ro-4956371 and Chromosome-Deletion

Human chromosome 16p11.2 microdeletion is the most common gene copy number variation in autism, but the synaptic pathophysiology caused by this mutation is largely unknown. Using a mouse with the same genetic deficiency, we found that metabotropic glutamate receptor 5 (mGluR5)-dependent synaptic plasticity and protein synthesis was altered in the hippocampus and that hippocampus-dependent memory was impaired. Notably, chronic treatment with a negative allosteric modulator of mGluR5 reversed the cognitive deficit.

Topics: Animals; Autistic Disorder; Behavior, Animal; Chromosome Deletion; Chromosome Disorders; Chromosomes, Human, Pair 16; Chromosomes, Mammalian; Disease Models, Animal; Hippocampus; Imidazoles; Intellectual Disability; Male; Memory Disorders; Mice; Mice, Inbred C57BL; Mice, Transgenic; Neuronal Plasticity; Pyridines; Receptor, Metabotropic Glutamate 5; Signal Transduction