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16 nips-2006-A Theory of Retinal Population Coding


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Author: Eizaburo Doi, Michael S. Lewicki

Abstract: Efficient coding models predict that the optimal code for natural images is a population of oriented Gabor receptive fields. These results match response properties of neurons in primary visual cortex, but not those in the retina. Does the retina use an optimal code, and if so, what is it optimized for? Previous theories of retinal coding have assumed that the goal is to encode the maximal amount of information about the sensory signal. However, the image sampled by retinal photoreceptors is degraded both by the optics of the eye and by the photoreceptor noise. Therefore, de-blurring and de-noising of the retinal signal should be important aspects of retinal coding. Furthermore, the ideal retinal code should be robust to neural noise and make optimal use of all available neurons. Here we present a theoretical framework to derive codes that simultaneously satisfy all of these desiderata. When optimized for natural images, the model yields filters that show strong similarities to retinal ganglion cell (RGC) receptive fields. Importantly, the characteristics of receptive fields vary with retinal eccentricities where the optical blur and the number of RGCs are significantly different. The proposed model provides a unified account of retinal coding, and more generally, it may be viewed as an extension of the Wiener filter with an arbitrary number of noisy units. 1

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Summary: the most important sentenses genereted by tfidf model

sentIndex sentText sentNum sentScore

1 edu Abstract Efficient coding models predict that the optimal code for natural images is a population of oriented Gabor receptive fields. [sent-6, score-0.724]

2 These results match response properties of neurons in primary visual cortex, but not those in the retina. [sent-7, score-0.14]

3 Does the retina use an optimal code, and if so, what is it optimized for? [sent-8, score-0.165]

4 Previous theories of retinal coding have assumed that the goal is to encode the maximal amount of information about the sensory signal. [sent-9, score-0.906]

5 However, the image sampled by retinal photoreceptors is degraded both by the optics of the eye and by the photoreceptor noise. [sent-10, score-0.977]

6 Therefore, de-blurring and de-noising of the retinal signal should be important aspects of retinal coding. [sent-11, score-1.231]

7 Furthermore, the ideal retinal code should be robust to neural noise and make optimal use of all available neurons. [sent-12, score-0.867]

8 When optimized for natural images, the model yields filters that show strong similarities to retinal ganglion cell (RGC) receptive fields. [sent-14, score-1.021]

9 Importantly, the characteristics of receptive fields vary with retinal eccentricities where the optical blur and the number of RGCs are significantly different. [sent-15, score-1.305]

10 The proposed model provides a unified account of retinal coding, and more generally, it may be viewed as an extension of the Wiener filter with an arbitrary number of noisy units. [sent-16, score-0.605]

11 The retina has numerous specialized classes of retinal ganglion cells (RGCs) that are likely to subserve a variety of different tasks [1]. [sent-18, score-0.749]

12 An important class directly subserving visual perception is the midget RGCs (mRGCs) which constitute 70% of RGCs with an even greater proportion at the fovea [1]. [sent-19, score-0.266]

13 The problem that mRGCs face should be to maximally preserve signal information in spite of the limited representational capacity, which is imposed both by neural noise and the population size. [sent-20, score-0.408]

14 This problem was recently addressed (although not specifically as a model of mRGCs) in [2], which derived the theoretically optimal linear coding method for a noisy neural population. [sent-21, score-0.393]

15 This model is not appropriate, however, for the mRGCs, because it does not take into account the noise in the retinal image (Fig. [sent-22, score-0.722]

16 Before being projected on the retina, the visual stimulus is distorted by the optics of the eye in a manner that depends on eccentricity [3]. [sent-24, score-0.282]

17 This retinal image is then sampled by cone photoreceptors whose sampling density also varies with eccentricity [1]. [sent-25, score-0.947]

18 Finally, the sampled image is noisier in the dimmer illumination condition [4]. [sent-26, score-0.142]

19 We conjecture that the computational goal of mRGCs is to represent the maximum amount of information about the underlying, non-degraded image signal subject to limited coding precision and neural population size. [sent-27, score-0.569]

