The Experts below are selected from a list of 240 Experts worldwide ranked by ideXlab platform
Katia Gysling - One of the best experts on this subject based on the ideXlab platform.
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Regulation of norepinephrine release from the rat bed nucleus of the Stria Terminalis: In vivo microdialysis studies
Journal of neuroscience research, 1997Co-Authors: María Inés Forray, Gonzalo Bustos, Katia GyslingAbstract:The microdialysis technique was used to study the in vivo extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis. A basal level of 2.34 ± 0.25 fmol/μl of norepinephrine was observed. Desipramine (2 and 10 μM), a norepinephrine uptake blocker, significantly increased extracellular levels of norepinephrine. Reversed perfusion with high potassium in the presence of 2 μM desipramine induced the release of norepinephrine. Instead, in the presence of 10 μM desipramine, a significant decrease in the induced release of norepinephrine was observed. Clonidine, an α2-adrenergic agonist, significantly decreased basal extracellular levels of norepinephrine and the K+-induced release of norepinephrine. In contrast, yohimbine and RX821002, two α2-adrenergic antagonists, significantly increased basal extracellular levels of norepinephrine but not the release of norepinephrine induced by 70 mM K+. Perfusion of tetrodotoxin through the probe located in the bed nucleus of the Stria Terminalis significantly decreased both the basal extracellular level and the K+-induced release of norepinephrine. Furthermore, perfusion of tetrodotoxin through a microdialysis probe implanted in the medial forebrain bundle also decreased basal extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis. The results show that in vivo there is a significant noradrenergic tonic activity in the bed nucleus of the Stria Terminalis. This tonic activity depends on the impulse flow through medial forebrain bundle nerve fibers. Under these conditions, extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis are regulated by the magnitude of norepinephrine uptake and by presynaptic α2-adrenergic receptors. J. Neurosci. Res. 50:1040–1046, 1997. © 1997 Wiley-Liss, Inc.
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Regulation of endogenous noradrenaline release from the bed nucleus of Stria Terminalis
Biochemical pharmacology, 1995Co-Authors: María Inés Forray, María Estela Andrés, Gonzalo Bustos, Katia GyslingAbstract:The bed nucleus of Stria Terminalis (BNST) contains the highest concentration of noradrenaline (NA) in the brain. Minislices of the ventral portion of the bed nucleus of Stria Terminalis (vBNST) were used to study the release of endogenous NA. High K+ induced a Ca(2+)-dependent and reserpine-sensitive release of NA. Clonidine (1 microM), an alpha 2-noradrenergic receptor agonist, significantly decreased K(+)-induced release of NA, whereas yohimbine (1 microM), an alpha 2-noradrenergic antagonist, increased this release. N-Methyl-D-aspartate (NMDA), a specific agonist of NMDA-type glutamate receptors, evoked the release of NA from vBNST minislices. In the presence of D-serine (10 microM), an agonist at the glycine site associated with the NMDA receptor, the NMDA effect was significantly higher. Glycine (1 microM) also increased NA release evoked by NMDA. However, glycine exhibited a significant effect by itself, suggesting the existence of strychnine-sensitive glycine receptors in vBNST. Endogenous NA release induced by 40 mM K+ and NMDA was not additive. Thus, vBNST minislices seem to be a good model to study the release of endogenous NA in the CNS. Such NA release in the vBNST is regulated by alpha 2-noradrenergic receptors and by glutamate through NMDA receptors.
