Paired whole-cell recordings from pyramidal neurons in Fmr1 KO mice revealed reductions in synchronized synaptic inhibition and coordinated spike synchrony in response to the group I metabotropic glutamate receptor (mGluRs) agonist 3,5-dihydroxyphenylalanine (DHPG), implying a weakened somatostatin-expressing, low-threshold-spiking (LTS) interneuron network in layer II/III of the somatosensory cortex, resulting in altered activity of the cortical network that was in line with the FXS phenotype [228]. The gene discussed is FMR1; the disease is fragile X syndrome.