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Inga D Neumann - One of the best experts on this subject based on the ideXlab platform.
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release of oxytocin in the rat central amygdala modulates stress coping behavior and the release of Excitatory Amino Acids
Neuropsychopharmacology, 2005Co-Authors: Karl Ebner, Oliver J Bosch, Simone A Kromer, Nicolas Singewald, Inga D NeumannAbstract:Release of Oxytocin in the Rat Central Amygdala Modulates Stress-Coping Behavior and the Release of Excitatory Amino Acids
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release of oxytocin in the rat central amygdala modulates stress coping behavior and the release of Excitatory Amino Acids
Neuropsychopharmacology, 2005Co-Authors: Karl Ebner, Oliver J Bosch, Simone A Kromer, Nicolas Singewald, Inga D NeumannAbstract:Previous experiments have indicated that the release of oxytocin (OXT) occurs in various hypothalamic and extrahypothalamic brain areas. In the present study, we investigated in male rats whether swim stress triggers the release of OXT in the central amygdala (CeA), a key area in processing emotions and stress responses. Further, we examined the physiological significance of OXT released within the CeA for behavioral responses during forced swimming as well as effects on the local release of selected Amino Acids including glutamate, aspartate, arginine, taurine, and GABA, which are thought to modulate processing of emotions. Exposure to a 10-min forced swimming session caused a significant increase in OXT release (200%, p<0.01) within, but not outside, the CeA as monitored by microdialysis. Administration of the OXT receptor antagonist des-Gly-NH2d(CH2)5(Tyr(Me)2Thr4)OVT via inverse microdialysis into the amygdala before and during exposure to swimming reduced the floating time by 55% (p<0.05) and increased the swimming time by 29% (p<0.05) indicative of a more active stress-coping strategy. Simultaneously, local administration of the OXT receptor antagonist caused a significant increase in the stress-induced release of the Excitatory Amino Acids glutamate and aspartate, whereas the basal release of these Amino Acids remained unchanged. Taken together, these findings demonstrate a significant activation of the oxytocinergic system in the CeA in response to swim stress. Furthermore, our data indicate that OXT receptor-mediated mechanisms within the amygdala are involved in the generation of passive stress-coping strategies, which might be mediated at least in part via its inhibitory influence on the local release of Excitatory Amino Acids during stress.
Karl Ebner - One of the best experts on this subject based on the ideXlab platform.
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release of oxytocin in the rat central amygdala modulates stress coping behavior and the release of Excitatory Amino Acids
Neuropsychopharmacology, 2005Co-Authors: Karl Ebner, Oliver J Bosch, Simone A Kromer, Nicolas Singewald, Inga D NeumannAbstract:Release of Oxytocin in the Rat Central Amygdala Modulates Stress-Coping Behavior and the Release of Excitatory Amino Acids
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release of oxytocin in the rat central amygdala modulates stress coping behavior and the release of Excitatory Amino Acids
Neuropsychopharmacology, 2005Co-Authors: Karl Ebner, Oliver J Bosch, Simone A Kromer, Nicolas Singewald, Inga D NeumannAbstract:Previous experiments have indicated that the release of oxytocin (OXT) occurs in various hypothalamic and extrahypothalamic brain areas. In the present study, we investigated in male rats whether swim stress triggers the release of OXT in the central amygdala (CeA), a key area in processing emotions and stress responses. Further, we examined the physiological significance of OXT released within the CeA for behavioral responses during forced swimming as well as effects on the local release of selected Amino Acids including glutamate, aspartate, arginine, taurine, and GABA, which are thought to modulate processing of emotions. Exposure to a 10-min forced swimming session caused a significant increase in OXT release (200%, p<0.01) within, but not outside, the CeA as monitored by microdialysis. Administration of the OXT receptor antagonist des-Gly-NH2d(CH2)5(Tyr(Me)2Thr4)OVT via inverse microdialysis into the amygdala before and during exposure to swimming reduced the floating time by 55% (p<0.05) and increased the swimming time by 29% (p<0.05) indicative of a more active stress-coping strategy. Simultaneously, local administration of the OXT receptor antagonist caused a significant increase in the stress-induced release of the Excitatory Amino Acids glutamate and aspartate, whereas the basal release of these Amino Acids remained unchanged. Taken together, these findings demonstrate a significant activation of the oxytocinergic system in the CeA in response to swim stress. Furthermore, our data indicate that OXT receptor-mediated mechanisms within the amygdala are involved in the generation of passive stress-coping strategies, which might be mediated at least in part via its inhibitory influence on the local release of Excitatory Amino Acids during stress.
Nicholas T Kouchoukos - One of the best experts on this subject based on the ideXlab platform.
