The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
Cathrin Schnell - One of the best experts on this subject based on the ideXlab platform.
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Atypical on-, off- and neutral cells in the rostral ventromedial medulla oblongata in rat.
Experimental Brain Research, 2002Co-Authors: Cathrin Schnell, Coskun Ulucan, Jens EllrichAbstract:It is generally assumed that the Response Pattern of on-, off- and neutral cells in the rostral ventromedial medulla (RVM) to noxious stimulation is independent of stimulation site. But recent studies have shown that a remarkable number of RVM neurons do not have whole-body receptive fields. These so-called atypical neurons were extracellularly recorded in lightly anaesthetized rats. The receptive fields to noxious thermal and mechanical stimulation applied to the tail, the extremities and the craniofacial region were determined in 57 RVM neurons. In 24 atypical off-cells, 12 on-cells and 21 neutral cells, the Response Pattern evoked by noxious pinch to the nose, forehead and ear most frequently differed from the Responses to noxious tail heat. The modulatory effects of intravenously administered morphine were examined in 21 cells. In contrast to the general assumption that morphine activates off-cells, inhibits on-cells and has no effect on neutral cells, in atypical RVM neurons 5 of 6 off-cells, 2 of 6 on-cells and 5 out 9 neutral cells showed a different Response Pattern to systemical administration of morphine. The results show that a RVM cell classification that is exclusively based on the behaviour to noxious tail heat can neither sufficiently predict the Response Pattern to different noxious stimuli, especially in the craniofacial region, nor reliably predict the modulatory effect of morphine in RVM neurons. The fact that the neutral cells responded in an off or on manner to noxious stimulation different from noxious tail heat and that morphine modulated activity in many neutral cells suggests that these cells are probably subtypes of on- and off-cells.
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Is the Response Pattern of on- and off-cells in the rostral ventromedial medulla to noxious stimulation independent of stimulation site?
Experimental Brain Research, 2001Co-Authors: Jens Ellrich, Coskun Ulucan, Cathrin SchnellAbstract:The classification of on- and off-cells in the rostral ventromedial medulla is based on the Response Pattern to noxious tail heat. It is generally assumed that on- and off-cells respond equally to noxious stimulation anywhere on the body surface, but so far this assumption has not been systematically examined. In the present study the effects of noxious thermal and mechanical stimuli applied to the tail, the extremities and the craniofacial region on the extracellularly recorded activity of 13 on- and 23 off-cells were investigated in lightly anesthetized rats. In 3 out of 13 on-cells and 11 out of 23 off-cells the Response Pattern evoked by noxious stimulation of the extremities or the craniofacial region differed from the Response Pattern elicited by noxious tail heat. In comparison with the Response Pattern to noxious tail heat, stimulation of the extremities or the craniofacial region reproducibly evoked opposite reactions in 2 on- and 9 off-cells and did not change neuronal activity in one on- and 2 off-cells. The results of the present study raise the question of whether the Response Pattern of on- and off-cells in the rostral ventromedial medulla can be sufficiently predicted by a classification that is exclusively based on the cellular behavior to noxious heat stimulation of the tail.
Hakan Gurdal - One of the best experts on this subject based on the ideXlab platform.