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Release of endogenous catecholamines from the Striatum and bed nucleus of Stria Terminalis evoked by potassium and N‐methyl‐D‐aspartate: In vitro microdialysis studies
Journal of neuroscience research, 1995Co-Authors: E. Aliaga, Gonzalo Bustos, Katia GyslingAbstract:Induced release of endogenous dopamine and noradrenaline from coronal slices containing the Striatum and the bed nucleus of the Stria Terminalis, respectively, was studied by means of in vitro microdialysis. A Ca+2-dependent and reserpine-sensitive K+-induced release of catecholamines was detected in both nuclei. We confirmed that N-methyl D-aspartate (2.5 and 5.0 mM in the dialysis perfusion solution) induces the release of dopamine from the Striatum, and this effect was blocked by prior dialysis perfusion with 500 μM MK-801, a noncompetitive N-methyl-D-aspartate receptor antagonist. Infusion of N-methyl-D-aspartate (1–10 mM) or glutamate through the dialysis probe did not produce any detectable modification in the extracellular levels of noradrenaline in the bed nucleus of the Stria Terminalis. In addition, perfusion with D-serine (100 μM)alone or in the presence of desipramine (10 μM) resulted in a slight increase in extracellular noradrenaline in the bed nucleus of the Stria Terminalis. However, N-methyl-D-aspartate in the presence of D-serine and desipramine produced a marked increase in extracellular noradrenaline from the bed nucleus of the Stria Terminalis. These results indicate that N-methyl-D-aspartate receptors might regulate the release of noradrenaline from the bed nucleus of the Stria Terminalis as is the case of dopamine release in the Striatum. The in vitro microdialysis seems to be a suitable complement to the in vivo microdialysis for the study of catecholamine release in discrete regions of the central nervous system and its local regulation by excitatory amino acid receptors. © 1995 Wiley-Liss, Inc.
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Studies of cholecystokinin in the rat bed nucleus of Stria Terminalis
Biochemical Pharmacology, 1993Co-Authors: María Estela Andrés, María Inés Forray, Carmen Gloria Barría, Katia GyslingAbstract:The release of cholecystokinin from the dorsal and ventral region of the rat bed nucleus of Stria Terminalis was studied. Minislices from both regions were superfused with Krebs-Ringer-phosphate, and the cholecystokinin released into the physiological medium was concentrated previous to radioimmunoassay determination. For this purpose, cholecystokinin was adsorbed onto a C18 reverse-phase column and eluted with acetonitrile. Cholecystokinin standards (10-50 pg) were subjected to the above procedure, which allowed a 20- to 50-fold concentration of the peptide with an 80% recovery. Potassium-induced release of cholecystokinin from minislices of dorsal and ventral regions of the bed nucleus of Stria Terminalis was measured successfully using the above procedure to concentrate the peptide. Lesion of the Stria Terminalis, a fiber tract originating in the amygdala, provoked a significant decrease in cholecystokinin levels in the ventral region of the bed nucleus of Strial Terminalis. Thus, cholecystokinin released from minislices of the ventral region of the Stria Terminalis may be of amygdaloid origin.
María Inés Forray - One of the best experts on this subject based on the ideXlab platform.
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Regulation of norepinephrine release from the rat bed nucleus of the Stria Terminalis: In vivo microdialysis studies
Journal of neuroscience research, 1997Co-Authors: María Inés Forray, Gonzalo Bustos, Katia GyslingAbstract:The microdialysis technique was used to study the in vivo extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis. A basal level of 2.34 ± 0.25 fmol/μl of norepinephrine was observed. Desipramine (2 and 10 μM), a norepinephrine uptake blocker, significantly increased extracellular levels of norepinephrine. Reversed perfusion with high potassium in the presence of 2 μM desipramine induced the release of norepinephrine. Instead, in the presence of 10 μM desipramine, a significant decrease in the induced release of norepinephrine was observed. Clonidine, an α2-adrenergic agonist, significantly decreased basal extracellular levels of norepinephrine and the K+-induced release of norepinephrine. In contrast, yohimbine and RX821002, two α2-adrenergic antagonists, significantly increased basal extracellular levels of norepinephrine but not the release of norepinephrine induced by 70 mM K+. Perfusion of tetrodotoxin through the probe located in the bed nucleus of the Stria Terminalis significantly decreased both the basal extracellular level and the K+-induced release of norepinephrine. Furthermore, perfusion of tetrodotoxin through a microdialysis probe implanted in the medial forebrain bundle also decreased basal extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis. The results show that in vivo there is a significant noradrenergic tonic activity in the bed nucleus of the Stria Terminalis. This tonic activity depends on the impulse flow through medial forebrain bundle nerve fibers. Under these conditions, extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis are regulated by the magnitude of norepinephrine uptake and by presynaptic α2-adrenergic receptors. J. Neurosci. Res. 50:1040–1046, 1997. © 1997 Wiley-Liss, Inc.
