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GABA neuronal deletion of Shank3 exons 14?16 in mice suppresses striatal excitatory synaptic input and induces social and locomotor abnormalities

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Title
GABA neuronal deletion of Shank3 exons 14?16 in mice suppresses striatal excitatory synaptic input and induces social and locomotor abnormalities
Author(s)
Taesun Yoo; Heejin Cho; Jiseok Lee; Haram Park; Ye-Eun Yoo; Esther Yang; Jin Yong Kim; Hyun Kim; Eunjoon Kim
Publication Date
2018-10
Journal
Frontiers in Cellular Neuroscience, v.12, no., pp.341 -
Publisher
FRONTIERS RES FOUND
Abstract
Shank3 is an excitatory postsynaptic scaffolding protein implicated in multiple brain disorders, including autism spectrum disorders (ASD) and Phelan-McDermid syndrome (PMS). Although previous neurobiological studies on Shank3 and Shank3-mutant mice have revealed diverse roles of Shank3 in the regulation of synaptic, neuronal and brain functions, whether Shank3 expression in specific cell types distinctly contributes to mouse phenotypes remains largely unclear. In the present study, we generated two Shank3-mutant mouse lines (exons 14?16) carrying global and GABA neuron-specific deletions and characterized their electrophysiological and behavioral phenotypes. These mouse lines show similar decreases in excitatory synaptic input onto dorsolateral striatal neurons. In addition, the abnormal social and locomotor behaviors observed in global Shank3-mutant mice are strongly mimicked by GABA neuron-specific Shank3-mutant mice, whereas the repetitive and anxiety-like behaviors are only partially mimicked. These results suggest that GABAergic Shank3 (exons 14?16) deletion has strong influences on striatal excitatory synaptic transmission and social and locomotor behaviors in mice. (c) 2018 Yoo, Cho, Lee, Park, Yoo, Yang, Kim, Kim and Kim
URI
https://pr.ibs.re.kr/handle/8788114/5156
ISSN
1662-5102
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > Journal Papers (저널논문)
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