The Experts below are selected from a list of 10554 Experts worldwide ranked by ideXlab platform
Y S Chan - One of the best experts on this subject based on the ideXlab platform.
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5 ht1a receptor mediated attenuation of synaptic transmission in rat medial vestibular nucleus impacts on vestibular related motor function
The Journal of Physiology, 2020Co-Authors: Lei Han, Puiyi Kwan, Oscar Wingho Chua, Daisy K Y Shum, Y S ChanAbstract:KEY POINTS Chemogenetic activation of medial vestibular nucleus-projecting 5-HT neurons resulted in deficits in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. The 5-HT1A receptor mediates the vestibular-related behavioural effects of 5-HT in the vestibular nucleus. 5-HT1A receptor activation attenuated evoked excitatory postsynaptic currents and evoked inhibitory postsynaptic currents via a Presynaptic Mechanism in the vestibular nucleus. ABSTRACT While the anxiolytic effects of serotonergic neuromodulation are well studied, its role in sensorimotor coordination and postural control is unclear. In this study, we show that an increase of serotonin (5-hydroxytryptamine, 5-HT) at the medial vestibular nucleus (MVN), a brainstem centre for vestibulospinal coordination, by either direct cannula administration or chemogenetic stimulation of MVN-projecting serotonergic neurons, adversely affected performance of rats in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. Application of the 5-HT1 and 5-HT7 receptor co-agonist 8-hydroxy-2-(di-n-propylamino) tetralin recapitulated the effect of 5-HT, while co-administration of the specific 5-HT1A receptor antagonist WAY 100135 effectively abolished all 5-HT-induced behavioural deficits. This indicated that 5-HT1A receptors mediated the effects of 5-HT in the rat MVN. Using whole-cell patch-clamp recording, we demonstrated that 5-HT1A receptor activation attenuated both evoked excitatory and evoked inhibitory postsynaptic currents through a Presynaptic Mechanism in the rat MVN. The results thus highlight the 5-HT1A receptor as the gain controller of vestibular-related brainstem circuits for posture and balance.
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5‐HT 1A receptor‐mediated attenuation of synaptic transmission in rat medial vestibular nucleus impacts on vestibular‐related motor function
The Journal of physiology, 2020Co-Authors: Lei Han, Puiyi Kwan, Daisy K Y Shum, Oscar Wing‐ho Chua, Y S ChanAbstract:KEY POINTS Chemogenetic activation of medial vestibular nucleus-projecting 5-HT neurons resulted in deficits in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. The 5-HT1A receptor mediates the vestibular-related behavioural effects of 5-HT in the vestibular nucleus. 5-HT1A receptor activation attenuated evoked excitatory postsynaptic currents and evoked inhibitory postsynaptic currents via a Presynaptic Mechanism in the vestibular nucleus. ABSTRACT While the anxiolytic effects of serotonergic neuromodulation are well studied, its role in sensorimotor coordination and postural control is unclear. In this study, we show that an increase of serotonin (5-hydroxytryptamine, 5-HT) at the medial vestibular nucleus (MVN), a brainstem centre for vestibulospinal coordination, by either direct cannula administration or chemogenetic stimulation of MVN-projecting serotonergic neurons, adversely affected performance of rats in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. Application of the 5-HT1 and 5-HT7 receptor co-agonist 8-hydroxy-2-(di-n-propylamino) tetralin recapitulated the effect of 5-HT, while co-administration of the specific 5-HT1A receptor antagonist WAY 100135 effectively abolished all 5-HT-induced behavioural deficits. This indicated that 5-HT1A receptors mediated the effects of 5-HT in the rat MVN. Using whole-cell patch-clamp recording, we demonstrated that 5-HT1A receptor activation attenuated both evoked excitatory and evoked inhibitory postsynaptic currents through a Presynaptic Mechanism in the rat MVN. The results thus highlight the 5-HT1A receptor as the gain controller of vestibular-related brainstem circuits for posture and balance.
