The Experts below are selected from a list of 216 Experts worldwide ranked by ideXlab platform
Tatsushi Onaka - One of the best experts on this subject based on the ideXlab platform.
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effects of rfamide related peptide rfrp 1 and rfrp 3 on oxytocin release and anxiety related behaviour in rats
Journal of Neuroendocrinology, 2011Co-Authors: Maroot Kaewwongse, Yuki Takayanagi, Tatsushi OnakaAbstract:RFamide-related peptides (RFRP-1 and RFRP-3) are localised in neurones of the dorsomedial Hypothalamus in rats. The dorsomedial Hypothalamus plays an essential role in neuroendocrine and behavioural stress responses. In the present study, we examined the role of RFRP in the control of neuroendocrine and behavioural responses in rats. Stressful stimuli increased expression of Fos protein in RFRP-immunoreactive neurones of the dorsomedial Hypothalamus, suggesting that stressful stimuli activate RFRP neurones. Intracerebroventricular injection of RFRPs increased the expression of Fos protein in oxytocin neurones in the Hypothalamus and plasma concentrations of adrenocorticotrophic hormone and oxytocin. The hypothalamic paraventricular and supraoptic nuclei expressed mRNA of GPR147, the putative RFRP receptor, and application of RFRPs to isolated supraoptic nuclei facilitated oxytocin release, suggesting that RFRPs activate oxytocin neurones directly. Furthermore, the administration of RFRPs induced anxiety-related behaviour in rats in open-field tests. All these data taken together suggest that RFRPs play a role in the control of neuroendocrine and behavioural stress responses in rats.
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Effects of RFamide‐Related Peptide (RFRP)‐1 and RFRP‐3 on Oxytocin Release and Anxiety‐Related Behaviour in Rats
Journal of Neuroendocrinology, 2010Co-Authors: Maroot Kaewwongse, Yuki Takayanagi, Tatsushi OnakaAbstract:RFamide-related peptides (RFRP-1 and RFRP-3) are localised in neurones of the dorsomedial Hypothalamus in rats. The dorsomedial Hypothalamus plays an essential role in neuroendocrine and behavioural stress responses. In the present study, we examined the role of RFRP in the control of neuroendocrine and behavioural responses in rats. Stressful stimuli increased expression of Fos protein in RFRP-immunoreactive neurones of the dorsomedial Hypothalamus, suggesting that stressful stimuli activate RFRP neurones. Intracerebroventricular injection of RFRPs increased the expression of Fos protein in oxytocin neurones in the Hypothalamus and plasma concentrations of adrenocorticotrophic hormone and oxytocin. The hypothalamic paraventricular and supraoptic nuclei expressed mRNA of GPR147, the putative RFRP receptor, and application of RFRPs to isolated supraoptic nuclei facilitated oxytocin release, suggesting that RFRPs activate oxytocin neurones directly. Furthermore, the administration of RFRPs induced anxiety-related behaviour in rats in open-field tests. All these data taken together suggest that RFRPs play a role in the control of neuroendocrine and behavioural stress responses in rats.
Maroot Kaewwongse - One of the best experts on this subject based on the ideXlab platform.
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effects of rfamide related peptide rfrp 1 and rfrp 3 on oxytocin release and anxiety related behaviour in rats
Journal of Neuroendocrinology, 2011Co-Authors: Maroot Kaewwongse, Yuki Takayanagi, Tatsushi OnakaAbstract:RFamide-related peptides (RFRP-1 and RFRP-3) are localised in neurones of the dorsomedial Hypothalamus in rats. The dorsomedial Hypothalamus plays an essential role in neuroendocrine and behavioural stress responses. In the present study, we examined the role of RFRP in the control of neuroendocrine and behavioural responses in rats. Stressful stimuli increased expression of Fos protein in RFRP-immunoreactive neurones of the dorsomedial Hypothalamus, suggesting that stressful stimuli activate RFRP neurones. Intracerebroventricular injection of RFRPs increased the expression of Fos protein in oxytocin neurones in the Hypothalamus and plasma concentrations of adrenocorticotrophic hormone and oxytocin. The hypothalamic paraventricular and supraoptic nuclei expressed mRNA of GPR147, the putative RFRP receptor, and application of RFRPs to isolated supraoptic nuclei facilitated oxytocin release, suggesting that RFRPs activate oxytocin neurones directly. Furthermore, the administration of RFRPs induced anxiety-related behaviour in rats in open-field tests. All these data taken together suggest that RFRPs play a role in the control of neuroendocrine and behavioural stress responses in rats.
