Cell-Type-Specific Shank2 Deletion in Mice Leads to Differential Synaptic and Behavioral Phenotypes

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Shank2 is an excitatory postsynaptic scaffolding protein implicated in synaptic regulation and psychiatric disorders including autism spectrum disorders. Conventional Shank2-mutant (Shank2(-/-)) mice display several autistic-like behaviors, including social deficits, repetitive behaviors, hyperactivity, and anxiety-like behaviors. However, cell-type-specific contributions to these behaviors have remained largely unclear. Here, we deleted Shank2 in specific cell types and found that male mice lacking Shank2 in excitatory neurons (CaMKII-Cre;Shank2(fl/fl)) show social interaction deficits and mild social communication deficits, hyperactivity, and anxiety-like behaviors. In particular, male mice lacking Shank2 in GABAergic inhibitory neurons (Viaat-Cre;Shank2(fl/fl)) display social communication deficits, repetitive self-grooming, and mild hyperactivity. These behavioral changes were associated with distinct changes in hippocampal and striatal synaptic transmission in the two mouse lines. These results indicate that cell-type-specific deletions of Shank2 in mice lead to differential synaptic and behavioral abnormalities.
Publisher
SOC NEUROSCIENCE
Issue Date
2018-04
Language
English
Article Type
Article
Keywords

POSTSYNAPTIC DENSITY PROTEINS; AUTISM SPECTRUM DISORDERS; CEREBELLAR PURKINJE-CELLS; BINDING-PROTEIN; SPINY NEURONS; NEUROPSYCHIATRIC DISORDERS; ULTRASONIC VOCALIZATIONS; DOPAMINERGIC MODULATION; SCAFFOLD PROTEINS; SUBSTRATE IRSP53

Citation

JOURNAL OF NEUROSCIENCE, v.38, no.17, pp.4076 - 4092

ISSN
0270-6474
DOI
10.1523/JNEUROSCI.2684-17.2018
URI
http://hdl.handle.net/10203/242364
Appears in Collection
BS-Journal Papers(저널논문)
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