metabolic response to Stress Hormone infusion was investigated. We studied 11 conscious dogs fasted for 20 h before (day 0) and after (day 3) a 70-h Stress Hormone infusion containing glucagon, cortisol, epinephrine, and norepinephrine that increased their respective levels approximately sixfold. Five additional dogs were studied on day 0 and were then infused with the same Stress Hormone infusion but without glucagon. Glucose production and gluconeogenesis were assessed using tracer and arteriovenous difference techniques. The absence of an increase in glucagon during Stress Hormone infusion attenuated the increase in arterial plasma glucose concentration (delta 81 +/- 16 vs. delta 28 +/- 6 mg/dl) but did not significantly alter the increase in the rate of glucose appearance (delta 1.7 +/- 0.3 vs. delta 1.1 +/- 0.4 mg.kg-1.min-1). However, it eliminated the increase in net hepatic glucose output (delta 0.7 +/- 0.3 vs. delta 0.0 +/- 0.4 mg.kg-1.min-1) primarily because of an increase in hepatic glucose uptake. In addition, the Stress Hormone-induced increase in net hepatic gluconeogenic precursor uptake (delta 0.7 +/- 0.3 vs. delta 0.2 +/- 0.1 mg of glucose.kg-1.min-1) and the efficiency of gluconeogenesis (delta 0.19 +/- 0.07 vs. delta 0.01 +/- 0.05) were attenuated. Glucagon thus plays a pivotal role in the metabolic response to Stress Hormone infusion by sustaining gluconeogenesis through a stimulatory effect on the hepatic gluconeogenic precursor uptake as well as on the efficiency of gluconeogenesis within the liver.
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The effect of acute glucagon removal on the metabolic response to Stress Hormone infusion in the conscious dog
Metabolism: clinical and experimental, 1994Co-Authors: Owen P. Mcguinness, Christopher Moran, Deanna P. Bracy, Sam Murrell, Alan D. CherringtonAbstract:The effect of acute glucagon removal on glucose metabolism following long-term (70-hour) Stress Hormone infusion (day 3) was investigated in 20-hour-fasted conscious dogs. Stress Hormone infusion increased arterial plasma glucagon, cortisol, epinephrine, and norepinephrine (∼ fivefold), as well as arterial plasma glucose (Δ82 ± 16 mg/dL) and insulin (Δ26 ± 5 μU/mL). After assessing basal glucose metabolism on day 3, the long-term glucagon infusion was discontinued (n = 6), and the remaining Hormones were infused for an additional 180 minutes. Constant glycemia was maintained by an exogenous glucose infusion. In five dogs, the Stress Hormone infusion containing glucagon was continued for 180 minutes. Glucose production and gluconeogenesis were assessed using tracer and arteriovenous-difference techniques. Acute removal of glucagon decreased arterial plasma glucagon from 220 ± 24 to 32 ± 4 pg/mL and net hepatic glucose output (Δ1.6 ± 0.3 mg/kg/min). Net hepatic handling of lactate, alanine, and glycerol was not altered. The efficiency of gluconeogenesis, on the other hand, was decreased by 40%. Liver biopsies taken following discontinuation of glucagon indicated that both3H- and14C-glucose accumulated in glycogen. The calculated rate of plasma glucose and gluconeogenic precursor diversion to glycogen increased by fivefold and fourfold, respectively. The increased gluconeogenic precursor diversion to glycogen accounted for 58% of the decrease in the efficiency of gluconeogenesis. In conclusion, acute removal of glucagon during Stress Hormone infusion decreased net hepatic glycogenolysis in the face of prevailing hyperglycemia and hyperinsulinemia, while having minimal effects on the gluconeogenic process per se.
Marian Joels - One of the best experts on this subject based on the ideXlab platform.