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Effects of RFamide‐Related Peptide (RFRP)‐1 and RFRP‐3 on Oxytocin Release and Anxiety‐Related Behaviour in Rats
Journal of Neuroendocrinology, 2010Co-Authors: Maroot Kaewwongse, Yuki Takayanagi, Tatsushi OnakaAbstract:RFamide-related peptides (RFRP-1 and RFRP-3) are localised in neurones of the dorsomedial Hypothalamus in rats. The dorsomedial Hypothalamus plays an essential role in neuroendocrine and behavioural stress responses. In the present study, we examined the role of RFRP in the control of neuroendocrine and behavioural responses in rats. Stressful stimuli increased expression of Fos protein in RFRP-immunoreactive neurones of the dorsomedial Hypothalamus, suggesting that stressful stimuli activate RFRP neurones. Intracerebroventricular injection of RFRPs increased the expression of Fos protein in oxytocin neurones in the Hypothalamus and plasma concentrations of adrenocorticotrophic hormone and oxytocin. The hypothalamic paraventricular and supraoptic nuclei expressed mRNA of GPR147, the putative RFRP receptor, and application of RFRPs to isolated supraoptic nuclei facilitated oxytocin release, suggesting that RFRPs activate oxytocin neurones directly. Furthermore, the administration of RFRPs induced anxiety-related behaviour in rats in open-field tests. All these data taken together suggest that RFRPs play a role in the control of neuroendocrine and behavioural stress responses in rats.
Yuki Takayanagi - One of the best experts on this subject based on the ideXlab platform.
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effects of rfamide related peptide rfrp 1 and rfrp 3 on oxytocin release and anxiety related behaviour in rats
Journal of Neuroendocrinology, 2011Co-Authors: Maroot Kaewwongse, Yuki Takayanagi, Tatsushi OnakaAbstract:RFamide-related peptides (RFRP-1 and RFRP-3) are localised in neurones of the dorsomedial Hypothalamus in rats. The dorsomedial Hypothalamus plays an essential role in neuroendocrine and behavioural stress responses. In the present study, we examined the role of RFRP in the control of neuroendocrine and behavioural responses in rats. Stressful stimuli increased expression of Fos protein in RFRP-immunoreactive neurones of the dorsomedial Hypothalamus, suggesting that stressful stimuli activate RFRP neurones. Intracerebroventricular injection of RFRPs increased the expression of Fos protein in oxytocin neurones in the Hypothalamus and plasma concentrations of adrenocorticotrophic hormone and oxytocin. The hypothalamic paraventricular and supraoptic nuclei expressed mRNA of GPR147, the putative RFRP receptor, and application of RFRPs to isolated supraoptic nuclei facilitated oxytocin release, suggesting that RFRPs activate oxytocin neurones directly. Furthermore, the administration of RFRPs induced anxiety-related behaviour in rats in open-field tests. All these data taken together suggest that RFRPs play a role in the control of neuroendocrine and behavioural stress responses in rats.
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Effects of RFamide‐Related Peptide (RFRP)‐1 and RFRP‐3 on Oxytocin Release and Anxiety‐Related Behaviour in Rats
Journal of Neuroendocrinology, 2010Co-Authors: Maroot Kaewwongse, Yuki Takayanagi, Tatsushi OnakaAbstract:RFamide-related peptides (RFRP-1 and RFRP-3) are localised in neurones of the dorsomedial Hypothalamus in rats. The dorsomedial Hypothalamus plays an essential role in neuroendocrine and behavioural stress responses. In the present study, we examined the role of RFRP in the control of neuroendocrine and behavioural responses in rats. Stressful stimuli increased expression of Fos protein in RFRP-immunoreactive neurones of the dorsomedial Hypothalamus, suggesting that stressful stimuli activate RFRP neurones. Intracerebroventricular injection of RFRPs increased the expression of Fos protein in oxytocin neurones in the Hypothalamus and plasma concentrations of adrenocorticotrophic hormone and oxytocin. The hypothalamic paraventricular and supraoptic nuclei expressed mRNA of GPR147, the putative RFRP receptor, and application of RFRPs to isolated supraoptic nuclei facilitated oxytocin release, suggesting that RFRPs activate oxytocin neurones directly. Furthermore, the administration of RFRPs induced anxiety-related behaviour in rats in open-field tests. All these data taken together suggest that RFRPs play a role in the control of neuroendocrine and behavioural stress responses in rats.
Rolf Gruetter - One of the best experts on this subject based on the ideXlab platform.
