Intrinsic Stability of Temporally Shifted Spike-Timing Dependent Plasticity
Figure 5
The effect of the inhibitory input on synaptic competition.
A. Transition from mean-driven to fluctuation-driven firing regimes when the rate of the inhibitory input is increased. The black curve is the coefficient of variation of postsynaptic interspike intervals (), the blue curve is the mean free-running membrane potential in units of the spiking threshold, and the red curve is the standard deviation of the membrane potential in the same units. For inhibitory input rates greater than 14 Hz, there is an abrupt switch from the mean-driven to the fluctuation-driven regime, corresponding to the transition from anti-Hebbian to Hebbian competition (figure 4). B. Postsynaptic causal bumps due to uncorrelated (cyan) and correlated (magenta) input spikes for different mean synaptic strengths (shading) when the inhibitory input rate is 10 Hz. The blue area shows the depression domain and the red area is the potentiation domain. Note that the correlated causal bumps (magenta) fall almost entirely into the depression domain (blue shading) in this case, so the correlated synapses lose the competition. C. Same as panel b, but for an inhibitory input rate of 20 Hz. Note the heavy tail of the correlated causal bumps (magenta), which extend into the potentiation domain of the STDP window. These curves were obtained by numerical simulations, changing the mean of the steady-state distribution of correlated or uncorrelated synapses to the desired value for each curve. Because the correlated synapses arrive in unison, their causal bump is the aggregate effect of all of their spikes. To show the contribution of individual correlated spikes, comparable to that of the uncorrelated ones, we therefore normalized the magnitude of the causal bump of the correlated synapses by their average cluster size (
).