GABAergic synaptic scaling in embryonic motoneurons is mediated by a shift in the chloride reversal potential.

Homeostatic synaptic plasticity ensures that networks maintain specific levels of activity by regulating synaptic strength in a compensatory manner. When spontaneous network activity was blocked in vivo in the embryonic spinal cord, compensatory increases in excitatory GABAergic synaptic inputs were observed. This homeostatic synaptic strengthening was observed as an increase in the amplitude of GABAergic miniature postsynaptic currents. We find that this process is mediated by an increase in chloride accumulation, which produces a depolarizing shift in the GABAergic reversal potential (E(GABA)). The findings demonstrate a previously unrecognized mechanism underlying homeostatic synaptic scaling. Similar shifts in E(GABA) have been described following various forms of neuronal injury, introducing the possibility that these shifts in E(GABA) represent a homeostatic response.