Table 1. Experimental and model cell numbers, along with incoming synaptic numbers, strengths, and time constants.

Cell	Number	Synapse	Number of synapses per cell	Experiment: PSP / PSC amplitude, peak / fall times	Modeling strategy	Model: max conductance & time constants; Simulated PSP amplitude & peak / fall times
ORN	104 / glomerulus				As Poisson spikes
PG	70–85% of juxtaglomerular (JG) cells (1500–2000 [20]) [21] i.e. ~1000 / glomerulus	ORN→PG	~50 spines (estimated from 25 in mice [22]).	EPSP 3 mV [23,24], τf ~ 5 ms [24]	1000 PG / glomerulus; 50 ORN→PG synapses per PG.	gmax = 0.45 nS for plateauing and 1.25 nS for low-threshold spiking PG cell, τ1 = 1 ms, τ2 = 1 ms (same for both synapses); simulated EPSP: ~7-8 mV, τp ~ 2 ms, τf ~ 5 ms.
		M/T→PG or ET→PG	Similar to above.	EPSP 6–10 mV [24,25], τf ~ 5 ms [24]	25 M→PG per PG.	Same as above.
ET	10% of JG cells (M.T. Shipley, email, 2010) [26,27]. Hence ~150–200 / glomerulus	ORN→ET; SA─┤ET			Absorbed into ORN Poisson spikes.
SA	15–20% of JG cells are ET / SA [26] (mice). 1:1 with M/T [27]. So, ~100 / glomerulus.				Not much inter-glomerular inhibition in vivo [28], so ignored.
M/T	25 M / 50 T per glomerulus [27]	ORN→M	460–1500 [29]	Conflicting EPSP amplitudes: ~3 mV [30], to ~0.1 mV [29], τp = 6 ms, τf = 12 ms [30].	2 mitral cells / glomerulus; 400 ORN→M on mitral tuft.	gmax = 6 nS, τ1 = 1 ms, τ2 = 1 ms; simulated EPSP: ~1 mV, τp ~ 7 ms, τf ~ 80 ms (Large time constant of our mitral cell model caused long EPSPs)
		G ─┤M	104 [11,31]	IPSC amplitude decays with distance [32]. IPSCs have τp ~ 5 ms, τf ~ 30 ms [33]; spontaneous IPSPs are not well resolved, but may have similar τp = 5 ms, τf = 30 ms [34,35].	104 G ─┤M on mitral soma, apical and lateral dendrites.	proximal gmax = 1 nS but 4× if ‘super-inhibitory’ in default network (1.5 nS in random / directed network as it had no ‘super-inhibitory’ synapses), τ1 = 1 ms, τ2 = 20 ms; simulated IPSP: ~ –0.9mV (proximal), τp ~ 26 ms, τf ~ 115 ms; (long IPSPs as above. We verified that reducing τ2 to 1 ms to get short IPSPs did not affect our results qualitatively, since gmax was set by activity-dependent inhibition, and its value had to increase (to 12 nS) to compensate. In any case, the composite IPSP due to multiple granule cells has τf > 200 ms [36,37].)
		PG ─┤M	~100 (PG spines are connected to both M/T and ET i.e. ~250 cells)	IPSCs are similar to above G ─┤M synapse [38].	100 PG ─┤M on mitral tuft,	gmax = 1 nS, τ1 = 1 ms, τ2 = 20 ms; simulated IPSP: ~ –0.2 mV, τp ~ 28 ms, τf ~ 117 ms; (as above, we verified that setting τ2 = 1 ms with gmax = 30 nS did not change our results qualitatively.)
G	50 to 100 G per M/T [27]	M→G	100 spines [27]. Assume each spine has a reciprocal synapse.	EPSP ~3.5 mV in vivo [39]; τ-s from sources [39,40,33]; Mg-block voltage-dependence and NMDA to AMPA ratio from experiment [33].	2500 G-s per glomerulus: shared G-s were retained 1:1; but non-shared were aggregated 100:1; unconnected were pruned.	AMPA: gmax = 0.2 nS, τ1 = 1 ms, τ2 = 4 ms; NMDA: gmax = 0.26 × AMPA gmax, τ1 = 25 ms, τ2 = 200 ms; (3× for distal ‘super-inhibitory’ synapses); simulated EPSP: ~2 mV, τp ~ 13 ms, τf ~ 50 ms.

τ_p is the time to peak, and τ_f the time to fall (to 20% of peak) in the relevant cell. All synaptic conductances were modeled as dual exponential