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agonist directed trafficking explaining the difference between Response Pattern of naratriptan and sumatriptan in rabbit common carotid artery
British Journal of Pharmacology, 2002Co-Authors: Demet Akin, Ongun H Onaran, Hakan GurdalAbstract:Sumatriptan or eletriptan produced vasocontraction in common carotid artery (CCA) by stimulating 5HT1B receptors (see also Akin & Gurdal, this issue). Naratriptan as a 5HT1B/D agonist, was unable to produce vasocontraction in this artery, but inhibited the vasocontractile Response induced by sumatriptan or eletriptan. All these agonists inhibited forskolin-stimulated cyclic AMP production with comparable potencies and maximal Responses. This inhibition was mediated by 5HT1B receptors: 5HT1B antagonist SB216641 (1 μM) completeley antagonized sumatriptan-, eletriptan- or naratriptan-induced cyclic AMP inhibition, but 5HT1D antagonist BRL15572 (1 μM) did not affect this Response. Naratriptan-induced stimulation of 5-HT1B receptors resulted only in adenylate cyclase inhibition, whereas stimulation of these receptors by sumatriptan or eletriptan produced vasocontraction as well. Hence, we concluded that the 5HT1B-mediated inhibition of adenylate cyclase was not a sufficient condition to couple the receptor stimulation to vasocontraction. We discussed agonist-induced trafficking as a plausible mechanism for the observed phenomenon. British Journal of Pharmacology (2002) 136, 171–176; doi:10.1038/sj.bjp.0704710
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Agonist‐directed trafficking explaining the difference between Response Pattern of naratriptan and sumatriptan in rabbit common carotid artery
British Journal of Pharmacology, 2002Co-Authors: Demet Akin, H. Ongun Onaran, Hakan GurdalAbstract:Sumatriptan or eletriptan produced vasocontraction in common carotid artery (CCA) by stimulating 5HT1B receptors (see also Akin & Gurdal, this issue). Naratriptan as a 5HT1B/D agonist, was unable to produce vasocontraction in this artery, but inhibited the vasocontractile Response induced by sumatriptan or eletriptan. All these agonists inhibited forskolin-stimulated cyclic AMP production with comparable potencies and maximal Responses. This inhibition was mediated by 5HT1B receptors: 5HT1B antagonist SB216641 (1 μM) completeley antagonized sumatriptan-, eletriptan- or naratriptan-induced cyclic AMP inhibition, but 5HT1D antagonist BRL15572 (1 μM) did not affect this Response. Naratriptan-induced stimulation of 5-HT1B receptors resulted only in adenylate cyclase inhibition, whereas stimulation of these receptors by sumatriptan or eletriptan produced vasocontraction as well. Hence, we concluded that the 5HT1B-mediated inhibition of adenylate cyclase was not a sufficient condition to couple the receptor stimulation to vasocontraction. We discussed agonist-induced trafficking as a plausible mechanism for the observed phenomenon. British Journal of Pharmacology (2002) 136, 171–176; doi:10.1038/sj.bjp.0704710
Jens Ellrich - One of the best experts on this subject based on the ideXlab platform.
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Atypical on-, off- and neutral cells in the rostral ventromedial medulla oblongata in rat.
Experimental Brain Research, 2002Co-Authors: Cathrin Schnell, Coskun Ulucan, Jens EllrichAbstract:It is generally assumed that the Response Pattern of on-, off- and neutral cells in the rostral ventromedial medulla (RVM) to noxious stimulation is independent of stimulation site. But recent studies have shown that a remarkable number of RVM neurons do not have whole-body receptive fields. These so-called atypical neurons were extracellularly recorded in lightly anaesthetized rats. The receptive fields to noxious thermal and mechanical stimulation applied to the tail, the extremities and the craniofacial region were determined in 57 RVM neurons. In 24 atypical off-cells, 12 on-cells and 21 neutral cells, the Response Pattern evoked by noxious pinch to the nose, forehead and ear most frequently differed from the Responses to noxious tail heat. The modulatory effects of intravenously administered morphine were examined in 21 cells. In contrast to the general assumption that morphine activates off-cells, inhibits on-cells and has no effect on neutral cells, in atypical RVM neurons 5 of 6 off-cells, 2 of 6 on-cells and 5 out 9 neutral cells showed a different Response Pattern to systemical administration of morphine. The results show that a RVM cell classification that is exclusively based on the behaviour to noxious tail heat can neither sufficiently predict the Response Pattern to different noxious stimuli, especially in the craniofacial region, nor reliably predict the modulatory effect of morphine in RVM neurons. The fact that the neutral cells responded in an off or on manner to noxious stimulation different from noxious tail heat and that morphine modulated activity in many neutral cells suggests that these cells are probably subtypes of on- and off-cells.
