Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2024-12-24 |
タイトル |
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タイトル |
Differential contribution of canonical and noncanonical NLGN3 pathways to early social development and memory performance |
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言語 |
en |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
著者 |
Li, Lin-Yu
Imai, Ayako
Izumi, Hironori
Inoue, Ran
Koshidaka, Yumie
Takao, Keizo
Mori, Hisashi
Yoshida, Tomoyuki
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Abstract |
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内容記述タイプ |
Abstract |
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内容記述 |
Neuroligin (NLGN) 3 is a postsynaptic cell adhesion protein organizing synapse formation through two different types of transsynaptic interactions, canonical interaction with neurexins (NRXNs) and a recently identified noncanonical interaction with protein tyrosine phosphatase (PTP) δ. Although, NLGN3 gene is known as a risk gene for neurodevelopmental disorders such as autism spectrum disorder (ASD) and intellectual disability (ID), the pathogenic contribution of the canonical NLGN3-NRXN and noncanonical NLGN3-PTPδ pathways to these disorders remains elusive. In this study, we utilized Nlgn3 mutant mice selectively lacking the interaction with either NRXNs or PTPδ and investigated their social and memory performance. Neither Nlgn3 mutants showed any social cognitive deficiency in the social novelty recognition test. However, the Nlgn3 mutant mice lacking the PTPδ pathway exhibited significant decline in the social conditioned place preference (sCPP) at the juvenile stage, suggesting the involvement of the NLGN3-PTPδ pathway in the regulation of social motivation and reward. In terms of learning and memory, disrupting the canonical NRXN pathway attenuated contextual fear conditioning while disrupting the noncanonical NLGN3-PTPδ pathway enhanced it. Furthermore, disruption of the NLGN3-PTPδ pathway negatively affected the remote spatial reference memory in the Barnes maze test. These findings highlight the differential contributions of the canonical NLGN3-NRXN and noncanonical NLGN3-PTPδ synaptogenic pathways to the regulation of higher order brain functions associated with ASD and ID. |
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言語 |
en |
書誌情報 |
Molecular Brain
巻 17,
号 1,
p. 16-16,
発行日 2024-03-12
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出版者 |
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出版者 |
Springer Nature |
DOI |
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識別子タイプ |
DOI |
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関連識別子 |
10.1186/s13041-024-01087-5 |
著者版フラグ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
査読 |
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内容記述タイプ |
Other |
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内容記述 |
査読あり |