The Experts below are selected from a list of 255 Experts worldwide ranked by ideXlab platform
Giuseppe Di Giovanni - One of the best experts on this subject based on the ideXlab platform.
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Magor Lőrincz, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Régis Lambert, Giuseppe Di GiovanniAbstract:Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Magor L. Lőrincz, Régis C. Lambert, Giuseppe Di GiovanniAbstract:The authors demonstrate that the thalamic output during absence seizures is controlled and synchronized by a combination of excitation from the cortex and fast feedforward inhibition from reticular thalamus, with little involvement of thalamocortical neuron intrinsic mechanisms. Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that, during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca^ 2+ channel (T-channel)-dependent burst firing in thalamocortical (TC) neurons and by temporally framing thalamic output via feedforward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing was markedly reduced and bursts rarely occurred. Moreover, blockade of T-channels in cortical and NRT neurons suppressed ASs, but such blockade in TC neurons had no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the first mechanistic understanding of cortico-thalamo-cortical network firing dynamics during ASs in behaving animals.
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures Europe PMC Funders Group Europe PMC Funders Author Manuscripts Europe PMC Funders Author Manuscripts
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Magor Lőrincz, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Régis Lambert, Giuseppe Di GiovanniAbstract:Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:
Cian Mccafferty - One of the best experts on this subject based on the ideXlab platform.
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Magor Lőrincz, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Régis Lambert, Giuseppe Di GiovanniAbstract:Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Magor L. Lőrincz, Régis C. Lambert, Giuseppe Di GiovanniAbstract:The authors demonstrate that the thalamic output during absence seizures is controlled and synchronized by a combination of excitation from the cortex and fast feedforward inhibition from reticular thalamus, with little involvement of thalamocortical neuron intrinsic mechanisms. Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that, during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca^ 2+ channel (T-channel)-dependent burst firing in thalamocortical (TC) neurons and by temporally framing thalamic output via feedforward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing was markedly reduced and bursts rarely occurred. Moreover, blockade of T-channels in cortical and NRT neurons suppressed ASs, but such blockade in TC neurons had no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the first mechanistic understanding of cortico-thalamo-cortical network firing dynamics during ASs in behaving animals.
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures Europe PMC Funders Group Europe PMC Funders Author Manuscripts Europe PMC Funders Author Manuscripts
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Magor Lőrincz, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Régis Lambert, Giuseppe Di GiovanniAbstract:Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:
Jeong-hwa Lee - One of the best experts on this subject based on the ideXlab platform.
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ERK-mediated phosphorylation of BIS regulates nuclear translocation of HSF1 under oxidative stress
Experimental & Molecular Medicine, 2016Co-Authors: Hye Yun Kim, Hye Hyeon Yun, Yong-sam Kim, Jeong-hwa LeeAbstract:South Korean researchers have investigated the activity of a protein that can help cancer Cells stay alive by suppressing normal Cell death. Jeong-Hwa Lee at the Catholic University of Korea in Seoul led a team from three research centers investigating the protein known as BIS, which is active in a variety of common cancers. They subjected Cells to oxidative stress, a chemical state that can adapt cancer Cells to survive. This caused another protein to add a chemical phosphate group to BIS, which in turn triggered a third protein to move from the Cell cytoplasm into the nucleus. This study identifies key steps in a pathway towards cancer. As scientists learn more about such protein interactions they become better equipped to devise drugs that might be useful in treating cancer. B-Cell lymphoma (BCL)-2-Interacting Cell death suppressor (BIS) has diverse Cellular functions depending on its binding partners. However, little is known about the effects of biochemical modification of BIS on its various activities under oxidative stress conditions. In this study, we showed that H_2O_2 reduced BIS mobility on SDS–polyacrylamide gels in a time-dependent manner via the activation of extraCellular signaling-regulated kinase (ERK). The combined results of mass spectroscopy and computational prediction identified Thr285 and Ser289 in BIS as candidate residues for phosphorylation by ERK under oxidative stress conditions. Deletion of these sites resulted in a partial reduction in the H_2O_2-induced mobility shift relative to that of the wild-type BIS protein; overexpression of the deletion mutant sensitized A172 Cells to H_2O_2-induced Cell death without increasing the level of intraCellular reactive oxygen species. Expression of the BIS deletion mutant decreased the level of heat shock protein (HSP) 70 mRNA following H_2O_2 treatment, which was accompanied by impaired nuclear translocation of heat shock transcription factor (HSF) 1. Co-immunoprecipitation assays revealed that the binding of wild-type BIS to HSF1 was decreased by oxidative stress, while the binding of the BIS deletion mutant to HSF1 was not affected. These results indicate that ERK-dependent phosphorylation of BIS has a role in the regulation of nuclear translocation of HSF1 likely through modulation of its interaction affinity with HSF1, which affects HSP70 expression and sensitivity to oxidative stress.