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Stress Hormone corticosterone enhances susceptibility to cortical spreading depression in familial hemiplegic migraine type 1 mutant mice
Experimental Neurology, 2015Co-Authors: Reinald Shyti, Marian Joels, Katharina Eikermannhaerter, Sandra H Van Heiningen, Onno C Meijer, Cenk Ayata, Michel D Ferrari, Arn M J M Van Den Maagdenberg, Else A TolnerAbstract:Abstract Stress is a putative migraine trigger, but the pathogenic mechanisms involved are unknown. Stress and Stress Hormones increase neuronal excitability by enhancing glutamatergic neurotransmission, but inhibitory effects have also been reported. We hypothesise that an acute rise in Stress Hormones, such as corticosteroids which are released after Stress, increase neuronal excitability and thereby may increase susceptibility to cortical spreading depression (CSD), the mechanism underlying the migraine aura. Here we investigated effects of acute restraint Stress and of the Stress Hormone corticosterone on CSD susceptibility as surrogate migraine marker, in a transgenic mouse model of familial hemiplegic migraine type 1 (FHM1), which displays increased glutamatergic cortical neurotransmission and increased propensity for CSD. We found that 20-min and 3-h restraint Stress did not influence CSD susceptibility in mutant or wild-type mice, despite elevated levels of plasma corticosterone. By contrast, subcutaneous administration of 20 mg/kg corticosterone increased CSD frequency exclusively in mutant mice, while corticosterone plasma levels were similarly elevated in mutants and wild types. The effect of corticosterone on CSD frequency was normalised by pre-administration of the glucocorticoid receptor (GR) antagonist mifepristone. These findings suggest that corticosteroid-induced GR activation can enhance susceptibility to CSD in genetically susceptible individuals, and may predispose to attacks of migraine. Although corticosterone levels rise also during acute Stress, the latter likely triggers a spatiotemporally more complex biological response with multiple positive and negative modulators which may not be adequately modeled by exogenous administration of corticosterone alone.
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metaplasticity of amygdalar responses to the Stress Hormone corticosterone
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Henk Karst, Stefan Berger, Gitta Erdmann, Gunther Schutz, Marian JoelsAbstract:High levels of corticosteroids (as circulate after Stress) quickly and reversibly enhance hippocampal glutamatergic transmission via nongenomic actions requiring mineralocorticoid receptors. Subsequently, the Hormone slowly and long-lastingly normalizes hippocampal cell function, through nuclear glucocorticoid receptors. Here we describe a rapid mineralocorticoid receptor-dependent enhancement of glutamatergic transmission in basolateral amygdala neurons. Contrary to the hippocampus, this rapid enhancement is long-lasting, potentially allowing an extended window for encoding of emotional aspects during Stressful events. Importantly, the long-lasting change in state of amygdala neurons greatly affects the responsiveness to subsequent surges of corticosterone, revealing a quick suppression of glutamatergic transmission, which requires the glucocorticoid receptor. Responses of basolateral amygdala neurons to the Stress Hormone corticosterone can thus switch from excitatory to inhibitory, depending on the recent Stress history of the organism.
Owen P. Mcguinness - One of the best experts on this subject based on the ideXlab platform.
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Role of epinephrine and norepinephrine in the metabolic response to Stress Hormone infusion in the conscious dog
The American journal of physiology, 1997Co-Authors: Owen P. Mcguinness, Vickie Shau, Eric M. Benson, Mike Lewis, Robert T. Snowden, James E. Greene, Doss W. Neal, Alan D. CherringtonAbstract:The role of epinephrine and norepinephrine in contributing to the alterations in hepatic glucose metabolism during a 70-h Stress Hormone infusion (SHI) was investigated in four groups of chronicall...
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Role of cortisol in the metabolic response to Stress Hormone infusion in the conscious dog
Metabolism: clinical and experimental, 1996Co-Authors: Fujiwara Toshihiko, Alan D. Cherrington, Doss Neal, Owen P. McguinnessAbstract:Abstract The role of cortisol in directing the metabolic response to a combined infusion of glucagon, epinephrine, norepinephrine, and cortisol (Stress Hormones) was investigated. Chronically catheterized, conscious fasted dogs were studied before Hormone infusion and after a 70-hour Stress Hormone infusion containing glucagon, epinephrine, norepinephrine, and cortisol (n = 11) or containing all these Hormones except cortisol (n = 5). Combined Stress Hormone infusion increased arterial plasma glucagon, cortisol, epinephrine, and norepinephrine approximately sixfold. Whole-body glucose production (R a ), glycogenolysis, and gluconeogenesis were assessed using tracer and arteriovenous-difference techniques. The absence of an increase in cortisol during Stress Hormone infusion attenuated the increase in arterial plasma glucose concentration and R a (Δ 81 ± 16 v 24 ± 3 mg/dL and 1.7 ± 0.3 v 0.8 ± 0.4 mg/kg/min, respectively). However, it did not alter the increase in net hepatic glucose output (Δ 0.7 ± 0.3 v 0.8 ± 0.4 mg / kg / min ). When the increase in cortisol was absent, the increase in net hepatic gluconeogenic precursor uptake was attenuated (Δ 0.7 ± 0.3 v 0.1 ± 0.3 mg glucose/kg/min) due to a decrease in gluconeogenic precursor levels. The efficiency of gluconeogenesis increased to a greater extent (Δ 0.19 ± 0.07 v 0.31 ± 0.11) when cortisol was not infused. The absence of an increase in cortisol also led to marked glycogen depletion in the liver (10 ± 4 v 55 ± 10 mg/g liver). Cortisol thus plays a pivotal role in the metabolic response to Stress Hormone infusion by sustaining gluconeogenesis through a stimulatory effect on hepatic gluconeogenic precursor supply and by maintaining hepatic glycogen availability.
