Atlastin‐1 modulates seizure activity and neuronal excitability
Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the disorder are not yet fully understood. Atlastin‐1, a dynamin‐like GTPase, interacts with microtubules and is responsible for vesicle formation, bo...
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| Published in | CNS neuroscience & therapeutics Vol. 26; no. 3; pp. 385 - 393 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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England
John Wiley & Sons, Inc
01.03.2020
John Wiley and Sons Inc |
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| Abstract | Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the disorder are not yet fully understood. Atlastin‐1, a dynamin‐like GTPase, interacts with microtubules and is responsible for vesicle formation, both of which are highly associated with the development of epilepsy. Here, we reported that the expression level of atlastin‐1 protein was reduced in the temporal neocortex of patients with temporal lobe epilepsy and in the hippocampus and adjacent cortex of a pentylenetetrazol‐kindled epileptic mouse model. Cells expressing atlastin‐1 coexpressed the inhibitory synaptic marker GAD67 in the temporal cortex and hippocampus of patients with epilepsy and an epileptic mouse model. The lentivirus‐mediated overexpression of atlastin‐1 protein in the hippocampus of mice suppressed seizure activity in behavioral experiments. Patch‐clamp recordings in the Mg2+‐free epilepsy cell model showed that atlastin‐1 overexpression inhibited neuronal excitability by suppressing the discharge frequency of spontaneous action potentials rather than by changing the passive and active properties of action potentials. Inhibitory synaptic transmission, but not excitatory synaptic currents, increased after atlastin‐1 overexpression. These findings suggest that atlastin‐1 likely contributes to the occurrence and development of epilepsy through inhibitory synaptic transmission. |
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| AbstractList | Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the disorder are not yet fully understood. Atlastin‐1, a dynamin‐like GTPase, interacts with microtubules and is responsible for vesicle formation, both of which are highly associated with the development of epilepsy. Here, we reported that the expression level of atlastin‐1 protein was reduced in the temporal neocortex of patients with temporal lobe epilepsy and in the hippocampus and adjacent cortex of a pentylenetetrazol‐kindled epileptic mouse model. Cells expressing atlastin‐1 coexpressed the inhibitory synaptic marker GAD67 in the temporal cortex and hippocampus of patients with epilepsy and an epileptic mouse model. The lentivirus‐mediated overexpression of atlastin‐1 protein in the hippocampus of mice suppressed seizure activity in behavioral experiments. Patch‐clamp recordings in the Mg2+‐free epilepsy cell model showed that atlastin‐1 overexpression inhibited neuronal excitability by suppressing the discharge frequency of spontaneous action potentials rather than by changing the passive and active properties of action potentials. Inhibitory synaptic transmission, but not excitatory synaptic currents, increased after atlastin‐1 overexpression. These findings suggest that atlastin‐1 likely contributes to the occurrence and development of epilepsy through inhibitory synaptic transmission. Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the disorder are not yet fully understood. Atlastin-1, a dynamin-like GTPase, interacts with microtubules and is responsible for vesicle formation, both of which are highly associated with the development of epilepsy. Here, we reported that the expression level of atlastin-1 protein was reduced in the temporal neocortex of patients with temporal lobe epilepsy and in the hippocampus and adjacent cortex of a pentylenetetrazol-kindled epileptic mouse model. Cells expressing atlastin-1 coexpressed the inhibitory synaptic marker GAD67 in the temporal cortex and hippocampus of patients with epilepsy and an epileptic mouse model. The lentivirus-mediated overexpression of atlastin-1 protein in the hippocampus of mice suppressed seizure activity in behavioral experiments. Patch-clamp recordings in the Mg -free epilepsy cell model showed that atlastin-1 overexpression inhibited neuronal excitability by suppressing the discharge frequency of spontaneous action potentials rather than by changing the passive and active properties of action potentials. Inhibitory synaptic transmission, but not excitatory synaptic currents, increased after atlastin-1 overexpression. These findings suggest that atlastin-1 likely contributes to the occurrence and development of epilepsy through inhibitory synaptic transmission. Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the disorder are not yet fully understood. Atlastin-1, a dynamin-like GTPase, interacts with microtubules and is responsible for vesicle formation, both of which are highly associated with the development of epilepsy. Here, we reported that the expression level of atlastin-1 protein was reduced in the temporal neocortex of patients with temporal lobe epilepsy and in the hippocampus and adjacent cortex of a pentylenetetrazol-kindled epileptic mouse model. Cells expressing atlastin-1 coexpressed the inhibitory synaptic marker GAD67 in the temporal cortex and hippocampus of patients with epilepsy and an epileptic mouse model. The lentivirus-mediated overexpression of atlastin-1 protein in the hippocampus of mice suppressed seizure activity in behavioral experiments. Patch-clamp recordings in the Mg2+ -free epilepsy cell model showed that atlastin-1 overexpression inhibited neuronal excitability by suppressing the discharge frequency of spontaneous action potentials rather than by changing the passive and active properties of action potentials. Inhibitory synaptic transmission, but not excitatory synaptic currents, increased after atlastin-1 overexpression. These findings suggest that atlastin-1 likely contributes to the occurrence and development of epilepsy through inhibitory synaptic transmission.Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the disorder are not yet fully understood. Atlastin-1, a dynamin-like GTPase, interacts with microtubules and is responsible for vesicle formation, both of which are highly associated with the development of epilepsy. Here, we reported that the expression level of atlastin-1 protein was reduced in the temporal neocortex of patients with temporal lobe epilepsy and in the hippocampus and adjacent cortex of a pentylenetetrazol-kindled epileptic mouse model. Cells expressing atlastin-1 coexpressed the inhibitory synaptic marker GAD67 in the temporal cortex and hippocampus of patients with epilepsy and an epileptic mouse model. The lentivirus-mediated overexpression of atlastin-1 protein in the hippocampus of mice suppressed seizure activity in behavioral experiments. Patch-clamp recordings in the Mg2+ -free epilepsy cell model showed that atlastin-1 overexpression inhibited neuronal excitability by suppressing the discharge frequency of spontaneous action potentials rather than by changing the passive and active properties of action potentials. Inhibitory synaptic transmission, but not excitatory synaptic currents, increased after atlastin-1 overexpression. These findings suggest that atlastin-1 likely contributes to the occurrence and development of epilepsy through inhibitory synaptic transmission. Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the disorder are not yet fully understood. Atlastin‐1, a dynamin‐like GTPase, interacts with microtubules and is responsible for vesicle formation, both of which are highly associated with the development of epilepsy. Here, we reported that the expression level of atlastin‐1 protein was reduced in the temporal neocortex of patients with temporal lobe epilepsy and in the hippocampus and adjacent cortex of a pentylenetetrazol‐kindled epileptic mouse model. Cells expressing atlastin‐1 coexpressed the inhibitory synaptic marker GAD67 in the temporal cortex and hippocampus of patients with epilepsy and an epileptic mouse model. The lentivirus‐mediated overexpression of atlastin‐1 protein in the hippocampus of mice suppressed seizure activity in behavioral experiments. Patch‐clamp recordings in the Mg 2+ ‐free epilepsy cell model showed that atlastin‐1 overexpression inhibited neuronal excitability by suppressing the discharge frequency of spontaneous action potentials rather than by changing the passive and active properties of action potentials. Inhibitory synaptic transmission, but not excitatory synaptic currents, increased after atlastin‐1 overexpression. These findings suggest that atlastin‐1 likely contributes to the occurrence and development of epilepsy through inhibitory synaptic transmission. |
