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Mishra, A.* ; Traut, M.H.* ; Becker, L. ; Klopstock, T. ; Stein, V.* ; Klein, R.*

Genetic evidence for the adhesion protein IgSF9/Dasm1 to regulate inhibitory synapse development independent of its intracellular domain.

J. Neurosci. 34, 4187-4199 (2014)
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Normal brain function requires balanced development of excitatory and inhibitory synapses. An imbalance in synaptic transmission underlies many brain disorders such as epilepsy, schizophrenia, and autism. Compared with excitatory synapses, relatively little is known about the molecular control of inhibitory synapse development. We used a genetic approach in mice to identify the Ig superfamily member IgSF9/Dasm1 as a candidate homophilic synaptic adhesion protein that regulates inhibitory synapse development. IgSF9 is expressed in pyramidal cells and subsets of interneurons in the CA1 region of hippocampus. Electrophysiological recordings of acute hippocampal slices revealed that genetic inactivation of the IgSF9 gene resulted in fewer functional inhibitory synapses; however, the strength of the remaining synapses was unaltered. These physiological abnormalities were correlated with decreased expression of inhibitory synapse markers in IgSF9.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Cell-adhesion; Dendrite Arborization; Seizure Susceptibility; Maturation-1 Dasm1; Ig Superfamily; Family-member; Neuroligin 2; In-vivo; Turtle; Differentiation
Language english
Publication Year 2014
HGF-reported in Year 2014
ISSN (print) / ISBN 0270-6474
e-ISSN 1529-2401
Quellenangaben Volume: 34, Issue: 12, Pages: 4187-4199 Article Number: , Supplement: ,
Publisher Society for Neuroscience
Publishing Place Washington
Reviewing status Peer reviewed
POF-Topic(s) 30201 - Metabolic Health
Research field(s) Genetics and Epidemiology
PSP Element(s) G-500600-001
PubMed ID 24647940
Scopus ID 84896276102
Erfassungsdatum 2014-03-24