TY  - JOUR
A1  - Muellerleile, Julia
A1  - Vnenčák, Matej
A1  - Ippolito, Angelo
A1  - Krueger-Burg, Dilja
A1  - Jungenitz, Tassilo
A1  - Schwarzacher, Stephan
A1  - Jedlička, Peter
T1  - Neuroligin-3 regulates excitatory synaptic transmission and EPSP-spike coupling in the dentate gyrus in vivo
T2  - Molecular neurobiology
N2  - Neuroligin-3 (Nlgn3), a neuronal adhesion protein implicated in autism spectrum disorder (ASD), is expressed at excitatory and inhibitory postsynapses and hence may regulate neuronal excitation/inhibition balance. To test this hypothesis, we recorded field excitatory postsynaptic potentials (fEPSPs) in the dentate gyrus of Nlgn3 knockout (KO) and wild-type mice. Synaptic transmission evoked by perforant path stimulation was reduced in KO mice, but coupling of the fEPSP to the population spike was increased, suggesting a compensatory change in granule cell excitability. These findings closely resemble those in neuroligin-1 (Nlgn1) KO mice and could be partially explained by the reduction in Nlgn1 levels we observed in hippocampal synaptosomes from Nlgn3 KO mice. However, unlike Nlgn1, Nlgn3 is not necessary for long-term potentiation. We conclude that while Nlgn1 and Nlgn3 have distinct functions, both are required for intact synaptic transmission in the mouse dentate gyrus. Our results indicate that interactions between neuroligins may play an important role in regulating synaptic transmission and that ASD-related neuroligin mutations may also affect the synaptic availability of other neuroligins.
KW  - Neuroligins
KW  - Autism Spectrum disorder
KW  - Synaptic transmission
KW  - In vivo electrophysiology
KW  - Synaptosomal preparation
Y1  - 2021
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/69578
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-695784
SN  - 1559-1182
N1  - Open Access funding enabled and organized by Projekt DEAL.
VL  - 59
IS  - 2
SP  - 1098
EP  - 1111
PB  - Humana Press
CY  - Totowa, NJ
ER  -