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Myosin heavy chain is stabilized by BCL-2 Interacting Cell death suppressor (BIS) in skeletal muscle
Experimental & molecular medicine, 2016Co-Authors: Jin Hong, Jun-sub Park, Jaemin Jeong, Hyun Geun Lee, Hye Hyeon Yun, Hye Yun Kim, Jeong-hwa LeeAbstract:BCL-2 Interacting Cell death suppressor (BIS), which is ubiquitously expressed, has important roles in various Cellular processes, such as apoptosis, the Cellular stress response, migration and invasion and protein quality control. In particular, BIS is highly expressed in skeletal and cardiac muscles, and BIS gene mutations result in human myopathy. In this study, we show that mRNA and protein levels of BIS were markedly increased during skeletal myogenesis in C2C12 Cells and mouse satellite Cells. BIS knockdown did not prevent the early stage of skeletal myogenesis, but did induce muscle atrophy and a decrease in the diameter of myotubes. BIS knockdown significantly suppressed the expression level of myosin heavy chain (MyHC) without changing the expression levels of myogenic marker proteins, such as Mgn, Cav-3 and MG53. In addition, BIS endogenously interacted with MyHC, and BIS knockdown induced MyHC ubiquitination and degradation. From these data, we conclude that molecular association of MyHC and BIS is necessary for MyHC stabilization in skeletal muscle.
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Myosin heavy chain is stabilized by BCL-2 Interacting Cell death suppressor (BIS) in skeletal muscle
Experimental & Molecular Medicine, 2016Co-Authors: Jin Hong, Jun-sub Park, Hyun Lee, Jaemin Jeong, Hye Hyeon Yun, Hye Yun Kim, Jeong-hwa LeeAbstract:The protein known as BCL-2 Interacting Cell death suppressor (BIS) is essential for the formation and maintenance of skeletal muscle. Mutations in the gene for BIS have previously been linked to muscle dysfunction in humans, but the mechanism of the protein's effect was unclear. Jeong-Hwa Lee and colleagues at The Catholic University of Korea, with co-workers elsewhere in South Korea, used genetic studies on mouse muscle Cells to investigate the role of BIS. Their results reveal a direct link between BIS and the heavy chain of the protein myosin, an essential component of muscle fibers. BIS binds to and stabilizes the myosin, protecting it from being degraded by Cell turnover processes. Modifying the activity of the gene that codes for BIS might offer a new approach for treating various muscle diseases. BCL-2 Interacting Cell death suppressor (BIS), which is ubiquitously expressed, has important roles in various Cellular processes, such as apoptosis, the Cellular stress response, migration and invasion and protein quality control. In particular, BIS is highly expressed in skeletal and cardiac muscles, and BIS gene mutations result in human myopathy. In this study, we show that mRNA and protein levels of BIS were markedly increased during skeletal myogenesis in C2C12 Cells and mouse satellite Cells. BIS knockdown did not prevent the early stage of skeletal myogenesis, but did induce muscle atrophy and a decrease in the diameter of myotubes. BIS knockdown significantly suppressed the expression level of myosin heavy chain (MyHC) without changing the expression levels of myogenic marker proteins, such as Mgn, Cav-3 and MG53. In addition, BIS endogenously interacted with MyHC, and BIS knockdown induced MyHC ubiquitination and degradation. From these data, we conclude that molecular association of MyHC and BIS is necessary for MyHC stabilization in skeletal muscle.