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Is the Response Pattern of on- and off-cells in the rostral ventromedial medulla to noxious stimulation independent of stimulation site?
Experimental Brain Research, 2001Co-Authors: Jens Ellrich, Coskun Ulucan, Cathrin SchnellAbstract:The classification of on- and off-cells in the rostral ventromedial medulla is based on the Response Pattern to noxious tail heat. It is generally assumed that on- and off-cells respond equally to noxious stimulation anywhere on the body surface, but so far this assumption has not been systematically examined. In the present study the effects of noxious thermal and mechanical stimuli applied to the tail, the extremities and the craniofacial region on the extracellularly recorded activity of 13 on- and 23 off-cells were investigated in lightly anesthetized rats. In 3 out of 13 on-cells and 11 out of 23 off-cells the Response Pattern evoked by noxious stimulation of the extremities or the craniofacial region differed from the Response Pattern elicited by noxious tail heat. In comparison with the Response Pattern to noxious tail heat, stimulation of the extremities or the craniofacial region reproducibly evoked opposite reactions in 2 on- and 9 off-cells and did not change neuronal activity in one on- and 2 off-cells. The results of the present study raise the question of whether the Response Pattern of on- and off-cells in the rostral ventromedial medulla can be sufficiently predicted by a classification that is exclusively based on the cellular behavior to noxious heat stimulation of the tail.
Gregor K Wenning - One of the best experts on this subject based on the ideXlab platform.
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L-dopa Response Pattern in a rat model of mild striatonigral degeneration.
PloS one, 2019Co-Authors: Christine Kaindlstorfer, Kurt A. Jellinger, Nadia Stefanova, Joanna Garcia, Florian Krismer, Máté D. Döbrössy, Georg Göbel, Roberta Granata, Gregor K WenningAbstract:Background Unresponsiveness to dopaminergic therapies is a key feature in the diagnosis of multiple system atrophy (MSA) and a major unmet need in the treatment of MSA patients caused by combined striatonigral degeneration (SND). Transgenic, alpha-synuclein animal models do not recapitulate this lack of levodopa responsiveness. In order to preclinically study interventions including striatal cell grafts, models that feature SND are required. Most of the previous studies focused on extensive nigral and striatal lesions corresponding to advanced MSA-P/SND. The aim of the current study was to replicate mild stage MSA-P/SND with L-dopa failure. Methods and results Two different striatal quinolinic acid (QA) lesions following a striatal 6-OHDA lesion replicating mild and severe MSA-P/SND, respectively, were investigated and compared to 6-OHDA lesioned animals. After the initial 6-OHDA lesion there was a significant improvement of motor performance after dopaminergic stimulation in the cylinder and stepping test (p
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l dopa Response Pattern in a rat model of mild striatonigral degeneration
PLOS ONE, 2019Co-Authors: Christine Kaindlstorfer, Kurt A. Jellinger, Nadia Stefanova, Joanna Garcia, Florian Krismer, Máté D. Döbrössy, Georg Göbel, Roberta Granata, Gregor K WenningAbstract:Background Unresponsiveness to dopaminergic therapies is a key feature in the diagnosis of multiple system atrophy (MSA) and a major unmet need in the treatment of MSA patients caused by combined striatonigral degeneration (SND). Transgenic, alpha-synuclein animal models do not recapitulate this lack of levodopa responsiveness. In order to preclinically study interventions including striatal cell grafts, models that feature SND are required. Most of the previous studies focused on extensive nigral and striatal lesions corresponding to advanced MSA-P/SND. The aim of the current study was to replicate mild stage MSA-P/SND with L-dopa failure. Methods and results Two different striatal quinolinic acid (QA) lesions following a striatal 6-OHDA lesion replicating mild and severe MSA-P/SND, respectively, were investigated and compared to 6-OHDA lesioned animals. After the initial 6-OHDA lesion there was a significant improvement of motor performance after dopaminergic stimulation in the cylinder and stepping test (p<0.001). Response to L-dopa treatment declined in both MSA-P/SND groups reflecting striatal damage of lateral motor areas in contrast to the 6-OHDA only lesioned animals (p<0.01). The remaining striatal volume correlated strongly with contralateral apomorphine induced rotation behaviour and contralateral paw use during L-dopa treatment in cylinder and stepping test (p<0.001). Conclusion Our novel L-dopa Response data suggest that L-dopa failure can be induced by restricted lateral striatal lesions combined with dopaminergic denervation. We propose that this sequential striatal double-lesion model replicates a mild stage of MSA-P/SND and is suitable to address neuro-regenerative therapies aimed at restoring dopaminergic responsiveness.
