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Activity-Dependent Validation of Excitatory versus Inhibitory Synapses by Neuroligin-1 versus Neuroligin-2
TLDR
It is shown that in cultured neurons, neuroligin-1 overexpression increases excitatory, but not inhibitory, synaptic responses, and potentiates synaptic NMDAR/AMPAR ratios, which indicates that neuroligins do not establish, but specify and validate, synapses via an activity-dependent mechanism. Expand
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
Munc13-1 is essential for fusion competence of glutamatergic synaptic vesicles
TLDR
It is shown that glutamatergic hippocampal neurons from mice lacking Munc13-1 form ultrastructurally normal synapses whose synaptic-vesicle cycle is arrested at the maturation step, demonstrating the existence of multiple and transmitter-specific synaptic vesicle maturation processes in synapses. 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
An essential role for vesicular glutamate transporter 1 (VGLUT1) in postnatal development and control of quantal size.
TLDR
The results show that the expression level of VGLUTs determines the amount of glutamate that is loaded into vesicles and released and thereby regulates the efficacy of neurotransmission. 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
Synaptotagmin: a calcium sensor on the synaptic vesicle surface.
TLDR
It is reported here that synaptotagmin, a highly conserved synaptic vesicle protein, binds calcium at physiological concentrations in a complex with negatively charged phospholipids, and this binding is specific for calcium and involves the cytoplasmic domain of synaptoagmin. 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
Ca2+-dependent and -independent activities of neural and non-neural synaptotagmins
TLDR
Four Syts are described, three of which (Syt VI, VII and VIII) are widely expressed in non-neural tissues and appear to be ubiquitous proteins with a role in exocytosis mediated by syntaxin binding. Expand
Functional Interaction of the Active Zone Proteins Munc13-1 and RIM1 in Synaptic Vesicle Priming
TLDR
The Munc13-1/RIM1 interaction may create a functional link between synaptic vesicle tethering and priming, or it may regulate the priming reaction itself, thereby determining the number of fusion-competent vesicles. Expand
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