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update 2001 dextrorphan inhibits the release of Excitatory Amino Acids during spinal cord ischemia
The Annals of Thoracic Surgery, 2001Co-Authors: Chris K Rokkas, Nicholas T KouchoukosAbstract:Abstract As Originally Published in 1994: by Chris K. Rokkas, MD, Loring R. Helfrich, Jr, BS, Douglas C. Lobner, PhD, Dennis W. Choi, MD, PhD, and Nicholas T. Kouchoukos, MD. Division of Cardiothoracic Surgery, Department of Surgery, and Department of Neurology, Washington University School of Medicine, St. Louis, Missouri. The release of Excitatory Amino Acids, particularly glutamate, into the extracellular space plays a causal role in irreversible neuronal damage after central nervous system ischemia. Dextrorphan, a noncompetitive N -methyl-d-aspartate receptor antagonist, has been shown to provide significant protection against cerebral damage after focal ischemia. We investigated the changes in extracellular neurotransmitter Amino acid concentrations using in vivo microdialysis in a swine model of spinal cord ischemia. After lumbar laminectomies were performed, all animals underwent left thoracotomy and right atrial–femoral cardiopulmonary bypass with additional aortic arch perfusion. Microdialysis probes were then inserted stereotactically into the lumbar spinal cord. The probes were perfused with artificial cerebrospinal fluid and 15-minute samples were assayed using high-performance liquid chromatography. Group 1 animals (n = 9) underwent aortic clamping distal to the left subclavian and proximal to the renal arteries for 60 minutes. Group 2 animals (n = 7) were treated with dextrorphan before application of aortic clamps, and during aortic occlusion and reperfusion. Five Amino Acids were studied, including two Excitatory neurotransmitters (glutamate and aspartate) and three putative inhibitory neurotransmitters (glycine, γ-Amino-butyric acid, and serine). Somatosensory-evoked potentials and motor-evoked potentials were monitored. Glutamate exhibited a threefold increase in extracellular concentration during normothermic ischemia compared with baseline values and remained elevated until 60 minutes after reperfusion. In animals treated with dextrorphan, glutamate concentrations decreased to one-third of baseline levels before aortic clamping and remained unchanged during ischemia and reperfusion. There was early loss of somato-sensory-evoked potentials and motor-evoked potentials during ischemia in group 1 animals. Group 2 animals demonstrated unchanged somatosensory-evoked potentials and only mild (20%) decrease in the amplitude of motor-evoked potentials. These results suggest that dextrorphan inhibits the release of Excitatory Amino Acids in the spinal cord during ischemia and, therefore, may have a protective effect on spinal cord function during operations on the thoracoabdominal aorta.
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dextrorphan inhibits the release of Excitatory Amino Acids during spinal cord ischemia
The Annals of Thoracic Surgery, 1994Co-Authors: Chris K Rokkas, Loring R Helfrich, Douglas C Lobner, Dennis W Choi, Nicholas T KouchoukosAbstract:The release of Excitatory Amino Acids, particularly glutamate, into the extracellular space plays a causal role in irreversible neuronal damage after central nervous system ischemia. Dextrorphan, a noncompetitive N-methylD-aspartate receptor antagonist, has been shown to provide significant protection against cerebral damage after focal ischemia. We investigated the changes in extracellular neurotransmitter Amino acid concentrations using in vivo microdialysis in a swine model of spinal cord ischemia. After lumbar laminectomies were performed, all animals underwent left thoracotomy and right atrial‐ femoral cardiopulmonary bypass with additional aortic arch perfusion. Microdialysis probes were then inserted stereotactically into the lumbar spinal cord. The probes were perfused with artificial cerebrospinal fluid and 15-minute samples were assayed using high-performance liquid chromatography. Group 1 animals (n 5 9) underwent aortic clamping distal to the left subclavian and proximal to the renal arteries for 60 minutes. Group 2 animals (n 5 7) were treated with dextrorphan before application of aortic clamps, and during aortic occlusion and reperfusion. Five Amino Acids were studied, including two Excitatory neurotransmitters (glutamate and aspartate) and three putative inhibitory neurotransmitters (glycine, g-Amino-butyric acid, and serine). Somatosensory-evoked potentials and motor-evoked potentials were monitored. Glutamate exhibited a threefold increase in extracellular concentration during normothermic ischemia compared with baseline values and remained elevated until 60 minutes after reperfusion. In animals treated with dextrorphan, glutamate concentrations decreased to one-third of baseline levels before aortic clamping and remained unchanged during ischemia and reperfusion. There was early loss of somatosensory-evoked potentials and motor-evoked potentials during ischemia in group 1 animals. Group 2 animals demonstrated unchanged somatosensory-evoked potentials and only mild (20%) decrease in the amplitude of motor-evoked potentials. These results suggest that dextrorphan inhibits the release of Excitatory Amino Acids in the spinal cord during ischemia and, therefore, may have a protective effect on spinal cord function during operations on the thoracoabdominal aorta. (Ann Thorac Surg 1994;58:312‐20)
Nicolas Singewald - One of the best experts on this subject based on the ideXlab platform.
