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Neuroligins Determine Synapse Maturation and Function
TLDR
It is shown that deletion mutant mice lacking neuroligin expression die shortly after birth due to respiratory failure, and that neuroligins are required for proper synapse maturation and brain function, but not for the initial formation of synaptic contacts. Expand
Neuroligin 2 Drives Postsynaptic Assembly at Perisomatic Inhibitory Synapses through Gephyrin and Collybistin
TLDR
Protein interactions of the synaptic adhesion molecule neuroligin 2 that drive postsynaptic differentiation at inhibitory synapses are identified and deleted in mice perturbs GABAergic and glycinergic synaptic transmission and leads to a loss of post Synaptic specializations specifically at perisomatic inhibitorysynaptic synapses. Expand
Total arrest of spontaneous and evoked synaptic transmission but normal synaptogenesis in the absence of Munc13-mediated vesicle priming
TLDR
It is concluded that Munc13-mediated vesicle priming is not a transmitter specific phenomenon but rather a general and essential feature of multiple fast neurotransmitter systems, and that synaptogenesis during development is not dependent on synaptic secretory activity. Expand
β Phorbol Ester- and Diacylglycerol-Induced Augmentation of Transmitter Release Is Mediated by Munc13s and Not by PKCs
TLDR
Modulation of Munc13-1 activity by second messengers via the DAG/beta phorbol ester binding C(1) domain is essential for use-dependent alterations of synaptic efficacy and survival. Expand
Neuroligin 2 is exclusively localized to inhibitory synapses.
TLDR
The findings identify neuroligin 2 as a new cell adhesion protein specific for inhibitory synapses and open new avenues for identifiying the constituents of this unique type of postsynaptic specialization. Expand
Calmodulin and Munc13 Form a Ca2+ Sensor/Effector Complex that Controls Short-Term Synaptic Plasticity
TLDR
A conserved calmodulin binding site is identified in UNC-13/Munc13s, which are essential regulators of synaptic vesicle priming and synaptic efficacy in response to a residual Ca2+ signal and thus shape short-term plasticity characteristics during periods of sustained synaptic activity. Expand
Complexins Regulate a Late Step in Ca2+-Dependent Neurotransmitter Release
TLDR
It is shown that Complexins, stoichiometric components of the exocytotic core complex, are important regulators of transmitter release at a step immediately preceding vesicle fusion. Expand
Differential Control of the Releasable Vesicle Pools by SNAP-25 Splice Variants and SNAP-23
TLDR
It is concluded that three alternative SNARE components support exocytosis, but they differ in their ability to stabilize vesicles in the primed state. Expand
Neuroligin‐3‐deficient mice: model of a monogenic heritable form of autism with an olfactory deficit
TLDR
The findings show that the NL‐3 knockout mouse represents a useful animal model for understanding pathophysiological events in monogenic heritable ASD and for developing novel treatment strategies in this devastating human disorder. Expand
Reduced social interaction and ultrasonic communication in a mouse model of monogenic heritable autism
TLDR
It is reported that mice with a loss-of-function mutation in the murine NLGN4 ortholog Nlgn4, which encodes the synaptic cell adhesion protein Neuroligin-4, exhibit highly selective deficits in reciprocal social interactions and communication that are reminiscent of ASCs in humans. Expand
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