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Regulation of endogenous noradrenaline release from the bed nucleus of Stria Terminalis
Biochemical pharmacology, 1995Co-Authors: María Inés Forray, María Estela Andrés, Gonzalo Bustos, Katia GyslingAbstract:The bed nucleus of Stria Terminalis (BNST) contains the highest concentration of noradrenaline (NA) in the brain. Minislices of the ventral portion of the bed nucleus of Stria Terminalis (vBNST) were used to study the release of endogenous NA. High K+ induced a Ca(2+)-dependent and reserpine-sensitive release of NA. Clonidine (1 microM), an alpha 2-noradrenergic receptor agonist, significantly decreased K(+)-induced release of NA, whereas yohimbine (1 microM), an alpha 2-noradrenergic antagonist, increased this release. N-Methyl-D-aspartate (NMDA), a specific agonist of NMDA-type glutamate receptors, evoked the release of NA from vBNST minislices. In the presence of D-serine (10 microM), an agonist at the glycine site associated with the NMDA receptor, the NMDA effect was significantly higher. Glycine (1 microM) also increased NA release evoked by NMDA. However, glycine exhibited a significant effect by itself, suggesting the existence of strychnine-sensitive glycine receptors in vBNST. Endogenous NA release induced by 40 mM K+ and NMDA was not additive. Thus, vBNST minislices seem to be a good model to study the release of endogenous NA in the CNS. Such NA release in the vBNST is regulated by alpha 2-noradrenergic receptors and by glutamate through NMDA receptors.
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Studies of cholecystokinin in the rat bed nucleus of Stria Terminalis
Biochemical Pharmacology, 1993Co-Authors: María Estela Andrés, María Inés Forray, Carmen Gloria Barría, Katia GyslingAbstract:The release of cholecystokinin from the dorsal and ventral region of the rat bed nucleus of Stria Terminalis was studied. Minislices from both regions were superfused with Krebs-Ringer-phosphate, and the cholecystokinin released into the physiological medium was concentrated previous to radioimmunoassay determination. For this purpose, cholecystokinin was adsorbed onto a C18 reverse-phase column and eluted with acetonitrile. Cholecystokinin standards (10-50 pg) were subjected to the above procedure, which allowed a 20- to 50-fold concentration of the peptide with an 80% recovery. Potassium-induced release of cholecystokinin from minislices of dorsal and ventral regions of the bed nucleus of Stria Terminalis was measured successfully using the above procedure to concentrate the peptide. Lesion of the Stria Terminalis, a fiber tract originating in the amygdala, provoked a significant decrease in cholecystokinin levels in the ventral region of the bed nucleus of Strial Terminalis. Thus, cholecystokinin released from minislices of the ventral region of the Stria Terminalis may be of amygdaloid origin.
Danny G. Winder - One of the best experts on this subject based on the ideXlab platform.
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Noradrenergic control of the bed nucleus of the Stria Terminalis in stress and reward
Neuropharmacology, 2013Co-Authors: Stephanie A. Flavin, Danny G. WinderAbstract:The bed nucleus of the Stria Terminalis (BNST) is a group of inter-connected subnuclei that play critical roles in stress-reward interactions. An interesting feature of this brain region is the massive noradrenergic input that it receives. Important roles for norepinephrine in this region have been documented in a number of stress and reward related behaviors. This work has been paralleled over the last several years by efforts to understand the actions of norepinephrine on neuronal function in the region. In this review, we will summarize the current state of these research areas.
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α1-Adrenergic Receptor-Induced Heterosynaptic Long-Term Depression in the Bed Nucleus of the Stria Terminalis Is Disrupted in Mouse Models of Affective Disorders
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2007Co-Authors: Zoe A. Mcelligott, Danny G. WinderAbstract:α 1 -Adrenergic Receptor-Induced Heterosynaptic Long-Term Depression in the Bed Nucleus of the Stria Terminalis Is Disrupted in Mouse Models of Affective Disorders
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Norepinephrine modulates glutamatergic transmission in the bed nucleus of the Stria Terminalis.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2004Co-Authors: Regula E. Egli, Thomas L. Kash, Kevin Choo, Valentina Savchenko, Robert T. Matthews, Randy D. Blakely, Danny G. WinderAbstract:Norepinephrine Modulates Glutamatergic Transmission in the Bed Nucleus of the Stria Terminalis
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Dorsal and Ventral Distribution of Excitable and Synaptic Properties of Neurons of the Bed Nucleus of the Stria Terminalis
Journal of neurophysiology, 2003Co-Authors: Regula E. Egli, Danny G. WinderAbstract:The bed nucleus of the Stria Terminalis (BNST) is a structure uniquely positioned to integrate stress information and regulate both stress and reward systems. Consistent with this arrangement, evid...