| Author | Lu, Xi Yang, Min Yang, Yong Wang, Xue‐Feng |
| AuthorAffiliation | 1 Department of Neurology The First Affiliated Hospital of Chongqing Medical University Chongqing Key Laboratory of Neurology Chongqing China 2 Department of Neurology The First Affiliated Hospital of Nanchang University Nanchang China |
| AuthorAffiliation_xml | – name: 1 Department of Neurology The First Affiliated Hospital of Chongqing Medical University Chongqing Key Laboratory of Neurology Chongqing China – name: 2 Department of Neurology The First Affiliated Hospital of Nanchang University Nanchang China |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31729196$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_ceca_2021_102399 crossref_primary_10_3390_cells10112870 crossref_primary_10_1016_j_jbc_2021_101438 crossref_primary_10_1155_2020_8864246 |
| Cites_doi | 10.1111/j.1528-1167.2011.03121.x 10.1016/j.neuropharm.2013.10.016 10.1111/j.1471-4159.2009.06258.x 10.1523/JNEUROSCI.20-18-06743.2000 10.1523/JNEUROSCI.21-04-01211.2001 10.1523/JNEUROSCI.22-15-06650.2002 10.1073/pnas.211132798 10.1016/j.ydbio.2009.03.019 10.1056/NEJM200002033420503 10.1172/JCI40979 10.1523/JNEUROSCI.4712-05.2006 10.1002/path.4903 10.1016/S0896-6273(03)00640-8 10.1016/j.neuron.2012.10.012 10.1152/jn.91339.2008 10.1016/j.neuron.2005.10.034 10.1113/jphysiol.2007.138131 10.1046/j.1528-1157.42.s6.10.x 10.1146/annurev.physiol.64.092501.114547 10.1002/0471142301.ns0937s58 10.1038/ejhg.2015.200 10.1016/0013-4694(72)90177-0 10.1007/s12035-015-9431-8 10.1016/j.neulet.2013.02.074 10.1074/jbc.M306702200 10.1016/j.neures.2013.08.007 10.1038/nature04050 10.1126/science.1097065 10.1093/hmg/ddu280 10.1093/hmg/ddl054 10.1093/cercor/bht118 10.1152/jn.00866.2003 10.1146/annurev.physiol.63.1.815 10.1523/JNEUROSCI.4437-15.2016 10.1093/cercor/bhx215 10.1126/science.1165209 10.1093/brain/aww280 |
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| Copyright | 2019 The Authors. Published by John Wiley & Sons Ltd. 2019 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd. 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | epilepsy seizure human patients inhibitory synaptic transmission neuronal excitability |
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| References_xml | – volume: 437 start-page: 1027 year: 2005 end-page: 1031 article-title: Repeated cocaine exposure in vivo facilitates LTP induction in midbrain dopamine neurons publication-title: Nature – volume: 342 start-page: 314 year: 2000 end-page: 319 article-title: Early identification of refractory epilepsy publication-title: N Engl J Med – volume: 305 start-page: 532 year: 2004 end-page: 535 article-title: Acquired dendritic channelopathy in temporal lobe epilepsy publication-title: Science – volume: 24 start-page: 857 year: 2016 end-page: 863 article-title: Hereditary spastic paraplegia in Greece: characterisation of a previously unexplored population using next‐generation sequencing publication-title: Eur J Hum Genet – volume: 64 start-page: 355 year: 2002 end-page: 405 article-title: Short‐term synaptic plasticity publication-title: Annu Rev Physiol – volume: 21 start-page: 1211 year: 2001 end-page: 1217 article-title: Laminar organization of the NMDA receptor complex within the postsynaptic density publication-title: J Neurosci – volume: 28 start-page: 3491 year: 2018 end-page: 3504 article-title: CNTNAP4 impacts epilepsy through GABAA receptors regulation: evidence from temporal lobe epilepsy patients and mouse models publication-title: Cereb Cortex – volume: 52 start-page: 2 issue: Suppl 7 year: 2011 end-page: 26 article-title: Standards for epidemiologic studies and surveillance of epilepsy publication-title: Epilepsia – volume: 26 start-page: 2513 year: 2006 end-page: 2521 