FMR1 and fragile X syndrome: Changes to ion channel function with loss of FMRP not only directly affect intrinsic excitability in a manner to promote hyperactivity, but can lead to profound changes in pre-synaptic release properties and post-synaptic dendritic integration, which in turn will influence synaptic function and plasticity in a variety of ways; and (4) FMRP is an important regulator of homeostatic plasticity, which is essential for stabilizing activity levels in the brain, and impairments to this stabilization mechanism are likely to contribute to circuit hyperexcitability in FXS.