Daisy K Y Shum - One of the best experts on this subject based on the ideXlab platform.
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5 ht1a receptor mediated attenuation of synaptic transmission in rat medial vestibular nucleus impacts on vestibular related motor function
The Journal of Physiology, 2020Co-Authors: Lei Han, Puiyi Kwan, Oscar Wingho Chua, Daisy K Y Shum, Y S ChanAbstract:KEY POINTS Chemogenetic activation of medial vestibular nucleus-projecting 5-HT neurons resulted in deficits in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. The 5-HT1A receptor mediates the vestibular-related behavioural effects of 5-HT in the vestibular nucleus. 5-HT1A receptor activation attenuated evoked excitatory postsynaptic currents and evoked inhibitory postsynaptic currents via a Presynaptic Mechanism in the vestibular nucleus. ABSTRACT While the anxiolytic effects of serotonergic neuromodulation are well studied, its role in sensorimotor coordination and postural control is unclear. In this study, we show that an increase of serotonin (5-hydroxytryptamine, 5-HT) at the medial vestibular nucleus (MVN), a brainstem centre for vestibulospinal coordination, by either direct cannula administration or chemogenetic stimulation of MVN-projecting serotonergic neurons, adversely affected performance of rats in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. Application of the 5-HT1 and 5-HT7 receptor co-agonist 8-hydroxy-2-(di-n-propylamino) tetralin recapitulated the effect of 5-HT, while co-administration of the specific 5-HT1A receptor antagonist WAY 100135 effectively abolished all 5-HT-induced behavioural deficits. This indicated that 5-HT1A receptors mediated the effects of 5-HT in the rat MVN. Using whole-cell patch-clamp recording, we demonstrated that 5-HT1A receptor activation attenuated both evoked excitatory and evoked inhibitory postsynaptic currents through a Presynaptic Mechanism in the rat MVN. The results thus highlight the 5-HT1A receptor as the gain controller of vestibular-related brainstem circuits for posture and balance.
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5‐HT 1A receptor‐mediated attenuation of synaptic transmission in rat medial vestibular nucleus impacts on vestibular‐related motor function
The Journal of physiology, 2020Co-Authors: Lei Han, Puiyi Kwan, Daisy K Y Shum, Oscar Wing‐ho Chua, Y S ChanAbstract:KEY POINTS Chemogenetic activation of medial vestibular nucleus-projecting 5-HT neurons resulted in deficits in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. The 5-HT1A receptor mediates the vestibular-related behavioural effects of 5-HT in the vestibular nucleus. 5-HT1A receptor activation attenuated evoked excitatory postsynaptic currents and evoked inhibitory postsynaptic currents via a Presynaptic Mechanism in the vestibular nucleus. ABSTRACT While the anxiolytic effects of serotonergic neuromodulation are well studied, its role in sensorimotor coordination and postural control is unclear. In this study, we show that an increase of serotonin (5-hydroxytryptamine, 5-HT) at the medial vestibular nucleus (MVN), a brainstem centre for vestibulospinal coordination, by either direct cannula administration or chemogenetic stimulation of MVN-projecting serotonergic neurons, adversely affected performance of rats in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. Application of the 5-HT1 and 5-HT7 receptor co-agonist 8-hydroxy-2-(di-n-propylamino) tetralin recapitulated the effect of 5-HT, while co-administration of the specific 5-HT1A receptor antagonist WAY 100135 effectively abolished all 5-HT-induced behavioural deficits. This indicated that 5-HT1A receptors mediated the effects of 5-HT in the rat MVN. Using whole-cell patch-clamp recording, we demonstrated that 5-HT1A receptor activation attenuated both evoked excitatory and evoked inhibitory postsynaptic currents through a Presynaptic Mechanism in the rat MVN. The results thus highlight the 5-HT1A receptor as the gain controller of vestibular-related brainstem circuits for posture and balance.