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Role of glucagon in the metabolic response to Stress Hormone infusion in the conscious dog
American Journal of Physiology-Endocrinology and Metabolism, 1994Co-Authors: Owen P. Mcguinness, K. Burgin, Christopher Moran, Deanna P. Bracy, Alan D. CherringtonAbstract:The impact of the absence of an increase in glucagon on the metabolic response to Stress Hormone infusion was investigated. We studied 11 conscious dogs fasted for 20 h before (day 0) and after (day 3) a 70-h Stress Hormone infusion containing glucagon, cortisol, epinephrine, and norepinephrine that increased their respective levels approximately sixfold. Five additional dogs were studied on day 0 and were then infused with the same Stress Hormone infusion but without glucagon. Glucose production and gluconeogenesis were assessed using tracer and arteriovenous difference techniques. The absence of an increase in glucagon during Stress Hormone infusion attenuated the increase in arterial plasma glucose concentration (delta 81 +/- 16 vs. delta 28 +/- 6 mg/dl) but did not significantly alter the increase in the rate of glucose appearance (delta 1.7 +/- 0.3 vs. delta 1.1 +/- 0.4 mg.kg-1.min-1). However, it eliminated the increase in net hepatic glucose output (delta 0.7 +/- 0.3 vs. delta 0.0 +/- 0.4 mg.kg-1.min-1) primarily because of an increase in hepatic glucose uptake. In addition, the Stress Hormone-induced increase in net hepatic gluconeogenic precursor uptake (delta 0.7 +/- 0.3 vs. delta 0.2 +/- 0.1 mg of glucose.kg-1.min-1) and the efficiency of gluconeogenesis (delta 0.19 +/- 0.07 vs. delta 0.01 +/- 0.05) were attenuated. Glucagon thus plays a pivotal role in the metabolic response to Stress Hormone infusion by sustaining gluconeogenesis through a stimulatory effect on the hepatic gluconeogenic precursor uptake as well as on the efficiency of gluconeogenesis within the liver.
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The effect of acute glucagon removal on the metabolic response to Stress Hormone infusion in the conscious dog
Metabolism: clinical and experimental, 1994Co-Authors: Owen P. Mcguinness, Christopher Moran, Deanna P. Bracy, Sam Murrell, Alan D. CherringtonAbstract:The effect of acute glucagon removal on glucose metabolism following long-term (70-hour) Stress Hormone infusion (day 3) was investigated in 20-hour-fasted conscious dogs. Stress Hormone infusion increased arterial plasma glucagon, cortisol, epinephrine, and norepinephrine (∼ fivefold), as well as arterial plasma glucose (Δ82 ± 16 mg/dL) and insulin (Δ26 ± 5 μU/mL). After assessing basal glucose metabolism on day 3, the long-term glucagon infusion was discontinued (n = 6), and the remaining Hormones were infused for an additional 180 minutes. Constant glycemia was maintained by an exogenous glucose infusion. In five dogs, the Stress Hormone infusion containing glucagon was continued for 180 minutes. Glucose production and gluconeogenesis were assessed using tracer and arteriovenous-difference techniques. Acute removal of glucagon decreased arterial plasma glucagon from 220 ± 24 to 32 ± 4 pg/mL and net hepatic glucose output (Δ1.6 ± 0.3 mg/kg/min). Net hepatic handling of lactate, alanine, and glycerol was not altered. The efficiency of gluconeogenesis, on the other hand, was decreased by 40%. Liver biopsies taken following discontinuation of glucagon indicated that both3H- and14C-glucose accumulated in glycogen. The calculated rate of plasma glucose and gluconeogenic precursor diversion to glycogen increased by fivefold and fourfold, respectively. The increased gluconeogenic precursor diversion to glycogen accounted for 58% of the decrease in the efficiency of gluconeogenesis. In conclusion, acute removal of glucagon during Stress Hormone infusion decreased net hepatic glycogenolysis in the face of prevailing hyperglycemia and hyperinsulinemia, while having minimal effects on the gluconeogenic process per se.