Gonzalo Bustos - One of the best experts on this subject based on the ideXlab platform.
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Regulation of norepinephrine release from the rat bed nucleus of the Stria Terminalis: In vivo microdialysis studies
Journal of neuroscience research, 1997Co-Authors: María Inés Forray, Gonzalo Bustos, Katia GyslingAbstract:The microdialysis technique was used to study the in vivo extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis. A basal level of 2.34 ± 0.25 fmol/μl of norepinephrine was observed. Desipramine (2 and 10 μM), a norepinephrine uptake blocker, significantly increased extracellular levels of norepinephrine. Reversed perfusion with high potassium in the presence of 2 μM desipramine induced the release of norepinephrine. Instead, in the presence of 10 μM desipramine, a significant decrease in the induced release of norepinephrine was observed. Clonidine, an α2-adrenergic agonist, significantly decreased basal extracellular levels of norepinephrine and the K+-induced release of norepinephrine. In contrast, yohimbine and RX821002, two α2-adrenergic antagonists, significantly increased basal extracellular levels of norepinephrine but not the release of norepinephrine induced by 70 mM K+. Perfusion of tetrodotoxin through the probe located in the bed nucleus of the Stria Terminalis significantly decreased both the basal extracellular level and the K+-induced release of norepinephrine. Furthermore, perfusion of tetrodotoxin through a microdialysis probe implanted in the medial forebrain bundle also decreased basal extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis. The results show that in vivo there is a significant noradrenergic tonic activity in the bed nucleus of the Stria Terminalis. This tonic activity depends on the impulse flow through medial forebrain bundle nerve fibers. Under these conditions, extracellular levels of norepinephrine in the bed nucleus of the Stria Terminalis are regulated by the magnitude of norepinephrine uptake and by presynaptic α2-adrenergic receptors. J. Neurosci. Res. 50:1040–1046, 1997. © 1997 Wiley-Liss, Inc.
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Regulation of endogenous noradrenaline release from the bed nucleus of Stria Terminalis
Biochemical pharmacology, 1995Co-Authors: María Inés Forray, María Estela Andrés, Gonzalo Bustos, Katia GyslingAbstract:The bed nucleus of Stria Terminalis (BNST) contains the highest concentration of noradrenaline (NA) in the brain. Minislices of the ventral portion of the bed nucleus of Stria Terminalis (vBNST) were used to study the release of endogenous NA. High K+ induced a Ca(2+)-dependent and reserpine-sensitive release of NA. Clonidine (1 microM), an alpha 2-noradrenergic receptor agonist, significantly decreased K(+)-induced release of NA, whereas yohimbine (1 microM), an alpha 2-noradrenergic antagonist, increased this release. N-Methyl-D-aspartate (NMDA), a specific agonist of NMDA-type glutamate receptors, evoked the release of NA from vBNST minislices. In the presence of D-serine (10 microM), an agonist at the glycine site associated with the NMDA receptor, the NMDA effect was significantly higher. Glycine (1 microM) also increased NA release evoked by NMDA. However, glycine exhibited a significant effect by itself, suggesting the existence of strychnine-sensitive glycine receptors in vBNST. Endogenous NA release induced by 40 mM K+ and NMDA was not additive. Thus, vBNST minislices seem to be a good model to study the release of endogenous NA in the CNS. Such NA release in the vBNST is regulated by alpha 2-noradrenergic receptors and by glutamate through NMDA receptors.
