Excitatory synapses and gap junctions cooperate to improve Pv neuronal burst firing and cortical social cognition in Shank2-mutant mice
| العنوان: | Excitatory synapses and gap junctions cooperate to improve Pv neuronal burst firing and cortical social cognition in Shank2-mutant mice |
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| المؤلفون: | Jihye Kim, Hyogeun Shin, Eunjoon Kim, Seung Joon Lee, Young Woo Noh, Tae Kyung Lee, Issac Rhim, Jisoo Kim, Suho Lee, Soo Yeon Lee, Joo Min Park, Ye-Eun Yoo, Seungmin Ha, Min Whan Jung, Karl Deisseroth, Woochul Choi, Woohyun Kim, Ryunhee Kim, Eunee Lee, Il-Joo Cho, Sang Jeong Kim, Changuk Chung, Taesun Yoo, Se-Bum Paik, Jae Jin Shin |
| المصدر: | Nature Communications, Vol 12, Iss 1, Pp 1-20 (2021) Nature Communications |
| بيانات النشر: | Nature Portfolio, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | Male, Social Cognition, Science, General Physics and Astronomy, Nerve Tissue Proteins, Optogenetics, Inhibitory postsynaptic potential, Receptors, N-Methyl-D-Aspartate, Article, General Biochemistry, Genetics and Molecular Biology, Mice, Bursting, Interneurons, mental disorders, Animals, Social Behavior, Prefrontal cortex, Mice, Knockout, Multidisciplinary, biology, musculoskeletal, neural, and ocular physiology, Gap Junctions, Neurotransmitters, General Chemistry, Autism spectrum disorders, SHANK2, Parvalbumins, Electrical Synapses, nervous system, Social behaviour, Synapses, biology.protein, Excitatory postsynaptic potential, biological phenomena, cell phenomena, and immunity, Neuroscience, Parvalbumin, psychological phenomena and processes |
| الوصف: | NMDA receptor (NMDAR) and GABA neuronal dysfunctions are observed in animal models of autism spectrum disorders, but how these dysfunctions impair social cognition and behavior remains unclear. We report here that NMDARs in cortical parvalbumin (Pv)-positive interneurons cooperate with gap junctions to promote high-frequency (>80 Hz) Pv neuronal burst firing and social cognition. Shank2–/– mice, displaying improved sociability upon NMDAR activation, show impaired cortical social representation and inhibitory neuronal burst firing. Cortical Shank2–/– Pv neurons show decreased NMDAR activity, which suppresses the cooperation between NMDARs and gap junctions (GJs) for normal burst firing. Shank2–/– Pv neurons show compensatory increases in GJ activity that are not sufficient for social rescue. However, optogenetic boosting of Pv neuronal bursts, requiring GJs, rescues cortical social cognition in Shank2–/– mice, similar to the NMDAR-dependent social rescue. Therefore, NMDARs and gap junctions cooperate to promote cortical Pv neuronal bursts and social cognition. How NMDAR and GABA neuronal dysfunctions result in impaired social behaviour is unclear. Here, the authors show that NMDARs and gap junctions in cortical PV interneurons modulate burst firing, affecting social behaviour. |
| اللغة: | English |
| تدمد: | 2041-1723 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::983dd565722ce47c6e7ebcfbdab7c2e6 https://doaj.org/article/be579d8154684279867ebaa15847607e |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....983dd565722ce47c6e7ebcfbdab7c2e6 |
| قاعدة البيانات: | OpenAIRE |
Find this article in full text from Springer Verlag. | تدمد: | 20411723 |
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