Pool-Size Effects Depend on Synaptic Scaling

Abstract

We asked whether inhibitory population size alters PING activity by adding inhibition or merely redistributing a fixed inhibitory budget. We compared pool-size sweeps that held either summed inhibition or individual synaptic strength fixed.

Firing rates stayed stable under fixed total inhibition but fell as the pool grew when individual synaptic strength was preserved. This supports inverse scaling as a compensation rule for this regime; it does not establish uniqueness or demonstrate gamma rhythmicity.

Results

Pool-size scaling response

At nominal 𝐺𝐼𝐸=2 μS, E rates changed from 6.01 to 6 Hz across 16–256 I neurons. At 𝑤̄𝐼𝐸7.81 nS, E rates fell from 16.62 to 6 Hz and I rates from 120.41 to 34.41 Hz. All tested fixed-mean levels showed this decrease, consistent with stronger summed inhibition and reduced E–I feedback (Fig. 1).

Four panels of E and I firing rates for inhibitory pools of 16, 64 and 256 neurons. Fixed summed coupling gives nearly flat rates; fixed expected synaptic strength gives falling rates.
Figure 1: Reanalysed population firing rates. (A) Excitatory (E) rate with fixed expected summed coupling 𝐺𝐼𝐸; (B) E rate with fixed expected synaptic strength 𝑤̄𝐼𝐸; (C) inhibitory (I) rate with fixed summed coupling; (D) I rate with fixed synaptic strength. Markers are means ±1 sample standard deviation across 3 seeds, with 8 trials per seed. Shared conditions reused the same simulations.

Methods

We compared two scaling controls using recorded outputs from simulations of untrained, dense recurrent excitatory–inhibitory networks, without additional simulation.

  1. Initialize fan-in-normalized weights. For an I→E matrix with 1024 excitatory columns and 𝑁𝐼 inhibitory rows, each weight was 𝑊𝑘𝑗𝐼𝐸=𝐺draw𝑁𝐼, with 𝐺draw=max(0,𝑋) and 𝑋𝒩︀(𝜇init,𝜎init2) a Gaussian draw of mean 𝜇init and standard deviation 𝜎init=0.1𝜇init, in μS. Defining expected summed coupling 𝐺𝐼𝐸=ℰ︀[𝐺draw] gives

    ℰ︀[𝑊𝑘𝑗𝐼𝐸]=𝑤̄𝐼𝐸=𝐺𝐼𝐸𝑁𝐼,ℰ︀[𝑘=1𝑁𝐼𝑊𝑘𝑗𝐼𝐸]=𝐺𝐼𝐸.
    (1)

    Here ℰ︀ averages over weight initialization, 𝑘 indexes inhibitory neurons and 𝑗 excitatory neurons; 𝑤̄𝐼𝐸 is the expected conductance of one synapse, not an identical realised weight. An inhibitory volley gives

    Δ𝑔inh,post=E,𝑗=𝑘ℐ︀active𝑊𝑘𝑗𝐼𝐸,
    (2)

    where ℐ︀active is the active inhibitory set and Δ𝑔inh,post=E,𝑗 the inhibitory conductance increment at E neuron 𝑗, in μS; both weights and participation therefore enter the increment.

  2. Apply paired pool-size controls. We swept 𝑁𝐼{16,64,256}. Fixed-summed controls used parent means 𝜇init{1,2,4} μS, so 𝑤̄𝐼𝐸1𝑁𝐼; fixed-mean-synapse controls scaled 𝜇init with 𝑁𝐼, giving nominal 𝑤̄𝐼𝐸{3.90625,7.8125,15.625} nS. Nominal values approximate the post-clamp expectations; the arms coincide at 256 I neurons, with one additional shared condition at 64 I neurons and nominal 1 μS summed coupling.

  1. Drive and measure the networks. Nominal E→I summed coupling stayed at 1 μS; input weights used parent mean 1.2 μS, 95% initial zeros, compensation for zeroing and fan-in normalization. Each network received 784 independent 25 Hz input channels, implemented as Bernoulli spikes per 0.1 ms timestep, for 500 ms and 8 trials, with seeds 40, 41, 42. We included all conditions and averaged spike counts over the full duration, trials and neurons within each population; overlapping controls reused measurements, giving 3 seeds at each of 18 conditions from 42 distinct simulations. The reanalysis used these rates, not raw spike trains; population rates alone do not establish gamma oscillations [1].
  1. Display pool-size comparisons. We displayed the recorded population-rate responses for fixed total and fixed per-synapse coupling with their shared controls and seed aggregation.

Dataset

References

  1. G. Buzsáki and X.-J. Wang. “Mechanisms of Gamma Oscillations.” Annual Review of Neuroscience 35, 203–225 (2012). doi:10.1146/annurev-neuro-062111-150444