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Release of endogenous catecholamines from the Striatum and bed nucleus of Stria Terminalis evoked by potassium and N‐methyl‐D‐aspartate: In vitro microdialysis studies
Journal of neuroscience research, 1995Co-Authors: E. Aliaga, Gonzalo Bustos, Katia GyslingAbstract:Induced release of endogenous dopamine and noradrenaline from coronal slices containing the Striatum and the bed nucleus of the Stria Terminalis, respectively, was studied by means of in vitro microdialysis. A Ca+2-dependent and reserpine-sensitive K+-induced release of catecholamines was detected in both nuclei. We confirmed that N-methyl D-aspartate (2.5 and 5.0 mM in the dialysis perfusion solution) induces the release of dopamine from the Striatum, and this effect was blocked by prior dialysis perfusion with 500 μM MK-801, a noncompetitive N-methyl-D-aspartate receptor antagonist. Infusion of N-methyl-D-aspartate (1–10 mM) or glutamate through the dialysis probe did not produce any detectable modification in the extracellular levels of noradrenaline in the bed nucleus of the Stria Terminalis. In addition, perfusion with D-serine (100 μM)alone or in the presence of desipramine (10 μM) resulted in a slight increase in extracellular noradrenaline in the bed nucleus of the Stria Terminalis. However, N-methyl-D-aspartate in the presence of D-serine and desipramine produced a marked increase in extracellular noradrenaline from the bed nucleus of the Stria Terminalis. These results indicate that N-methyl-D-aspartate receptors might regulate the release of noradrenaline from the bed nucleus of the Stria Terminalis as is the case of dopamine release in the Striatum. The in vitro microdialysis seems to be a suitable complement to the in vivo microdialysis for the study of catecholamine release in discrete regions of the central nervous system and its local regulation by excitatory amino acid receptors. © 1995 Wiley-Liss, Inc.
Bruce M. King - One of the best experts on this subject based on the ideXlab platform.
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Role of the Stria Terminalis in food intake and body weight in rats.
Physiology & behavior, 2006Co-Authors: Bethany L. Rollins, Samuel G. Stines, Bruce M. KingAbstract:Previous studies have shown that lesions of the posterodorsal amygdala result in hyperphagia and obesity in female rats. In the present study, lesions of the Stria Terminalis at its most dorsal point (before it separates into dorsal and ventral components) also resulted in hyperphagia and excessive weight gains in female rats compared to female rats with sham lesions, as did coronal knife cuts anterior to the ventromedial hypothalamus. Identical lesions and knife cuts did not elevate food intake or weight gains in male rats compared to male control animals. Examination of the anterograde degeneration with the amino-cupric-silver method in the brains of two female rats with hypothalamic knife cuts revealed degenerating terminals in the capsule of the ventromedial hypothalamus and in the premammillary nuclei, two classic indicators of damage to the dorsal component of the Stria Terminalis. No degenerating axon terminals were observed in the paraventricular nucleus. Differences from previous studies that used male rats were attributed to a sex difference for the effects of amygdaloid and ventromedial hypothalamic lesions. It is proposed that the posterodorsal amygdala, dorsal component of the Stria Terminalis, and ventromedial hypothalamus are part of an inhibitory pathway in the regulation of feeding behavior.
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Excessive weight gains in female rats with transections of the Stria Terminalis
Physiology & Behavior, 2003Co-Authors: Bruce M. King, Bethany L. Rollins, Scott J. Grundmann, Leslie G. OlivierAbstract:Recent studies have demonstrated hyperphagia and excessive weight gains in female rats with small lesions in the most posterodorsal aspects of the medial amygdala. In the present study, similar results were observed in female rats with bilateral transections of the Stria Terminalis just as it exits the amygdala to begin its dorsal ascent (mean weight gain of 35.9 g/20 days compared to 0.1 g/20 days for operated control animals). Cellular damage caused by the retractable wire knife was limited to the caudal globus pallidus. The results of previous studies that failed to observe weight gains after Stria Terminalis transections were attributed to the use of male animals. The present results, along with the pattern of anterograde degeneration that is observed after obesity-inducing amygdaloid lesions, suggest a medial amygdala-Stria Terminalis-medial hypothalamic pathway in the regulation of food intake and body weight, but other possibilities are considered.