Lei Han - One of the best experts on this subject based on the ideXlab platform.
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5 ht1a receptor mediated attenuation of synaptic transmission in rat medial vestibular nucleus impacts on vestibular related motor function
The Journal of Physiology, 2020Co-Authors: Lei Han, Puiyi Kwan, Oscar Wingho Chua, Daisy K Y Shum, Y S ChanAbstract:KEY POINTS Chemogenetic activation of medial vestibular nucleus-projecting 5-HT neurons resulted in deficits in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. The 5-HT1A receptor mediates the vestibular-related behavioural effects of 5-HT in the vestibular nucleus. 5-HT1A receptor activation attenuated evoked excitatory postsynaptic currents and evoked inhibitory postsynaptic currents via a Presynaptic Mechanism in the vestibular nucleus. ABSTRACT While the anxiolytic effects of serotonergic neuromodulation are well studied, its role in sensorimotor coordination and postural control is unclear. In this study, we show that an increase of serotonin (5-hydroxytryptamine, 5-HT) at the medial vestibular nucleus (MVN), a brainstem centre for vestibulospinal coordination, by either direct cannula administration or chemogenetic stimulation of MVN-projecting serotonergic neurons, adversely affected performance of rats in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. Application of the 5-HT1 and 5-HT7 receptor co-agonist 8-hydroxy-2-(di-n-propylamino) tetralin recapitulated the effect of 5-HT, while co-administration of the specific 5-HT1A receptor antagonist WAY 100135 effectively abolished all 5-HT-induced behavioural deficits. This indicated that 5-HT1A receptors mediated the effects of 5-HT in the rat MVN. Using whole-cell patch-clamp recording, we demonstrated that 5-HT1A receptor activation attenuated both evoked excitatory and evoked inhibitory postsynaptic currents through a Presynaptic Mechanism in the rat MVN. The results thus highlight the 5-HT1A receptor as the gain controller of vestibular-related brainstem circuits for posture and balance.
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5‐HT 1A receptor‐mediated attenuation of synaptic transmission in rat medial vestibular nucleus impacts on vestibular‐related motor function
The Journal of physiology, 2020Co-Authors: Lei Han, Puiyi Kwan, Daisy K Y Shum, Oscar Wing‐ho Chua, Y S ChanAbstract:KEY POINTS Chemogenetic activation of medial vestibular nucleus-projecting 5-HT neurons resulted in deficits in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. The 5-HT1A receptor mediates the vestibular-related behavioural effects of 5-HT in the vestibular nucleus. 5-HT1A receptor activation attenuated evoked excitatory postsynaptic currents and evoked inhibitory postsynaptic currents via a Presynaptic Mechanism in the vestibular nucleus. ABSTRACT While the anxiolytic effects of serotonergic neuromodulation are well studied, its role in sensorimotor coordination and postural control is unclear. In this study, we show that an increase of serotonin (5-hydroxytryptamine, 5-HT) at the medial vestibular nucleus (MVN), a brainstem centre for vestibulospinal coordination, by either direct cannula administration or chemogenetic stimulation of MVN-projecting serotonergic neurons, adversely affected performance of rats in vestibular-mediated tasks, including negative geotaxis, balance beam and rota-rod tests. Application of the 5-HT1 and 5-HT7 receptor co-agonist 8-hydroxy-2-(di-n-propylamino) tetralin recapitulated the effect of 5-HT, while co-administration of the specific 5-HT1A receptor antagonist WAY 100135 effectively abolished all 5-HT-induced behavioural deficits. This indicated that 5-HT1A receptors mediated the effects of 5-HT in the rat MVN. Using whole-cell patch-clamp recording, we demonstrated that 5-HT1A receptor activation attenuated both evoked excitatory and evoked inhibitory postsynaptic currents through a Presynaptic Mechanism in the rat MVN. The results thus highlight the 5-HT1A receptor as the gain controller of vestibular-related brainstem circuits for posture and balance.
