Formation of excitation-inhibition balance: inhibition listens and changes its tune

Abstract

Recently, Xue, Atallah, and Scanziani reported that excitation/inhibition ratios across cortical pyramidal neurons are equalized by activity-dependent modulations of parvalbumin-neuron mediated feedforward inhibition. Their results raise questions about the developmental formation of this excitation-inhibition balance and the potential activity-dependent synaptic plasticity rules that mediate this process.

Fig. 1

Plasticity rules underlying the formation of E-I balance. (A) High levels of spiking activity of the pyramidal cell resulting from strong excitation (green arrow) or overexpression of Na⁺ channels induce potentiation of its inhibitory input (red bar), decreasing the E/I ratio. Conversely, low levels of spiking activity resulting from weak excitation or overexpression of Kir channels induce depression of the inhibitory input, increasing the E/I ratio. (B) Repetitive visual stimulation induced changes of GABAergic input strength in relation to the strength of the GABAergic input and its co-activated gultamatergic input prior to the stimulation (adapted from [12]). (C) The magnitude of GABAergic plasticity as a function of E/I ratio (adapted from [12]). The vertical dash line indicates an “optimal” E/I ratio. Solid red and blue lines are linear regression lines for data points above and below this optimal value, respectively. (D) Matching of excitatory (green) and inhibitory (red) tuning. S1 and S2 are two different stimuli in the sensory space. In early circuits, S1 evokes much stronger excitation than inhibition, while S2 evokes stronger inhibition than excitation. Repetitive S1 and S2 stimulation would induce potentiation (upward arrow) of S1 activated inhibition, but depression (downward arrow) of S2 activated inhibition, leading to a progressive matching of excitatory and inhibitory tuning, as previously described [15].