Inhibition of Group I Metabotropic Glutamate Receptors Reverses Autistic-Like Phenotypes Caused by Deficiency of the Translation Repressor eIF4E Binding Protein 2.
Argel Aguilar-VallesEdna Matta-CamachoArkady KhoutorskyChristos G GkogkasKarim NaderJean-Claude LacailleNahum SonenbergPublished in: The Journal of neuroscience : the official journal of the Society for Neuroscience (2015)
Exacerbated mRNA translation during brain development is associated with several autism spectrum disorders (ASDs). We recently demonstrated that the deletion of a negative regulator of mRNA translation initiation, the eukaryotic initiation factor 4E-binding protein 2, leads to ASD-like behaviors and increased excitatory synaptic activity. Here we demonstrated that autistic behavioral and electrophysiological phenotypes can be treated in adult mice with antagonists of group I metabotropic glutamate receptors (mGluRs), which have been previously used in other ASD models (i.e., fragile X syndrome). These findings support the use of group I mGluR antagonists as a potential therapy that extends to autism models involving exacerbated mRNA translation initiation.
Keyphrases
- binding protein
- autism spectrum disorder
- intellectual disability
- attention deficit hyperactivity disorder
- resting state
- transcription factor
- type diabetes
- stem cells
- multiple sclerosis
- white matter
- functional connectivity
- high fat diet induced
- insulin resistance
- subarachnoid hemorrhage
- bone marrow
- brain injury
- replacement therapy
- skeletal muscle
- smoking cessation
- newly diagnosed
- blood brain barrier
- prefrontal cortex