Uwe Heinemann - One of the best experts on this subject based on the ideXlab platform.
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Glutamate transporters and metabotropic receptors regulate excitatory neurotransmission in the medial entorhinal cortex of the rat.
Brain Research, 2004Co-Authors: Claudia Iserhot, Dietmar Schmitz, Christine Gebhardt, Uwe HeinemannAbstract:In layer III of the medial entorhinal cortex (mEC), a region that is especially prone to cell damage in Alzheimer's disease, schizophrenia and epilepsy, effects of blocking glutamate uptake on excitatory synaptic transmission were studied. Two competitive glutamate transporter antagonists, TBOA and tPDC, reduced the amplitude of pharmacologically isolated AMPAR and NMDAR mediated EPSPs/EPSCs without changing the time course of the events. This effect was mimicked by tACPD, an agonist of groups I and II metabotropic glutamate receptors (mGluRs). The competitive groups I and II mGluR antagonist MCPG blocked the depression of the EPSC amplitude induced by tACPD and also prevented the effect of either TBOA or tPDC. Furthermore, EGLU, which selectively antagonizes group II mGluRs, blocked the effect of tPDC and LY3414965, a specific group I mGluR antagonist, abolished the reduction of amplitude caused by TBOA. Additionally, application of TBOA increased the paired-pulse index, suggesting a Presynaptic Mechanism for the depression of EPSP/EPSC amplitude. The present data suggest that glutamate transporters and group I/II mGluRs regulate excitatory synaptic transmission in the mEC. Presynaptic mGluRs may limit excessive glutamate accumulation if uptake becomes compromised.
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dopamine suppresses stimulus induced field potentials in layer iii of rat medial entorhinal cortex
Neuroscience Letters, 1998Co-Authors: Kerstin Stenkamp, Uwe Heinemann, Dietmar SchmitzAbstract:Abstract We studied the effect of dopamine (DA) on field potential responses in layer III of the medial entorhinal cortex (mEC) evoked by synaptic stimulation of superficial layers of the lateral EC either by single or paired-pulses. The maximum amplitude of the field response was reduced to 50.6±2.6% by DA (500 μ M) bath-applied for 5 min. Both the D1 antagonist SCH 23390 (20 μ M) and the D2 antagonist sulpiride (20–50 μ M) reduced the effect of DA to the same extent, namely 18% less reduction in their presence. The D2 agonist quinelorane (500 μ M) reduced the field response to 75±4.0%, whereas the D1 agonist SKF38393 was without significant effect. The paired-pulse ratio increased significantly during DA application. These results suggest predominant D2 receptor involvement in the decrement of synaptic transmission in layer III by dopamine. Paired-pulse experiments may be indicative of a Presynaptic Mechanism of action.
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Serotonin reduces synaptic excitation in the superficial medial entorhinal cortex of the rat via a Presynaptic Mechanism
The Journal of Physiology, 1998Co-Authors: Dietmar Schmitz, Tengis Gloveli, Andreas Draguhn, Ruth M. Empson, Uwe HeinemannAbstract:1. The superficial layers II and III of the entorhinal cortex, which form the main cortical input to the hippocampus, receive a large serotonergic projection from the raphe nuclei and express 5-HT receptors at high density. Here, we studied the effects of serotonin on the intrinsic properties and excitatory synaptic transmission of the superficial medial entorhinal cortex. 2. Intracellular and patch clamp recordings revealed that serotonin hyperpolarized only one-third of the cells, approximately, through a potassium conductance via a GTP-dependent process. 3. Serotonin depressed mixed as well as isolated alpha-amino-3-hydroxy-5-methyl-4-isoxazole- propionic acid receptor (AMPAR)- and N-methyl-D-aspartic acid receptor (NMDAR)-mediated excitatory postsynaptic potentials/currents (EPSPs/EPSCsapproximately 40 % reduction with 1 microM serotonin). 4. The effect of serotonin on EPSPs/EPSCs was similar in whole-cell versus intracellular recordings; it did not require intracellular GTP and was not visible in glutamate applications to excised patches. Miniature EPSCs recorded in the presence of tetrodotoxin and bicuculline were reduced in frequency, but not altered in amplitude. 5. The effects of serotonin on intrinsic properties and EPSPs were partially mimicked by 5-HT1A receptor agonists (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT) and 5-carboxamido-tryptamine maleate (5-CT), and reduced by 5-HT1A receptor antagonists S-(-)-5-fluoro-8-hydroxy-DPAT hydrochloride (S-UH-301), 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]piperazine hydrobromide (NAN-190) and spiperone. 6. We conclude that serotonin potently suppresses excitatory synaptic transmission via 5-HT1A receptors in layers II and III of the medial entorhinal cortex by a Presynaptic Mechanism.
