A Neuroligin-3 Mutation Implicated in Autism Increases Inhibitory Synaptic Transmission in Mice

By K. Tabuchi, J. Blundell, M. Etherton, R. Hammer, Xinran Liu, Craig M. Powell, T. Sūdhof. Science, 2007

987 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Developmental Neuroscience, Genetics

View Paper: https://www.semanticscholar.org/paper/5d1e180b9bc3610ebe69f3dfe25c031a6b02986a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cognitive Neuroscience

1. Thomas Bourgeron
2. O. Marín
3. Mark F. Bear
4. T. Sūdhof
5. Takao K. Hensch
6. Nadine Gogolla
7. J. LeBlanc
8. K. Quast

In Developmental Neuroscience

1. Thomas Bourgeron
2. Mark F. Bear
3. O. Marín
4. Takao K. Hensch
5. T. Sūdhof
6. R. J. Kelleher

In Genetics

1. Thomas Bourgeron
2. Mark F. Bear
3. H. Zoghbi
4. O. Marín
5. R. J. Kelleher
6. T. Sūdhof
7. Mark Gerstein
8. Takao K. Hensch

Citations in the corpus

• Common circuit defect of excitatory-inhibitory balance in mouse models of autism (2009, positive): “To address the possibility that the lack of PV-cells in neocortex and an interhemispheric imbalance in inhibitory circuits is a more robust hallmark of ASD models, we investigated a single-gene mutation model of ASD, the Table 1 PV-cell deficits across ASD mouse models NL-3 R451C mutant mouse [6].”
• FOXG1-dependent dysregulation of GABA/glutamate neuron differentiation in autism spectrum disorders (2015, positive): “However, a gain-of-function mutation in NLGN3 (R451C) found in ASD confers an increase in GABAergic synaptic signaling (Etherton et al., 2011; Pizzarelli and Cherubini, 2013; Tabuchi et al., 2007).”
• Interneuron dysfunction in psychiatric disorders (2012, background): “, and analyses of their function in mice indicates that they are important for the maintenance of an adequate balance between neuronal excitation and inhibition in the cerebral corte”
• A synaptic trek to autism. (2009, background): “The mutant mice carrying a R451C Nlgn3 mutation identified in two brothers with ASD displays an increased number of GABAergic synapses and inhibitory currents [32].”
• Dendritic spine pathology in neuropsychiatric disorders (2011, background): “NLGN3-R451C transgenic mice display impaired social interaction behavior, but show enhanced performance in the Morris water maze, as well as enhanced inhibitory synaptic strengt”
• Neuronal Activity Promotes Glioma Growth through Neuroligin-3 Secretion (2015, neutral): “While wild-type neuroligins play a central role in normal synaptic function, NLGN3mutations are implicated in altered synaptic function in autism (Jamain et al., 2003; Rothwell et al., 2014; Tabuchi et al., 2007).”
• The autistic neuron: troubled translation? (2008, background): “…of mutations that cause ASDs in humans consistently point to disrupted synaptic function: excessive or diminished excitatory synaptic connectivity (Chao et al., 2007; Hanson and Madison, 2007) and alterations in the balance of excitation and inhibition (Dani et al., 2005; Tabuchi et al., 2007).”