The Experts below are selected from a list of 210 Experts worldwide ranked by ideXlab platform
Lijuan Shen - One of the best experts on this subject based on the ideXlab platform.
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Post-treatment with a Hydrogen Sulfide Donor Limits Neuronal Injury and Modulates Potassium Voltage-Gated Channel Subfamily D Member 2 (Kv4.2) and Potassium Channel Interacting Protein 3 (KChIP3) During Transient Global Cerebral Ischemia
Current Neurovascular Research, 2018Co-Authors: Chenliang Zhao, Lijuan ShenAbstract:Although the neuroprotective effect of sodium hydrosulfide (NaHS, a hydrogen sulfide donor) pretreatment has been revealed, the effect of NaHS post-conditioning remains largely unknown. We aimed to investigate the neuroprotective effect of NaHS post-conditioning against transient Global Cerebral Ischemia (tGCI)-induced hippocampal CA1 injury and its underlying molecular mechanism. A tGCI rat model was established using the four-vessel occlusion method for 15 min of ischemia. The survival of hippocampal neurons was determined by Nissl staining and NeuN immunostaining. Protein expression of potassium Voltage-Gated Channel subfamily D member 2 (Kv4.2) and potassium Channel interacting protein 3 (KChIP3) was assessed by Immunohistochemistry (IHC) and Western blot. Decreased concentrations (12 and 24 µmol/kg) of NaHS post-conditioning significantly increased the numbers of survival neurons and NeuN-positive neurons in the hippocampal CA1 region at 7 days post-tGCI (all P<0.05). NaHS post-conditioning (24 µmol/kg) at 12 and 24 hr posttGCI can achieve the best protective effect (both P<0.05). IHC data demonstrated that NaHS postconditioning (24 µmol/kg) markedly attenuated tGCI-induced down-regulation of Kv4.2 protein in the hippocampal CA1 region at 26 hr post-tGCI. Confocal images showed that Kv4.2 did not express in the neuronal nuclei but predominantly express in the neuronal dendrites. In addition, NaHS post-conditioning significantly up-regulated Kv4.2 and down-regulated KChIP3 in tGCI rats at 26 and 168 hr post- tGCI (all P<0.05). Decreased concentrations of NaHS post-conditioning at 12-24 hr post-tGCI effectively protected hippocampal CA1 neurons from tGCI-induced injury, which may be through regulating the expression of Kv4.2 and KChIP3. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
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Post-treatment with a Hydrogen Sulfide Donor Limits Neuronal Injury and Modulates Potassium Voltage-Gated Channel Subfamily D Member 2 (Kv4.2) and Potassium Channel Interacting Protein 3 (KChIP3) During Transient Global Cerebral Ischemia
Current Neurovascular Research, 2018Co-Authors: Cheng Ping Bai, Chenliang Zhao, Lijuan ShenAbstract:BACKGROUND: Although the neuroprotective effect of sodium hydrosulfide (NaHS, a hydrogen sulfide donor) pretreatment has been revealed, the effect of NaHS post-conditioning remains largely unknown. OBJECTIVE: We aimed to investigate the neuroprotective effect of NaHS post-conditioning against transient Global Cerebral Ischemia (tGCI)-induced hippocampal CA1 injury and its underlying molecular mechanism. METHODS: A tGCI rat model was established using the four-vessel occlusion method for 15 min of ischemia. The survival of hippocampal neurons was determined by Nissl staining and NeuN immunostaining. Protein expression of potassium Voltage-Gated Channel subfamily D member 2 (Kv4.2) and potassium Channel interacting protein 3 (KChIP3) was assessed by Immunohistochemistry (IHC) and Western blot. RESULTS: Decreased concentrations (12 and 24 micromol/kg) of NaHS post-conditioning significantly increased the numbers of survival neurons and NeuN-positive neurons in the hippocampal CA1 region at 7 days post-tGCI (all P
Cheng Ping Bai - One of the best experts on this subject based on the ideXlab platform.