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Dopamine suppresses stimulus-induced field potentials in layer III of rat medial entorhinal cortex
Neuroscience Letters, 1998Co-Authors: Kerstin Stenkamp, Uwe Heinemann, Dietmar SchmitzAbstract:We studied the effect of dopamine (DA) on field potential responses in layer III of the medial entorhinal cortex (mEC) evoked by synaptic stimulation of superficial layers of the lateral EC either by single or paired-pulses. The maximum amplitude of the field response was reduced to 50.6+/-2.6% by DA (500 microM) bath-applied for 5 min. Both the D1 antagonist SCH 23390 (20 microM) and the D2 antagonist sulpiride (20-50 microM) reduced the effect of DA to the same extent, namely 18% less reduction in their presence. The D2 agonist quinelorane (500 microM) reduced the field response to 75+/-4.0%, whereas the D1 agonist SKF38393 was without significant effect. The paired-pulse ratio increased significantly during DA application. These results suggest predominant D2 receptor involvement in the decrement of synaptic transmission in layer III by dopamine. Paired-pulse experiments may be indicative of a Presynaptic Mechanism of action.
Dietmar Schmitz - One of the best experts on this subject based on the ideXlab platform.
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Glutamate transporters and metabotropic receptors regulate excitatory neurotransmission in the medial entorhinal cortex of the rat.
Brain Research, 2004Co-Authors: Claudia Iserhot, Dietmar Schmitz, Christine Gebhardt, Uwe HeinemannAbstract:In layer III of the medial entorhinal cortex (mEC), a region that is especially prone to cell damage in Alzheimer's disease, schizophrenia and epilepsy, effects of blocking glutamate uptake on excitatory synaptic transmission were studied. Two competitive glutamate transporter antagonists, TBOA and tPDC, reduced the amplitude of pharmacologically isolated AMPAR and NMDAR mediated EPSPs/EPSCs without changing the time course of the events. This effect was mimicked by tACPD, an agonist of groups I and II metabotropic glutamate receptors (mGluRs). The competitive groups I and II mGluR antagonist MCPG blocked the depression of the EPSC amplitude induced by tACPD and also prevented the effect of either TBOA or tPDC. Furthermore, EGLU, which selectively antagonizes group II mGluRs, blocked the effect of tPDC and LY3414965, a specific group I mGluR antagonist, abolished the reduction of amplitude caused by TBOA. Additionally, application of TBOA increased the paired-pulse index, suggesting a Presynaptic Mechanism for the depression of EPSP/EPSC amplitude. The present data suggest that glutamate transporters and group I/II mGluRs regulate excitatory synaptic transmission in the mEC. Presynaptic mGluRs may limit excessive glutamate accumulation if uptake becomes compromised.