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The rate-limiting step for glucose transport into the Hypothalamus is across the blood-Hypothalamus interface.
Journal of neurochemistry, 2020Co-Authors: Carol Poitry-yamate, Rolf GruetterAbstract:Specialized glucosensing neurons are present in the Hypothalamus, some of which neighbor the median eminence, where the blood-brain barrier has been reported leaky. A leaky blood-brain barrier implies high tissue glucose levels and obviates a role for endothelial glucose transporters in the control of hypothalamic glucose concentration, important in understanding the mechanisms of glucose sensing We therefore addressed the question of blood-brain barrier integrity at the Hypothalamus for glucose transport by examining the brain tissue-to-plasma glucose ratio in the Hypothalamus relative to other brain regions. We also examined glycogenolysis in Hypothalamus because its occurrence is unlikely in the potential absence of a Hypothalamus-blood interface. Across all regions the concentration of glucose was comparable at a given plasma glucose concentration and was a near linear function of plasma glucose. At steady-state, hypothalamic glucose concentration was similar to the extracellular hypothalamic glucose concentration reported by others. Hypothalamic glycogen fell at a rate of approximately 1.5 micromol/g/h and remained present in substantial amounts. We conclude for the Hypothalamus, a putative primary site of brain glucose sensing that: the rate-limiting step for glucose transport into brain cells is at the blood-Hypothalamus interface, and that glycogenolysis is consistent with a substantial blood -to- intracellular glucose concentration gradient.
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Neurochemical profile of the mouse Hypothalamus using in vivo1H MRS at 14.1T
NMR in Biomedicine, 2010Co-Authors: Hongxia Lei, Carol Poitry-yamate, Frédéric Preitner, Bernard Thorens, Rolf GruetterAbstract:The Hypothalamus plays an essential role in the central nervous system of mammals by among others regulating glucose homeostasis, food intake, temperature, and to some extent blood pressure. Assessments of hypothalamic metabolism using, e.g. (1)H MRS in mouse models can provide important insights into its function. To date, direct in vivo (1)H MRS measurements of Hypothalamus have not been reported. Here, we report that in vivo single voxel measurements of mouse Hypothalamus are feasible using (1)H MRS at 14.1T. Localized (1)H MR spectra from Hypothalamus were obtained unilaterally (2-2.2 microL, VOI) and bilaterally (4-4.4 microL) with a quality comparable to that of hippocampus (3-3.5 microL). Using LCModel, a neurochemical profile consisting of 21 metabolites was quantified for both Hypothalamus and hippocampus with most of the Cramér-Rao lower bounds within 20%. Relative to the hippocampus, the Hypothalamus was characterized by high gamma-aminobutryric acid and myo-inositol, and low taurine concentrations. When studying transgenic mice with no glucose transporter isoform 8 expressed, small metabolic changes were observed, yet glucose homeostasis was well maintained. We conclude that a specific neurochemical profile of mouse Hypothalamus can be measured by (1)H MRS which will allow identifying and following metabolic alterations longitudinally in the Hypothalamus of genetic modified models.
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The rate-limiting step for glucose transport into the Hypothalamus is across the blood-Hypothalamus interface
Journal of Neurochemistry, 2009Co-Authors: Carol Poitry-yamate, Rolf GruetterAbstract:Specialized glucosensing neurons are present in the Hypothalamus, some of which neighbor the median eminence, where the blood–brain barrier has been reported leaky. A leaky blood–brain barrier implies high tissue glucose levels and obviates a role for endothelial glucose transporters in the control of hypothalamic glucose concentration, important in understanding the mechanisms of glucose sensing We therefore addressed the question of blood–brain barrier integrity at the Hypothalamus for glucose transport by examining the brain tissue-to-plasma glucose ratio in the Hypothalamus relative to other brain regions. We also examined glycogenolysis in Hypothalamus because its occurrence is unlikely in the potential absence of a Hypothalamus–blood interface. Across all regions the concentration of glucose was comparable at a given plasma glucose concentration and was a near linear function of plasma glucose. At steady-state, hypothalamic glucose concentration was similar to the extracellular hypothalamic glucose concentration reported by others. Hypothalamic glycogen fell at a rate of ∼1.5 μmol/g/h and remained present in substantial amounts. We conclude for the Hypothalamus, a putative primary site of brain glucose sensing that: the rate-limiting step for glucose transport into brain cells is at the blood–Hypothalamus interface, and that glycogenolysis is consistent with a substantial blood -to- intracellular glucose concentration gradient.
Carol Poitry-yamate - One of the best experts on this subject based on the ideXlab platform.
