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dc.contributor.authorLee, Seung Eun-
dc.contributor.authorLee, Jaekwang-
dc.contributor.authorLatchoumane, Charles-
dc.contributor.authorLee, Boyoung-
dc.contributor.authorOh, Soo-Jin-
dc.contributor.authorSaud, Zahangir Alam-
dc.contributor.authorPark, Cheongdahm-
dc.contributor.authorSun, Ning-
dc.contributor.authorCheong, Eunji-
dc.contributor.authorChen, Chien-Chang-
dc.contributor.authorChoi, Eui-Ju-
dc.contributor.authorLee, C. Justin-
dc.contributor.authorShin, Hee-Sup-
dc.date.accessioned2024-01-20T09:03:38Z-
dc.date.available2024-01-20T09:03:38Z-
dc.date.created2021-09-02-
dc.date.issued2014-08-12-
dc.identifier.issn0027-8424-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/126474-
dc.description.abstractIntrinsic burst and rhythmic burst discharges (RBDs) are elicited by activation of T-type Ca2+ channels in the thalamic reticular nucleus (TRN). TRN bursts are believed to be critical for generation and maintenance of thalamocortical oscillations, leading to the spike-and-wave discharges (SWDs), which are the hallmarks of absence seizures. We observed that the RBDs were completely abolished, whereas tonic firing was significantly increased, in TRN neurons from mice in which the gene for the T-type Ca2+ channel, Ca(V)3.3, was deleted (Ca(V)3.3(-/-)). Contrary to expectations, there was an increased susceptibility to drug-induced SWDs both in Ca(V)3.3(-/-)mice and in mice in which the CaV3.3 gene was silenced predominantly in the TRN. Ca(V)3.3(-/)-mice also showed enhanced inhibitory synaptic drive onto TC neurons. Finally, a double knockout of both Ca(V)3.3 and Ca(V)3.2, which showed complete elimination of burst firing and RBDs in TRN neurons, also displayed enhanced drug-induced SWDs and absence seizures. On the other hand, tonic firing in the TRN was increased in these mice, suggesting that increased tonic firing in the TRN may be sufficient for drug-induced SWD generation in the absence of burst firing. These results call into question the role of burst firing in TRN neurons in the genesis of SWDs, calling for a rethinking of the mechanism for absence seizure induction.-
dc.languageEnglish-
dc.publisherNATL ACAD SCIENCES-
dc.subjectGAMMA-HYDROXYBUTYRIC ACID-
dc.subjectELECTROPHYSIOLOGICAL PROPERTIES-
dc.subjectDIFFERENTIAL DISTRIBUTION-
dc.subjectCALCIUM-CHANNEL-
dc.subjectNEURONS-
dc.subjectOSCILLATIONS-
dc.subjectNUCLEUS-
dc.subjectMECHANISMS-
dc.subjectEPILEPSY-
dc.subjectCACNA1H-
dc.titleRebound burst firing in the reticular thalamus is not essential for pharmacological absence seizures in mice-
dc.typeArticle-
dc.identifier.doi10.1073/pnas.1408609111-
dc.description.journalClass1-
dc.identifier.bibliographicCitationPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.111, no.32, pp.11828 - 11833-
dc.citation.titlePROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-
dc.citation.volume111-
dc.citation.number32-
dc.citation.startPage11828-
dc.citation.endPage11833-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000340097900060-
dc.identifier.scopusid2-s2.0-84905967103-
dc.relation.journalWebOfScienceCategoryMultidisciplinary Sciences-
dc.relation.journalResearchAreaScience & Technology - Other Topics-
dc.type.docTypeArticle-
dc.subject.keywordPlusGAMMA-HYDROXYBUTYRIC ACID-
dc.subject.keywordPlusELECTROPHYSIOLOGICAL PROPERTIES-
dc.subject.keywordPlusDIFFERENTIAL DISTRIBUTION-
dc.subject.keywordPlusCALCIUM-CHANNEL-
dc.subject.keywordPlusNEURONS-
dc.subject.keywordPlusOSCILLATIONS-
dc.subject.keywordPlusNUCLEUS-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusEPILEPSY-
dc.subject.keywordPlusCACNA1H-
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KIST Article > 2014
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