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dopamine suppresses stimulus induced field potentials in layer iii of rat medial entorhinal cortex
Neuroscience Letters, 1998Co-Authors: Kerstin Stenkamp, Uwe Heinemann, Dietmar SchmitzAbstract:Abstract We studied the effect of dopamine (DA) on field potential responses in layer III of the medial entorhinal cortex (mEC) evoked by synaptic stimulation of superficial layers of the lateral EC either by single or paired-pulses. The maximum amplitude of the field response was reduced to 50.6±2.6% by DA (500 μ M) bath-applied for 5 min. Both the D1 antagonist SCH 23390 (20 μ M) and the D2 antagonist sulpiride (20–50 μ M) reduced the effect of DA to the same extent, namely 18% less reduction in their presence. The D2 agonist quinelorane (500 μ M) reduced the field response to 75±4.0%, whereas the D1 agonist SKF38393 was without significant effect. The paired-pulse ratio increased significantly during DA application. These results suggest predominant D2 receptor involvement in the decrement of synaptic transmission in layer III by dopamine. Paired-pulse experiments may be indicative of a Presynaptic Mechanism of action.
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Serotonin reduces synaptic excitation in the superficial medial entorhinal cortex of the rat via a Presynaptic Mechanism
The Journal of Physiology, 1998Co-Authors: Dietmar Schmitz, Tengis Gloveli, Andreas Draguhn, Ruth M. Empson, Uwe HeinemannAbstract:1. The superficial layers II and III of the entorhinal cortex, which form the main cortical input to the hippocampus, receive a large serotonergic projection from the raphe nuclei and express 5-HT receptors at high density. Here, we studied the effects of serotonin on the intrinsic properties and excitatory synaptic transmission of the superficial medial entorhinal cortex. 2. Intracellular and patch clamp recordings revealed that serotonin hyperpolarized only one-third of the cells, approximately, through a potassium conductance via a GTP-dependent process. 3. Serotonin depressed mixed as well as isolated alpha-amino-3-hydroxy-5-methyl-4-isoxazole- propionic acid receptor (AMPAR)- and N-methyl-D-aspartic acid receptor (NMDAR)-mediated excitatory postsynaptic potentials/currents (EPSPs/EPSCsapproximately 40 % reduction with 1 microM serotonin). 4. The effect of serotonin on EPSPs/EPSCs was similar in whole-cell versus intracellular recordings; it did not require intracellular GTP and was not visible in glutamate applications to excised patches. Miniature EPSCs recorded in the presence of tetrodotoxin and bicuculline were reduced in frequency, but not altered in amplitude. 5. The effects of serotonin on intrinsic properties and EPSPs were partially mimicked by 5-HT1A receptor agonists (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT) and 5-carboxamido-tryptamine maleate (5-CT), and reduced by 5-HT1A receptor antagonists S-(-)-5-fluoro-8-hydroxy-DPAT hydrochloride (S-UH-301), 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]piperazine hydrobromide (NAN-190) and spiperone. 6. We conclude that serotonin potently suppresses excitatory synaptic transmission via 5-HT1A receptors in layers II and III of the medial entorhinal cortex by a Presynaptic Mechanism.
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Dopamine suppresses stimulus-induced field potentials in layer III of rat medial entorhinal cortex
Neuroscience Letters, 1998Co-Authors: Kerstin Stenkamp, Uwe Heinemann, Dietmar SchmitzAbstract:We studied the effect of dopamine (DA) on field potential responses in layer III of the medial entorhinal cortex (mEC) evoked by synaptic stimulation of superficial layers of the lateral EC either by single or paired-pulses. The maximum amplitude of the field response was reduced to 50.6+/-2.6% by DA (500 microM) bath-applied for 5 min. Both the D1 antagonist SCH 23390 (20 microM) and the D2 antagonist sulpiride (20-50 microM) reduced the effect of DA to the same extent, namely 18% less reduction in their presence. The D2 agonist quinelorane (500 microM) reduced the field response to 75+/-4.0%, whereas the D1 agonist SKF38393 was without significant effect. The paired-pulse ratio increased significantly during DA application. These results suggest predominant D2 receptor involvement in the decrement of synaptic transmission in layer III by dopamine. Paired-pulse experiments may be indicative of a Presynaptic Mechanism of action.