Collectively, with regards to the mouse model of FXS, these findings have several implications [1]: in vitro gamma oscillations (CCh- and DHPG-induced) which depend on an intact AMPAR-driven excitatory synaptic transmission are elevated [2], inhibition-driven KA-induced gamma oscillations are reduced in their synchrony and show an increase in gamma peak frequency [3], excitation-inhibition balance during gamma oscillations may underlie the distinct changes in the properties of gamma network activity induced by CCh, DHPG or KA in the hippocampal CA3 of Fmr1 KO mice. Here, FMR1 is linked to fragile X syndrome.