article-title: Dopamine D3 receptors regulate GABAA receptor function through a phospho‐dependent endocytosis mechanism in nucleus accumbens publication-title: J Neurosci – volume: 24 start-page: 2533 year: 2014 end-page: 2540 article-title: Association of mitochondrial letm1 with epileptic seizures publication-title: Cereb Cortex – volume: 120 start-page: 1097 year: 2010 end-page: 1110 article-title: Hereditary spastic paraplegia proteins REEP1, spastin, and atlastin‐1 coordinate microtubule interactions with the tubular ER network publication-title: J Clin Invest – volume: 42 start-page: 3 issue: Suppl 6 year: 2001 article-title: Intractable epilepsy: definition and neurobiology publication-title: Epilepsia – volume: 53 start-page: 5013 year: 2016 end-page: 5024 article-title: Association of microtubule dynamics with chronic epilepsy publication-title: Mol Neurobiol – volume: 15 start-page: 1343 year: 2006 end-page: 1353 article-title: SPG3A protein atlastin‐1 is enriched in growth cones and promotes axon elongation during neuronal development publication-title: Hum Mol Genet – volume: 110 start-page: 1607 year: 2009 end-page: 1616 article-title: Atlastin‐1, the dynamin‐like GTPase responsible for spastic paraplegia SPG3A, remodels lipid membranes and may form tubules and vesicles in the endoplasmic reticulum publication-title: J Neurochem – year: 2012 article-title: Pentylenetetrazol (PTZ) kindling model of epilepsy publication-title: Curr Protoc Neurosci – volume: 140 start-page: 68 year: 2017 end-page: 82 article-title: Preoperative automated fibre quantification predicts postoperative seizure outcome in temporal lobe epilepsy publication-title: Brain – volume: 98 start-page: 11725 year: 2001 end-page: 11730 article-title: Interaction of the AMPA receptor subunit GluR2/3 with PDZ domains regulates hippocampal long‐term depression publication-title: Proc Natl Acad Sci USA – volume: 20 start-page: 6743 year: 2000 end-page: 6751 article-title: Regulation of somatodendritic GABAA receptor channels in rat hippocampal neurons: evidence for a role of the small GTPase Rac1 publication-title: J Neurosci – volume: 322 start-page: 1555 year: 2008 end-page: 1559 article-title: Activation of pannexin‐1 hemichannels augments aberrant bursting in the hippocampus publication-title: Science – volume: 101 start-page: 3126 year: 2009 end-page: 3134 article-title: Electrophysiological properties of dural afferents in the absence and presence of inflammatory mediators publication-title: J Neurophysiol – volume: 91 start-page: 2524 year: 2004 end-page: 2531 article-title: Cutaneous and colonic rat DRG neurons differ with respect to both baseline and PGE2‐induced changes in passive and active electrophysiological properties publication-title: J Neurophysiol – volume: 77 start-page: 379 year: 2014 end-page: 386 article-title: Synaptic plasticity in glutamatergic and GABAergic neurotransmission following chronic memantine treatment in an in vitro model of limbic epileptogenesis publication-title: Neuropharmacology – volume: 242 start-page: 297 year: 2017 end-page: 308 article-title: Tubulin beta‐III modulates seizure activity in epilepsy publication-title: J Pathol – volume: 543 start-page: 12 year: 2013 end-page: 16 article-title: Parawixin2, a novel non‐selective GABA uptake inhibitor from spider venom, inhibits pentylenetetrazole‐induced chemical kindling in rats publication-title: Neurosci Lett – volume: 22 start-page: 6650 year: 2002 end-page: 6658 article-title: Axon sprouting in a model of temporal lobe epilepsy creates a predominantly excitatory feedback circuit publication-title: J Neurosci – volume: 77 start-page: 137 year: 2013 end-page: 142 article-title: Atlastin‐1 regulates dendritic morphogenesis in mouse cerebral cortex publication-title: Neurosci Res – volume: 76 start-page: 945 year: 2012 end-page: 961 article-title: Molecular motor KIF5A is essential for GABA(A) receptor transport, and KIF5A deletion causes epilepsy publication-title: Neuron – volume: 584 start-page: 867 year: 2007 end-page: 883 article-title: Factors defining a pacemaker region for synchrony in the hippocampus publication-title: J Physiol – volume: 49 start-page: 131 year: 2006 end-page: 142 