Recombinant Mouse Neuroligin-3 (Nlgn3), partial

1. male Nlgn3 knockout mice and their wild-type littermates displayed deficits in sociability, female mice lacking Nlgn3 were insensitive to their peers' behavior but modified the social behavior of their littermates. PMID: 28795135
2. Data suggest an unanticipated mechanism of developmental compensation whereby cerebellin-1 and neuroligin-3 functionally occlude each other during development of calyx synapses. PMID: 27725662
3. Nlgn3(R451C) knock-in mice, an established genetic model for autism spectrum disorders, exhibited normal duration and distribution of sleep/wake states but significantly altered electroencephalography (EEG) power spectral profiles for wake and sleep. PMID: 28385162
4. The NL3 deletion-mutant mouse was a dramatic reduction of the number of GABAAalpha2-subunit containing GABAA receptor clusters at the retinal inner plexiform layer. PMID: 28708891
5. that neuroligin-3 specifies the properties of excitatory synapses on parvalbumin-containing interneurons by a retrograde trans-synaptic mechanism and suggest a molecular pathway whereby neuroligin-3 mutations contribute to neuropsychiatric disorders PMID: 28067903
6. Study shows altered mating behavior in the Neuroligin-3(R451C mutation) mouse and has provides new insights into the aggressive phenotype in this model. PMID: 28255463
7. Results identify impaired tonic endocannabinoid signaling as a common mechanism of Nlgn3R451C-induced excitatory/inhibitory imbalance in cortex, consistent with that identified in hippocampus. PMID: 26469287
8. Nlgn3 and Nrxn1 are differentially expressed in cerebral cortex and hippocampus which might be responsible for alternations in synaptic plasticity during aging. PMID: 25693924
9. These findings suggest that structural changes in the brain of NL-3 mice are induced by the mutation in the NL-3 gene PMID: 25299583
10. Thus our data suggest that perinatal exposure to BPA impairs spatial memory through upregulation of expression of synaptic proteins Nrxn1 and Nlgn3 and increased dendritic spine density in cerebral cortex and hippocampus of postnatal male mice. PMID: 25330104
11. Therefore, we sought to replicate our findings in the neuroligin-3 R451C point mutant knock-in mouse model (NL3R451C) in a different genetic background. PMID: 24619977
12. We used MRI to image three genetic mouse models with single mutations implicated in autism: Neuroligin-3 R451C knock-in, Methyl-CpG binding protein-2 (MECP2) 308-truncation and integrin beta3 homozygous knockout. PMID: 24151012
13. Results indicate that autism spectrum disorders (ASD)-associated NL3 mutations commonly disrupt striatal circuits in a subregion-, cell-type-, and synapse-specific fashion and suggest that this disruption may shape repetitive and stereotypic behaviors associated with ASD. PMID: 24995986
14. Neuroligin-3 R704C-mutant induced neurons exhibit a large and selective decrease in AMPA-type glutamate receptor-mediated synaptic transmission without changes in NMDA-type glutamate receptor- or in GABAA receptor-mediated synaptic transmission. PMID: 24046374
15. Our data thus suggest that neuroligin-3 is specifically required for tonic endocannabinoid signaling PMID: 23583622
16. in NL3(R451C) mutant mice, a single point mutation in a synaptic cell adhesion molecule causes context-dependent changes in synaptic transmission PMID: 21808020
17. The NL-3 acts redundantly to maintain excitatory synapses and that synapse elimination caused by the absence of NL-3 is promoted by synaptic activity and mediated by a postsynaptic Ca(2+)/CaM-dependent signaling pathway. PMID: 21788371
18. An autism-associated point mutation in the neuroligin cytoplasmic tail selectively impairs AMPA receptor-mediated synaptic transmission in hippocampus. PMID: 21642956
19. exposure to valproic acid (VPA) on gestational day 11 in mice results in a long-term, global reduction of NLGN3 at the level of gene expression, this lowered expression may be linked to autistic-like behavioral phenotype observed in the VPA mice PMID: 19607885
20. Data show that neuroligin 3 is required for proper synapse maturation and brain function, but not for the initial formation of synaptic contacts. PMID: 16982420
21. R451C(Arg451-->Cys451 substitution implicated in autism) mutants had impaired social interactions but enhanced spatial learning ability; changes were accompanied by increased inhibitory synaptic transmission with no apparent effect on excitatory synapses PMID: 17823315
22. NL-3-deficient mice display a behavioral phenotype reminiscent of the lead symptoms of autism spectrum disorder PMID: 19243448
23. these data support the hypothesis that the autism-associated NL3 mutation affects information processing in neuronal networks by altering network architecture and synchrony PMID: 19406211

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KEGG: mmu:245537

STRING: 10090.ENSMUSP00000066304

UniGene: Mm.121508