Cognitive Deficits in Calsyntenin-2-deficient Mice Associated with Reduced GABAergic Transmission
2016 | journal article; research paper. A publication with affiliation to the University of Göttingen.
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Cognitive Deficits in Calsyntenin-2-deficient Mice Associated with Reduced GABAergic Transmission
Lipina, T. V; Prasad, T.; Yokomaku, D.; Luo, L.; Connor, S. A; Kawabe, H. & Wang, Y. T. et al. (2016)
Neuropsychopharmacology, 41 pp. 802-810. DOI: https://doi.org/10.1038/npp.2015.206
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- Authors
- Lipina, Tatiana V; Prasad, Tuhina; Yokomaku, Daisaku; Luo, Lin; Connor, Steven A; Kawabe, Hiroshi; Wang, Yu Tian; Brose, Nils ; Roder, John C; Craig, Ann Marie
- Abstract
- Calsyntenin-2 has an evolutionarily conserved role in cognition. In a human genome-wide screen, the CLSTN2 locus was associated with verbal episodic memory, and expression of human calsyntenin-2 rescues the associative learning defect in orthologous Caenorhabditis elegans mutants. Other calsyntenins promote synapse development, calsyntenin-1 selectively of excitatory synapses and calsyntenin-3 of excitatory and inhibitory synapses. We found that targeted deletion of calsyntenin-2 in mice results in a selective reduction in functional inhibitory synapses. Reduced inhibitory transmission was associated with a selective reduction of parvalbumin interneurons in hippocampus and cortex. Clstn2(-/-) mice showed normal behavior in elevated plus maze, forced swim test, and novel object recognition assays. However, Clstn2(-/-) mice were hyperactive in the open field and showed deficits in spatial learning and memory in the Morris water maze and Barnes maze. These results confirm a function for calsyntenin-2 in cognitive performance and indicate an underlying mechanism that involves parvalbumin interneurons and aberrant inhibitory transmission.
- Issue Date
- 2016
- Journal
- Neuropsychopharmacology
- ISSN
- 0893-133X
- eISSN
- 1740-634X
- Language
- English