DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Hyosang | ko |
dc.contributor.author | Kim, Eunjoon | ko |
dc.date.accessioned | 2024-09-11T06:00:17Z | - |
dc.date.available | 2024-09-11T06:00:17Z | - |
dc.date.created | 2024-09-11 | - |
dc.date.issued | 2024-03 | - |
dc.identifier.citation | FRONTIERS IN PSYCHIATRY, v.14 | - |
dc.identifier.issn | 1664-0640 | - |
dc.identifier.uri | http://hdl.handle.net/10203/322891 | - |
dc.description.abstract | ARID1B, a chromatin remodeler, is strongly implicated in autism spectrum disorders (ASD). Two previous studies on Arid1b-mutant mice with the same exon 5 deletion in different genetic backgrounds revealed distinct synaptic phenotypes underlying the behavioral abnormalities: The first paper reported decreased inhibitory synaptic transmission in layer 5 pyramidal neurons in the medial prefrontal cortex (mPFC) region of the heterozygous Arid1b-mutant (Arid1b(+/-)) brain without changes in excitatory synaptic transmission. In the second paper, in contrast, we did not observe any inhibitory synaptic change in layer 5 mPFC pyramidal neurons, but instead saw decreased excitatory synaptic transmission in layer 2/3 mPFC pyramidal neurons without any inhibitory synaptic change. In the present report, we show that when we changed the genetic background of Arid1b(+/-) mice from C57BL/6 N to C57BL/6 J, to mimic the mutant mice of the first paper, we observed both the decreased inhibitory synaptic transmission in layer 5 mPFC pyramidal neurons reported in the first paper, and the decreased excitatory synaptic transmission in mPFC layer 2/3 pyramidal neurons reported in the second paper. These results suggest that genetic background can be a key determinant of the inhibitory synaptic phenotype in Arid1b-mutant mice while having minimal effects on the excitatory synaptic phenotype. | - |
dc.language | English | - |
dc.publisher | FRONTIERS MEDIA SA | - |
dc.title | Genetic background determines synaptic phenotypes in Arid1b-mutant mice | - |
dc.type | Article | - |
dc.identifier.wosid | 001187948700001 | - |
dc.type.rims | ART | - |
dc.citation.volume | 14 | - |
dc.citation.publicationname | FRONTIERS IN PSYCHIATRY | - |
dc.identifier.doi | 10.3389/fpsyt.2023.1341348 | - |
dc.contributor.localauthor | Kim, Eunjoon | - |
dc.contributor.nonIdAuthor | Kim, Hyosang | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | ARID1B mutation | - |
dc.subject.keywordAuthor | genetic background | - |
dc.subject.keywordAuthor | miniature excitatory postsynaptic currents | - |
dc.subject.keywordAuthor | miniature inhibitory postsynaptic currents | - |
dc.subject.keywordAuthor | synaptic phenotype | - |
dc.subject.keywordPlus | HOMEOSTASIS | - |
dc.subject.keywordPlus | MUTATIONS | - |
dc.subject.keywordPlus | NICOTINAMIDE NUCLEOTIDE TRANSHYDROGENASE | - |
dc.subject.keywordPlus | CHROMATIN-REMODELING COMPLEX | - |
dc.subject.keywordPlus | INTELLECTUAL DISABILITY | - |
dc.subject.keywordPlus | AUTISM | - |
dc.subject.keywordPlus | CYFIP2 | - |
dc.subject.keywordPlus | BALANCE | - |
dc.subject.keywordPlus | ARID1B | - |
dc.subject.keywordPlus | HAPLOINSUFFICIENCY | - |
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