Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathy
Summary: Absence seizures, manifested by spike-wave discharges (SWD) in the electroencephalogram, display synchronous reciprocal excitation between the neocortex and thalamus. Recent studies have revealed that inhibitory neurons in the reticular thalamic (RT) nucleus and excitatory thalamocortical (...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2022-11-01
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| Series: | iScience |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2589004222017606 |
| _version_ | 1798019276864487424 |
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| author | Sasa Teng Fenghua Zhen Briana R. McRae Elaine Zhu Wayne N. Frankel Yueqing Peng |
| author_facet | Sasa Teng Fenghua Zhen Briana R. McRae Elaine Zhu Wayne N. Frankel Yueqing Peng |
| author_sort | Sasa Teng |
| collection | DOAJ |
| description | Summary: Absence seizures, manifested by spike-wave discharges (SWD) in the electroencephalogram, display synchronous reciprocal excitation between the neocortex and thalamus. Recent studies have revealed that inhibitory neurons in the reticular thalamic (RT) nucleus and excitatory thalamocortical (TC) neurons are two subcortical players in generating SWD. However, the signals that drive SWD-related activity remain elusive. Here, we show that SWD predominately occurs during wakefulness in several mouse models of absence epilepsy. In more focused studies of Gnb1 mutant mice, we found that sensory input regulates SWD. Using in vivo recording, we demonstrate that TC cells are activated prior to the onset of SWD and then inhibited during SWD. On the contrary, RT cells are slightly inhibited prior to SWD, but are strongly activated during SWD. Furthermore, chemogenetic activation of TC cells leads to the enhancement of SWD. Together, our results indicate that sensory input can regulate SWD by activating the thalamocortical pathway. |
| first_indexed | 2024-04-11T16:38:13Z |
| format | Article |
| id | doaj.art-4c7c55f5d77a40318a07919d5d65739d |
| institution | Directory Open Access Journal |
| issn | 2589-0042 |
| language | English |
| last_indexed | 2024-04-11T16:38:13Z |
| publishDate | 2022-11-01 |
| publisher | Elsevier |
| record_format | Article |
| series | iScience |
| spelling | doaj.art-4c7c55f5d77a40318a07919d5d65739d2022-12-22T04:13:45ZengElsevieriScience2589-00422022-11-012511105488Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathySasa Teng0Fenghua Zhen1Briana R. McRae2Elaine Zhu3Wayne N. Frankel4Yueqing Peng5Institute for Genomic Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA; Department of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USAInstitute for Genomic Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA; Department of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USADepartment of Neuroscience, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USAColumbia College, Columbia University, New York, NY 10027, USADepartment of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA; Department of Genetics and Development, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USAInstitute for Genomic Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA; Department of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA; Corresponding authorSummary: Absence seizures, manifested by spike-wave discharges (SWD) in the electroencephalogram, display synchronous reciprocal excitation between the neocortex and thalamus. Recent studies have revealed that inhibitory neurons in the reticular thalamic (RT) nucleus and excitatory thalamocortical (TC) neurons are two subcortical players in generating SWD. However, the signals that drive SWD-related activity remain elusive. Here, we show that SWD predominately occurs during wakefulness in several mouse models of absence epilepsy. In more focused studies of Gnb1 mutant mice, we found that sensory input regulates SWD. Using in vivo recording, we demonstrate that TC cells are activated prior to the onset of SWD and then inhibited during SWD. On the contrary, RT cells are slightly inhibited prior to SWD, but are strongly activated during SWD. Furthermore, chemogenetic activation of TC cells leads to the enhancement of SWD. Together, our results indicate that sensory input can regulate SWD by activating the thalamocortical pathway.http://www.sciencedirect.com/science/article/pii/S2589004222017606Biological sciencesNeuroscienceMolecular neuroscienceSensory neuroscience |
| spellingShingle | Sasa Teng Fenghua Zhen Briana R. McRae Elaine Zhu Wayne N. Frankel Yueqing Peng Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathy iScience Biological sciences Neuroscience Molecular neuroscience Sensory neuroscience |
| title | Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathy |
| title_full | Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathy |
| title_fullStr | Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathy |
| title_full_unstemmed | Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathy |
| title_short | Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathy |
| title_sort | sensory regulation of absence seizures in a mouse model of gnb1 encephalopathy |
| topic | Biological sciences Neuroscience Molecular neuroscience Sensory neuroscience |
| url | http://www.sciencedirect.com/science/article/pii/S2589004222017606 |
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