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The rate-limiting step for glucose transport into the Hypothalamus is across the blood-Hypothalamus interface.
Journal of neurochemistry, 2020Co-Authors: Carol Poitry-yamate, Rolf GruetterAbstract:Specialized glucosensing neurons are present in the Hypothalamus, some of which neighbor the median eminence, where the blood-brain barrier has been reported leaky. A leaky blood-brain barrier implies high tissue glucose levels and obviates a role for endothelial glucose transporters in the control of hypothalamic glucose concentration, important in understanding the mechanisms of glucose sensing We therefore addressed the question of blood-brain barrier integrity at the Hypothalamus for glucose transport by examining the brain tissue-to-plasma glucose ratio in the Hypothalamus relative to other brain regions. We also examined glycogenolysis in Hypothalamus because its occurrence is unlikely in the potential absence of a Hypothalamus-blood interface. Across all regions the concentration of glucose was comparable at a given plasma glucose concentration and was a near linear function of plasma glucose. At steady-state, hypothalamic glucose concentration was similar to the extracellular hypothalamic glucose concentration reported by others. Hypothalamic glycogen fell at a rate of approximately 1.5 micromol/g/h and remained present in substantial amounts. We conclude for the Hypothalamus, a putative primary site of brain glucose sensing that: the rate-limiting step for glucose transport into brain cells is at the blood-Hypothalamus interface, and that glycogenolysis is consistent with a substantial blood -to- intracellular glucose concentration gradient.
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Neurochemical profile of the mouse Hypothalamus using in vivo1H MRS at 14.1T
NMR in Biomedicine, 2010Co-Authors: Hongxia Lei, Carol Poitry-yamate, Frédéric Preitner, Bernard Thorens, Rolf GruetterAbstract:The Hypothalamus plays an essential role in the central nervous system of mammals by among others regulating glucose homeostasis, food intake, temperature, and to some extent blood pressure. Assessments of hypothalamic metabolism using, e.g. (1)H MRS in mouse models can provide important insights into its function. To date, direct in vivo (1)H MRS measurements of Hypothalamus have not been reported. Here, we report that in vivo single voxel measurements of mouse Hypothalamus are feasible using (1)H MRS at 14.1T. Localized (1)H MR spectra from Hypothalamus were obtained unilaterally (2-2.2 microL, VOI) and bilaterally (4-4.4 microL) with a quality comparable to that of hippocampus (3-3.5 microL). Using LCModel, a neurochemical profile consisting of 21 metabolites was quantified for both Hypothalamus and hippocampus with most of the Cramér-Rao lower bounds within 20%. Relative to the hippocampus, the Hypothalamus was characterized by high gamma-aminobutryric acid and myo-inositol, and low taurine concentrations. When studying transgenic mice with no glucose transporter isoform 8 expressed, small metabolic changes were observed, yet glucose homeostasis was well maintained. We conclude that a specific neurochemical profile of mouse Hypothalamus can be measured by (1)H MRS which will allow identifying and following metabolic alterations longitudinally in the Hypothalamus of genetic modified models.
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The rate-limiting step for glucose transport into the Hypothalamus is across the blood-Hypothalamus interface
Journal of Neurochemistry, 2009Co-Authors: Carol Poitry-yamate, Rolf GruetterAbstract:Specialized glucosensing neurons are present in the Hypothalamus, some of which neighbor the median eminence, where the blood–brain barrier has been reported leaky. A leaky blood–brain barrier implies high tissue glucose levels and obviates a role for endothelial glucose transporters in the control of hypothalamic glucose concentration, important in understanding the mechanisms of glucose sensing We therefore addressed the question of blood–brain barrier integrity at the Hypothalamus for glucose transport by examining the brain tissue-to-plasma glucose ratio in the Hypothalamus relative to other brain regions. We also examined glycogenolysis in Hypothalamus because its occurrence is unlikely in the potential absence of a Hypothalamus–blood interface. Across all regions the concentration of glucose was comparable at a given plasma glucose concentration and was a near linear function of plasma glucose. At steady-state, hypothalamic glucose concentration was similar to the extracellular hypothalamic glucose concentration reported by others. Hypothalamic glycogen fell at a rate of ∼1.5 μmol/g/h and remained present in substantial amounts. We conclude for the Hypothalamus, a putative primary site of brain glucose sensing that: the rate-limiting step for glucose transport into brain cells is at the blood–Hypothalamus interface, and that glycogenolysis is consistent with a substantial blood -to- intracellular glucose concentration gradient.