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Post-treatment with a Hydrogen Sulfide Donor Limits Neuronal Injury and Modulates Potassium Voltage-Gated Channel Subfamily D Member 2 (Kv4.2) and Potassium Channel Interacting Protein 3 (KChIP3) During Transient Global Cerebral Ischemia
Current Neurovascular Research, 2018Co-Authors: Cheng Ping Bai, Chenliang Zhao, Lijuan ShenAbstract:BACKGROUND: Although the neuroprotective effect of sodium hydrosulfide (NaHS, a hydrogen sulfide donor) pretreatment has been revealed, the effect of NaHS post-conditioning remains largely unknown. OBJECTIVE: We aimed to investigate the neuroprotective effect of NaHS post-conditioning against transient Global Cerebral Ischemia (tGCI)-induced hippocampal CA1 injury and its underlying molecular mechanism. METHODS: A tGCI rat model was established using the four-vessel occlusion method for 15 min of ischemia. The survival of hippocampal neurons was determined by Nissl staining and NeuN immunostaining. Protein expression of potassium Voltage-Gated Channel subfamily D member 2 (Kv4.2) and potassium Channel interacting protein 3 (KChIP3) was assessed by Immunohistochemistry (IHC) and Western blot. RESULTS: Decreased concentrations (12 and 24 micromol/kg) of NaHS post-conditioning significantly increased the numbers of survival neurons and NeuN-positive neurons in the hippocampal CA1 region at 7 days post-tGCI (all P
Chenliang Zhao - One of the best experts on this subject based on the ideXlab platform.
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Post-treatment with a Hydrogen Sulfide Donor Limits Neuronal Injury and Modulates Potassium Voltage-Gated Channel Subfamily D Member 2 (Kv4.2) and Potassium Channel Interacting Protein 3 (KChIP3) During Transient Global Cerebral Ischemia
Current Neurovascular Research, 2018Co-Authors: Chenliang Zhao, Lijuan ShenAbstract:Although the neuroprotective effect of sodium hydrosulfide (NaHS, a hydrogen sulfide donor) pretreatment has been revealed, the effect of NaHS post-conditioning remains largely unknown. We aimed to investigate the neuroprotective effect of NaHS post-conditioning against transient Global Cerebral Ischemia (tGCI)-induced hippocampal CA1 injury and its underlying molecular mechanism. A tGCI rat model was established using the four-vessel occlusion method for 15 min of ischemia. The survival of hippocampal neurons was determined by Nissl staining and NeuN immunostaining. Protein expression of potassium Voltage-Gated Channel subfamily D member 2 (Kv4.2) and potassium Channel interacting protein 3 (KChIP3) was assessed by Immunohistochemistry (IHC) and Western blot. Decreased concentrations (12 and 24 µmol/kg) of NaHS post-conditioning significantly increased the numbers of survival neurons and NeuN-positive neurons in the hippocampal CA1 region at 7 days post-tGCI (all P<0.05). NaHS post-conditioning (24 µmol/kg) at 12 and 24 hr posttGCI can achieve the best protective effect (both P<0.05). IHC data demonstrated that NaHS postconditioning (24 µmol/kg) markedly attenuated tGCI-induced down-regulation of Kv4.2 protein in the hippocampal CA1 region at 26 hr post-tGCI. Confocal images showed that Kv4.2 did not express in the neuronal nuclei but predominantly express in the neuronal dendrites. In addition, NaHS post-conditioning significantly up-regulated Kv4.2 and down-regulated KChIP3 in tGCI rats at 26 and 168 hr post- tGCI (all P<0.05). Decreased concentrations of NaHS post-conditioning at 12-24 hr post-tGCI effectively protected hippocampal CA1 neurons from tGCI-induced injury, which may be through regulating the expression of Kv4.2 and KChIP3. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
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Post-treatment with a Hydrogen Sulfide Donor Limits Neuronal Injury and Modulates Potassium Voltage-Gated Channel Subfamily D Member 2 (Kv4.2) and Potassium Channel Interacting Protein 3 (KChIP3) During Transient Global Cerebral Ischemia
Current Neurovascular Research, 2018Co-Authors: Cheng Ping Bai, Chenliang Zhao, Lijuan ShenAbstract:BACKGROUND: Although the neuroprotective effect of sodium hydrosulfide (NaHS, a hydrogen sulfide donor) pretreatment has been revealed, the effect of NaHS post-conditioning remains largely unknown. OBJECTIVE: We aimed to investigate the neuroprotective effect of NaHS post-conditioning against transient Global Cerebral Ischemia (tGCI)-induced hippocampal CA1 injury and its underlying molecular mechanism. METHODS: A tGCI rat model was established using the four-vessel occlusion method for 15 min of ischemia. The survival of hippocampal neurons was determined by Nissl staining and NeuN immunostaining. Protein expression of potassium Voltage-Gated Channel subfamily D member 2 (Kv4.2) and potassium Channel interacting protein 3 (KChIP3) was assessed by Immunohistochemistry (IHC) and Western blot. RESULTS: Decreased concentrations (12 and 24 micromol/kg) of NaHS post-conditioning significantly increased the numbers of survival neurons and NeuN-positive neurons in the hippocampal CA1 region at 7 days post-tGCI (all P
Fred J. Sigworth - One of the best experts on this subject based on the ideXlab platform.
