1. Patterns of Ongoing Activity and the Functional Architecture of the Primary Visual Cortex 
Joshua A. Goldberg, Uri Rokni, Haim Sompolinsky 
Neuron 
Volume 42, Issue 3, Pages (May 2004)
DOI: /S (04)

2. Figure 1
Histogram of the Raw and Spike-Triggered Similarity Indices from the Experimental Optical Imaging Data
(A) All-times histogram of the SI.
(B) Histogram of the spike-triggered SI. These histograms were pooled from 12 recording sessions from five cats (adapted with permission from Tsodyks et al., Science 286, 1943–1946. Copyright 1999 American Association for the Advancement of Science).
Neuron  , DOI: ( /S (04) )

3. Figure 2
Schematic Representation of Evoked and Spontaneous Maps According to the Single and Multiple State Hypotheses
(A) In the ring model, the columns are arranged in a circle in orientation space according to their PO θ. Note that the circle ranges from 0° to 180° of orientation. The mean rate of each column is represented by its height above this circle. In the evoked state, the profile of firing rates in the network is hill shaped, centered about some orientation (here this orientation is zero).
(B) The time-averaged synaptic inputs h(θ) as a function of θ corresponding to the evoked state in panel (A). The dashed line marks the threshold.
(C) The set of evoked maps resides along a circle embedded within the two-dimensional subspace, termed the subspace of evoked maps. This subspace is spanned by two evoked maps and . The vector h(θ) in panel (B) corresponds to and is marked by a green arrow. The spontaneous maps (represented by the colored vectors) reside in the full N-dimensional space. In the single state scenario, the projection of the spontaneous map (blue vector) onto the subspace of evoked maps (blue dashed line) is small, whereas its component within the other N − 2 dimensions is large. In the multiple state scenario, the spontaneous map (red vector) is very close to one of the evoked maps. Consequently, its projection within the subspace of evoked maps (red dashed line) is large and it has a relatively small orthogonal component within the other dimensions.
Neuron  , DOI: ( /S (04) )

4. Figure 3 Network States of the Ring Model
(A) Phase diagram of the model. Abscissa: λ, gain of cortical interactions. Ordinate: T/σn is the ratio of the mean LGN drive to its standard deviation. H denotes the homogeneous phase. M denotes the marginal phase. I denotes the amplitude instability phase.
(B) Snapshot of the input h(θ) to the columns in the network as a function of their PO, θ, in the homogeneous phase (simulated for the point in the phase diagram in panel (A) marked by a diamond, λ = 1.2 and T/σn = −0.5).
(C) Snapshot of the input h(θ) in the marginal phase (calculated for the point in the phase diagram marked by an asterisk, λ = 1.2 and T/σn = 2).
Neuron  , DOI: ( /S (04) )

5. Figure 4
Spontaneous Map Fluctuations in the H and M Regimes of the Ring Model
(A–E) Fluctuations in the H regime (for the point in parameter space marked by a diamond in Figure 3A).
(F–J) Fluctuations in the M regime (for the point marked by an asterisk).
(A and F) Scatter plot of the projections of the spontaneous maps onto the evoked maps and .
(B and G) Distribution of the SI ρ. (Inset) The width σ of the distribution in the linear region of the H regime as a function of the cortical gain λ. Solid line, analytical solution (see Equation [S6] in the Supplemental Data at points, simulation results. σn = 1 and T = 3.
(C and H) Distribution of the spike-triggered SI ρspike. (Inset) The bias in the distribution of ρspike as a function of in the H regime, where N is the number of columns in the network. The bias is defined as the mean of this distribution normalized by the standard deviation of the distribution of ρ. Points, simulation results; solid line, linear fit.
(D and I) Temporal evolution of the SI ρ(t) as a function of time.
(E and J) Autocorrelation function (ACF) of ρ(t) as a function of the time lag Δ. Note the different time bases in panels (D) versus (I) and in (E) versus (J).
Neuron  , DOI: ( /S (04) )

6. Figure 5 Encoding Multiple Features in V1
(A–C) The unary multiple feature scenario.
(D–H) The combinatorial multiple feature scenario.
(A) The cortical states of orientation and direction are arranged on two distinct rings.
(B) The temporal evolution of the SIs of the network state with a state of orientation (ρo, thin line) and a state of direction (ρd, thick line).
(C) The distribution of ρo.
(D) The cortical states of orientation and spatial frequency are arranged on a sphere, such that the longitudinal angle θ represents orientation and the latitudinal angle φ represents spatial frequency.
(E) Scatter plot of the projections of the spontaneous maps onto the evoked maps and in the M regime, corresponding to the point in parameter space marked by an asterisk in Figure 3A.
(F) Distribution of the SI, ρ, in the M regime (for the point in parameter space marked by an asterisk in Figure 3A).
(G) The decay time τW of the ACF as a function of N, in the M regimes of the ring model (points) and the three-dimensional spherical model (crosses), calculated from network simulations. Solid lines, linear fit. τw was ex-tracted by fitting an exponential decay to the ACF for lags between 0 and 0.5 s.
(H) Analytical solution of the probability density function (pdf) of the SI, ρ, in the M regime of a d + 1 sphere of cortical states encoding d features at the large N limit (see Equation [S7] in the Supplemental Data at The number of features is indicated below each pdf.
Neuron  , DOI: ( /S (04) )

7. Figure 6 An Empirical Two-Dimensional Map of Preferred Orientations
(A) A color-coded angle map of POs (θ between −90° and 90°) derived from the optical imaging of a 3 mm × 3 mm region of the primary visual cortex (V1) of a cat (courtesy of T. Kenet, A. Arieli, and A. Grinvald).
(B) The distribution of POs derived from the angle map depicted in panel (A).
Neuron  , DOI: ( /S (04) )

8. Figure 7 The 2D Model—Uniform Distribution of POs
(A) The width of the distribution of the SI ρ, denoted σ, in the single state regime for λ = 0 as a function of the length-scale ξ of the correlations in the LGN input.
(B) Dependence of the width of distribution of the SI σ on the strength of cortical interactions λ. Here and for the remainder of the simulations of the full model, we chose ξ = 120 μm and T/σn = 2.
(C) A spontaneous map occurring in a simulation of the full model for λ = 0.6.
(D) An evoked map of zero orientation. The SI with the spontaneous map in panel (C) is 0.69.
(E) The histogram of the SI ρ for λ = 0.6.
(F) Distribution of ρspike for an ordinary column in the network.
(G) Tuning curve (arbitrary units) of an ordinary column in the network (dash-dotted line) and that of a “selective” column whose afferent cortical interactions were strengthened by a factor of 8 (solid line).
(H) Distribution of ρspike for the “selective” column.
(I) The decay time τW of the ACF as a function of ξ in the multiple state regime.
(J) Color-coded profile of cortical interactions with a spatial falloff impinging on a column located at the center of the patch. Length-scale of spatial falloff is 0.3 mm. red, excitation; dark blue, inhibition; light blue, zero.
Neuron  , DOI: ( /S (04) )

9. Figure 8 The 2D Model—Nonuniform Distribution of POs
(A) The scatter plot of the projections of the spontaneous maps onto the evoked maps and for λ = 0.6.
(B) Dependence of σ on the orientation ψ of the evoked map for λ = 0.6.
(C) The distribution of ρ for λ = 1.5.
Neuron  , DOI: ( /S (04) )