article-title: Threshold behavior in the initiation of hippocampal population bursts publication-title: Neuron – volume: 63 start-page: 815 year: 2001 end-page: 846 article-title: On the cellular and network bases of epileptic seizures publication-title: Annu Rev Physiol – volume: 330 start-page: 250 year: 2009 end-page: 262 article-title: Drosophila Atlastin regulates the stability of muscle microtubules and is required for synapse development publication-title: Dev Biol – volume: 32 start-page: 281 year: 1972 end-page: 294 article-title: Modification of seizure activity by electrical stimulation: II. Motor seizure publication-title: Electroencephalogr Clin Neurophysiol – volume: 278 start-page: 49063 year: 2003 end-page: 49071 article-title: Cellular localization, oligomerization, and membrane association of the hereditary spastic paraplegia 3A (SPG3A) protein atlastin publication-title: J Biol Chem – volume: 36 start-page: 2677 year: 2016 end-page: 2690 article-title: 17beta‐Estradiol acutely potentiates glutamatergic synaptic transmission in the hippocampus through distinct mechanisms in males and females publication-title: J Neurosci – volume: 23 start-page: 5638 year: 2014 end-page: 5648 article-title: Pharmacologic rescue of axon growth defects in a human iPSC model of hereditary spastic paraplegia SPG3A publication-title: Hum Mol Genet – volume: 40 start-page: 361 year: 2003 end-page: 379 article-title: AMPA receptor trafficking at excitatory synapses publication-title: Neuron – ident: e_1_2_7_2_1 doi: 10.1111/j.1528-1167.2011.03121.x – ident: e_1_2_7_33_1 doi: 10.1016/j.neuropharm.2013.10.016 – ident: e_1_2_7_11_1 doi: 10.1111/j.1471-4159.2009.06258.x – ident: e_1_2_7_37_1 doi: 10.1523/JNEUROSCI.20-18-06743.2000 – ident: e_1_2_7_26_1 doi: 10.1523/JNEUROSCI.21-04-01211.2001 – ident: e_1_2_7_14_1 doi: 10.1523/JNEUROSCI.22-15-06650.2002 – ident: e_1_2_7_20_1 doi: 10.1073/pnas.211132798 – ident: e_1_2_7_6_1 doi: 10.1016/j.ydbio.2009.03.019 – ident: e_1_2_7_3_1 doi: 10.1056/NEJM200002033420503 – ident: e_1_2_7_7_1 doi: 10.1172/JCI40979 – ident: e_1_2_7_21_1 doi: 10.1523/JNEUROSCI.4712-05.2006 – ident: e_1_2_7_12_1 doi: 10.1002/path.4903 – ident: e_1_2_7_25_1 doi: 10.1016/S0896-6273(03)00640-8 – ident: e_1_2_7_38_1 doi: 10.1016/j.neuron.2012.10.012 – ident: e_1_2_7_24_1 doi: 10.1152/jn.91339.2008 – ident: e_1_2_7_30_1 doi: 10.1016/j.neuron.2005.10.034 – ident: e_1_2_7_32_1 doi: 10.1113/jphysiol.2007.138131 – ident: e_1_2_7_17_1 doi: 10.1046/j.1528-1157.42.s6.10.x – ident: e_1_2_7_27_1 doi: 10.1146/annurev.physiol.64.092501.114547 – ident: e_1_2_7_28_1 doi: 10.1002/0471142301.ns0937s58 – ident: e_1_2_7_35_1 doi: 10.1038/ejhg.2015.200 – ident: e_1_2_7_19_1 doi: 10.1016/0013-4694(72)90177-0 – ident: e_1_2_7_13_1 doi: 10.1007/s12035-015-9431-8 – ident: e_1_2_7_18_1 doi: 10.1016/j.neulet.2013.02.074 – ident: e_1_2_7_5_1 doi: 10.1074/jbc.M306702200 – ident: e_1_2_7_8_1 doi: 10.1016/j.neures.2013.08.007 – ident: e_1_2_7_22_1 doi: 10.1038/nature04050 – ident: e_1_2_7_29_1 doi: 10.1126/science.1097065 – ident: e_1_2_7_9_1 doi: 10.1093/hmg/ddu280 – ident: e_1_2_7_10_1 doi: 10.1093/hmg/ddl054 – ident: e_1_2_7_16_1 doi: 10.1093/cercor/bht118 – ident: e_1_2_7_23_1 doi: 10.1152/jn.00866.2003 – ident: e_1_2_7_36_1 doi: 10.1146/annurev.physiol.63.1.815 – ident: e_1_2_7_34_1 doi: 10.1523/JNEUROSCI.4437-15.2016 – ident: e_1_2_7_15_1 doi: 10.1093/cercor/bhx215 – ident: e_1_2_7_31_1 doi: 10.1126/science.1165209 – ident: e_1_2_7_4_1 doi: 10.1093/brain/aww280 |
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| Snippet | Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the... |
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| SubjectTerms | Brain Convulsions & seizures Dynamin Epilepsy Etiology Excitability Guanosine triphosphatases Hippocampus human patients Human subjects Immunoglobulins inhibitory synaptic transmission Insects Magnesium Microtubules Neurological diseases neuronal excitability Original Proteins seizure Seizures Synaptic transmission Temporal cortex Temporal lobe |
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| Title | Atlastin‐1 modulates seizure activity and neuronal excitability |
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