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Expression, Purification and Functional Reconstitution of Slack Sodium-Activated Potassium Channels
The Journal of Membrane Biology, 2012Co-Authors: Youshan Yang, Shumin Bian, Fred J. SigworthAbstract:The slack ( slo 2.2) gene codes for a potassium-Channel α-subunit of the 6TM Voltage-Gated Channel family. Expression of slack results in Na^+-activated potassium Channel activity in various cell types. We describe the purification and reconstitution of Slack protein and show that the Slack α-subunit alone is sufficient for potassium Channel activity activated by sodium ions as assayed in planar bilayer membranes and in membrane vesicles.
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The Last Few Frames of the Voltage-Gating Movie
Biophysical Journal, 2007Co-Authors: Fred J. SigworthAbstract:In the voltage sensor domain (VSD) of a Voltage-Gated Channel, electrical charge is driven from the intracellular to the extracellular surface of a membrane as conformational changes occur and the Channel gates are opened. This charge displacement, which in Voltage-Gated potassium Channels occurs in ∼1 ms, is measured as a “gating current.”
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Structural biology: Life's transistors
Nature, 2003Co-Authors: Fred J. SigworthAbstract:Voltage-Gated ion Channels control electrical activity in nerve, muscle and many other cell types. The crystal structure of a bacterial Voltage-Gated Channel reveals the astonishingly simple design of its voltage sensor.
Michael Häusser - One of the best experts on this subject based on the ideXlab platform.
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Propagation of action potentials in dendrites depends on dendritic morphology.
Journal of neurophysiology, 2001Co-Authors: Pascal Vetter, A. Roth, Michael HäusserAbstract:Action potential propagation links information processing in different regions of the dendritic tree. To examine the contribution of dendritic morphology to the efficacy of propagation, simulations were performed in detailed reconstructions of eight different neuronal types. With identical complements of Voltage-Gated Channels, different dendritic morphologies exhibit distinct patterns of propagation. Remarkably, the range of backpropagation efficacies observed experimentally can be reproduced by the variations in dendritic morphology alone. Dendritic geometry also determines the extent to which modulation of Channel densities can affect propagation. Thus in Purkinje cells and dopamine neurons, backpropagation is relatively insensitive to changes in Channel densities, whereas in pyramidal cells, backpropagation can be modulated over a wide range. We also demonstrate that forward propagation of dendritically initiated action potentials is influenced by morphology in a similar manner. We show that these functional consequences of the differences in dendritic geometries can be explained quantitatively using simple anatomical measures of dendritic branching patterns, which are captured in a reduced model of dendritic geometry. These findings indicate that differences in dendritic geometry act in concert with differences in Voltage-Gated Channel density and kinetics to generate the diversity in dendritic action potential propagation observed between neurons. They also suggest that changes in dendritic geometry during development and plasticity will critically affect propagation. By determining the spatial pattern of action potential signaling, dendritic morphology thus helps to define the size and interdependence of functional compartments in the neuron.