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release of oxytocin in the rat central amygdala modulates stress coping behavior and the release of Excitatory Amino Acids
Neuropsychopharmacology, 2005Co-Authors: Karl Ebner, Oliver J Bosch, Simone A Kromer, Nicolas Singewald, Inga D NeumannAbstract:Release of Oxytocin in the Rat Central Amygdala Modulates Stress-Coping Behavior and the Release of Excitatory Amino Acids
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release of oxytocin in the rat central amygdala modulates stress coping behavior and the release of Excitatory Amino Acids
Neuropsychopharmacology, 2005Co-Authors: Karl Ebner, Oliver J Bosch, Simone A Kromer, Nicolas Singewald, Inga D NeumannAbstract:Previous experiments have indicated that the release of oxytocin (OXT) occurs in various hypothalamic and extrahypothalamic brain areas. In the present study, we investigated in male rats whether swim stress triggers the release of OXT in the central amygdala (CeA), a key area in processing emotions and stress responses. Further, we examined the physiological significance of OXT released within the CeA for behavioral responses during forced swimming as well as effects on the local release of selected Amino Acids including glutamate, aspartate, arginine, taurine, and GABA, which are thought to modulate processing of emotions. Exposure to a 10-min forced swimming session caused a significant increase in OXT release (200%, p<0.01) within, but not outside, the CeA as monitored by microdialysis. Administration of the OXT receptor antagonist des-Gly-NH2d(CH2)5(Tyr(Me)2Thr4)OVT via inverse microdialysis into the amygdala before and during exposure to swimming reduced the floating time by 55% (p<0.05) and increased the swimming time by 29% (p<0.05) indicative of a more active stress-coping strategy. Simultaneously, local administration of the OXT receptor antagonist caused a significant increase in the stress-induced release of the Excitatory Amino Acids glutamate and aspartate, whereas the basal release of these Amino Acids remained unchanged. Taken together, these findings demonstrate a significant activation of the oxytocinergic system in the CeA in response to swim stress. Furthermore, our data indicate that OXT receptor-mediated mechanisms within the amygdala are involved in the generation of passive stress-coping strategies, which might be mediated at least in part via its inhibitory influence on the local release of Excitatory Amino Acids during stress.
Simone A Kromer - One of the best experts on this subject based on the ideXlab platform.
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release of oxytocin in the rat central amygdala modulates stress coping behavior and the release of Excitatory Amino Acids
Neuropsychopharmacology, 2005Co-Authors: Karl Ebner, Oliver J Bosch, Simone A Kromer, Nicolas Singewald, Inga D NeumannAbstract:Release of Oxytocin in the Rat Central Amygdala Modulates Stress-Coping Behavior and the Release of Excitatory Amino Acids
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release of oxytocin in the rat central amygdala modulates stress coping behavior and the release of Excitatory Amino Acids
Neuropsychopharmacology, 2005Co-Authors: Karl Ebner, Oliver J Bosch, Simone A Kromer, Nicolas Singewald, Inga D NeumannAbstract:Previous experiments have indicated that the release of oxytocin (OXT) occurs in various hypothalamic and extrahypothalamic brain areas. In the present study, we investigated in male rats whether swim stress triggers the release of OXT in the central amygdala (CeA), a key area in processing emotions and stress responses. Further, we examined the physiological significance of OXT released within the CeA for behavioral responses during forced swimming as well as effects on the local release of selected Amino Acids including glutamate, aspartate, arginine, taurine, and GABA, which are thought to modulate processing of emotions. Exposure to a 10-min forced swimming session caused a significant increase in OXT release (200%, p<0.01) within, but not outside, the CeA as monitored by microdialysis. Administration of the OXT receptor antagonist des-Gly-NH2d(CH2)5(Tyr(Me)2Thr4)OVT via inverse microdialysis into the amygdala before and during exposure to swimming reduced the floating time by 55% (p<0.05) and increased the swimming time by 29% (p<0.05) indicative of a more active stress-coping strategy. Simultaneously, local administration of the OXT receptor antagonist caused a significant increase in the stress-induced release of the Excitatory Amino Acids glutamate and aspartate, whereas the basal release of these Amino Acids remained unchanged. Taken together, these findings demonstrate a significant activation of the oxytocinergic system in the CeA in response to swim stress. Furthermore, our data indicate that OXT receptor-mediated mechanisms within the amygdala are involved in the generation of passive stress-coping strategies, which might be mediated at least in part via its inhibitory influence on the local release of Excitatory Amino Acids during stress.