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Aggravation of diabetic nephropathy in BCL-2 Interacting Cell death suppressor (BIS)-haploinsufficient mice together with impaired induction of superoxide dismutase (SOD) activity
Diabetologia, 2013Co-Authors: Ji Hee Lim, Dong-ye Youn, Hyung Jae Yoo, Hye Hyeon Yoon, Min Young Kim, Sungjin Chung, Yong-soo Kim, Yoon Sik Chang, Cheol Whee Park, Jeong-hwa LeeAbstract:Aims/hypothesis B Cell CLL/lymphoma 2 (BCL-2)-Interacting Cell death suppressor (BIS), known as an anti-stress and anti-apoptotic protein, has been reported to modulate susceptibility to oxidative stress. This study investigated the potential role of BIS as an antioxidant protein in diabetic nephropathy.
Gergely Orban - One of the best experts on this subject based on the ideXlab platform.
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Magor Lőrincz, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Régis Lambert, Giuseppe Di GiovanniAbstract:Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Magor L. Lőrincz, Régis C. Lambert, Giuseppe Di GiovanniAbstract:The authors demonstrate that the thalamic output during absence seizures is controlled and synchronized by a combination of excitation from the cortex and fast feedforward inhibition from reticular thalamus, with little involvement of thalamocortical neuron intrinsic mechanisms. Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that, during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca^ 2+ channel (T-channel)-dependent burst firing in thalamocortical (TC) neurons and by temporally framing thalamic output via feedforward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing was markedly reduced and bursts rarely occurred. Moreover, blockade of T-channels in cortical and NRT neurons suppressed ASs, but such blockade in TC neurons had no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the first mechanistic understanding of cortico-thalamo-cortical network firing dynamics during ASs in behaving animals.
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures Europe PMC Funders Group Europe PMC Funders Author Manuscripts Europe PMC Funders Author Manuscripts
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Magor Lőrincz, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Régis Lambert, Giuseppe Di GiovanniAbstract:Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:
Francois David - One of the best experts on this subject based on the ideXlab platform.
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Magor Lőrincz, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Régis Lambert, Giuseppe Di GiovanniAbstract:Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Magor L. Lőrincz, Régis C. Lambert, Giuseppe Di GiovanniAbstract:The authors demonstrate that the thalamic output during absence seizures is controlled and synchronized by a combination of excitation from the cortex and fast feedforward inhibition from reticular thalamus, with little involvement of thalamocortical neuron intrinsic mechanisms. Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that, during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca^ 2+ channel (T-channel)-dependent burst firing in thalamocortical (TC) neurons and by temporally framing thalamic output via feedforward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing was markedly reduced and bursts rarely occurred. Moreover, blockade of T-channels in cortical and NRT neurons suppressed ASs, but such blockade in TC neurons had no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the first mechanistic understanding of cortico-thalamo-cortical network firing dynamics during ASs in behaving animals.
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Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures Europe PMC Funders Group Europe PMC Funders Author Manuscripts Europe PMC Funders Author Manuscripts
Nature Neuroscience, 2018Co-Authors: Cian Mccafferty, Francois David, Marcello Venzi, Magor Lőrincz, Francis Delicata, Zoe Atherton, Gregorio Recchia, Gergely Orban, Régis Lambert, Giuseppe Di GiovanniAbstract:Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse Interacting Cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: