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dc.contributor.authorZheng, Thomas
dc.contributor.authorCarcak, Nihan
dc.contributor.authorPowell, Kim
dc.contributor.authorONAT, FİLİZ
dc.contributor.authorO'Brien, Terence J.
dc.contributor.authorAli, Idrish
dc.date.accessioned2021-03-02T22:05:22Z
dc.date.available2021-03-02T22:05:22Z
dc.date.issued2019
dc.identifier.citationCarcak N., Ali I., Powell K., Zheng T., ONAT F., O'Brien T. J. , "Ca(v)3.2 T-type calcium channel mutation influences kindling-induced thalamic neuronal firing patterns in Genetic Absence Epilepsy Rats From Strasbourg", EPILEPSIA, cilt.60, sa.7, ss.1378-1386, 2019
dc.identifier.issn0013-9580
dc.identifier.otherav_0a9f73cd-d7e3-407c-947b-ffdd0b0cc856
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/12873
dc.identifier.urihttps://doi.org/10.1111/epi.16076
dc.description.abstractObjective: Recent data indicate that amygdala kindling leads to significant changes in interictal neuronal firing patterns of thalamic reticular nucleus (TRN) neurons by decreasing the spontaneous firing rate and increasing burst firing in nonepileptic control (NEC) rats. Genetic Absence Epilepsy Rats From Strasbourg (GAERS) were resistant to these kindling-induced firing changes in TRN neurons, and are also resistant to the progression of kindling. We investigated whether a homozygous, missense, single nucleotide mutation (R1584P) in the Ca(v)3.2 T-type Ca2+ channel gene, which has been correlated with the expression of absence seizures in GAERS, influenced kindling progression and TRN firing patterns.
dc.language.isoeng
dc.subjectNöroloji
dc.subjectDahili Tıp Bilimleri
dc.subjectSağlık Bilimleri
dc.subjectTıp
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectKLİNİK NEUROLOJİ
dc.titleCa(v)3.2 T-type calcium channel mutation influences kindling-induced thalamic neuronal firing patterns in Genetic Absence Epilepsy Rats From Strasbourg
dc.typeMakale
dc.relation.journalEPILEPSIA
dc.contributor.departmentRoyal Melbourne Hospital , ,
dc.identifier.volume60
dc.identifier.issue7
dc.identifier.startpage1378
dc.identifier.endpage1386
dc.contributor.firstauthorID265873


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