Demet Akin - One of the best experts on this subject based on the ideXlab platform.
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agonist directed trafficking explaining the difference between Response Pattern of naratriptan and sumatriptan in rabbit common carotid artery
British Journal of Pharmacology, 2002Co-Authors: Demet Akin, Ongun H Onaran, Hakan GurdalAbstract:Sumatriptan or eletriptan produced vasocontraction in common carotid artery (CCA) by stimulating 5HT1B receptors (see also Akin & Gurdal, this issue). Naratriptan as a 5HT1B/D agonist, was unable to produce vasocontraction in this artery, but inhibited the vasocontractile Response induced by sumatriptan or eletriptan. All these agonists inhibited forskolin-stimulated cyclic AMP production with comparable potencies and maximal Responses. This inhibition was mediated by 5HT1B receptors: 5HT1B antagonist SB216641 (1 μM) completeley antagonized sumatriptan-, eletriptan- or naratriptan-induced cyclic AMP inhibition, but 5HT1D antagonist BRL15572 (1 μM) did not affect this Response. Naratriptan-induced stimulation of 5-HT1B receptors resulted only in adenylate cyclase inhibition, whereas stimulation of these receptors by sumatriptan or eletriptan produced vasocontraction as well. Hence, we concluded that the 5HT1B-mediated inhibition of adenylate cyclase was not a sufficient condition to couple the receptor stimulation to vasocontraction. We discussed agonist-induced trafficking as a plausible mechanism for the observed phenomenon. British Journal of Pharmacology (2002) 136, 171–176; doi:10.1038/sj.bjp.0704710
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Agonist‐directed trafficking explaining the difference between Response Pattern of naratriptan and sumatriptan in rabbit common carotid artery
British Journal of Pharmacology, 2002Co-Authors: Demet Akin, H. Ongun Onaran, Hakan GurdalAbstract:Sumatriptan or eletriptan produced vasocontraction in common carotid artery (CCA) by stimulating 5HT1B receptors (see also Akin & Gurdal, this issue). Naratriptan as a 5HT1B/D agonist, was unable to produce vasocontraction in this artery, but inhibited the vasocontractile Response induced by sumatriptan or eletriptan. All these agonists inhibited forskolin-stimulated cyclic AMP production with comparable potencies and maximal Responses. This inhibition was mediated by 5HT1B receptors: 5HT1B antagonist SB216641 (1 μM) completeley antagonized sumatriptan-, eletriptan- or naratriptan-induced cyclic AMP inhibition, but 5HT1D antagonist BRL15572 (1 μM) did not affect this Response. Naratriptan-induced stimulation of 5-HT1B receptors resulted only in adenylate cyclase inhibition, whereas stimulation of these receptors by sumatriptan or eletriptan produced vasocontraction as well. Hence, we concluded that the 5HT1B-mediated inhibition of adenylate cyclase was not a sufficient condition to couple the receptor stimulation to vasocontraction. We discussed agonist-induced trafficking as a plausible mechanism for the observed phenomenon. British Journal of Pharmacology (2002) 136, 171–176; doi:10.1038/sj.bjp.0704710