20 This may be viewed as a generalization of both Wiener filtering [5] and robust coding [2]. [sent-29, score-0.23]

21 One significant characteristic of the proposed model is that it can make optimal use of an arbitrary number of neurons in order to preserve the maximum amount of signal information. [sent-30, score-0.236]

22 This allows the model to predict theoretically optimal representations at any retinal eccentricity in contrast to the earlier studies [4, 6, 7, 8]. [sent-31, score-0.831]

23 (b) Fovea retinal image (c) 40 degrees eccentricity Intensity (a) Undistorted image -4 0 -4 4 Visual angle [arc min] 0 4 Figure 1: Simulation of retinal images at different retinal eccentricities. [sent-32, score-2.092]

24 (b) The convolution kernel at the fovea [3] superimposed on the photoreceptor array indicated by triangles under the x-axis [1]. [sent-34, score-0.33]

25 (c) The same as in (b) but at 40 degrees of retinal eccentricity. [sent-35, score-0.633]

26 We assume that data sampled by photoreceptors (referred to as the observation) x ∈ RN are blurred versions of the underlying image signal s ∈ RN with 2 additive white noise ν ∼ N (0, σν IN ), x = Hs + ν (1) where H ∈ RN ×N implements the optical blur. [sent-38, score-0.531]

27 To model limited neural pre2 cision, it is assumed that the representation is subject to additive channel noise, δ ∼ N (0, σδ IM ). [sent-40, score-0.21]

28 The noisy neural representation is therefore expressed as r = W(Hs + ν) + δ (2) M ×N where each row of W ∈ R corresponds to a receptive field. [sent-41, score-0.416]

29 To evaluate the amount of signal information preserved in the representation, we consider a linear reconstruciton ˆ = Ar where s A ∈ RN ×M . [sent-42, score-0.091]

30 To model limited neural capacity, the representation r must have limited SNR. [sent-45, score-0.162]

31 This constraint is T 2 equivalent to fixing the variance of filter output wj x = σu , where wj is the j-th row of W (here we assume all neurons have the same capacity). [sent-46, score-0.091]

32 It can further be simplified to diag[VVT ] W = 1M , = ν s image H δ encoder x observation (7) channel noise sensory noise optical blur (6) σu VS−1 ET , x W decoder r representation A ˆ s reconstruction 2 Figure 2: The model diagram. [sent-48, score-0.933]

33 If there is no degradation of the image (H = I and σν = 0), the 2 model is reduced to the original robust coding model [2]. [sent-49, score-0.342]

34 If channel noise is zero as well (σδ = 0), it boils down to conventional block coding such as PCA, ICA, or wavelet transforms. [sent-50, score-0.32]

35 Note that αk defines the modulation transfer function of the optical blur H, i. [sent-52, score-0.484]

36 , the attenuation of the amplitude of the signal along the k-th eigenvector. [sent-54, score-0.091]

37 This implies that the optimal A is determined once the optimal V is found. [sent-57, score-0.108]

38 Solutions for 2-D data In this section we present the explicit characterization of the optimal solutions for two-dimensional data. [sent-62, score-0.122]

39 It entails under-complete, complete, and over-complete representations, and provides precise insights into the numerical solutions for the high-dimensional image data (Section 3). [sent-63, score-0.135]

40 This is a generalization of the analysis in [2] with the addition of optical blur and additive sensory noise. [sent-64, score-0.58]

41 cos θM (11) where θj ∈ [0, 2π), j = 1, · · · , M , which yields 2 E= λk (1 − φk ) + (ψ1 + ψ2 ) k=1 M 2 2 γ M 2 2 γ γ2 2 (ψ1 − ψ2 ) Re(Z) , 2 − 1 γ 4 |Z|2 4 +1 − +1 (12) with ψk ≡ φk λk and Z ≡ j (cos 2θj + i sin 2θj ). [sent-72, score-0.129]

42 (In the previous analysis of robust coding [2], these cases depend only on the ratio between λ1 and λ2 , i. [sent-75, score-0.268]

43 In the current, general model, these also depend on the isotropy of the 2 optical blur (α1 and α2 ) and the variance of sensory noise (σν ), and no simple meaning is attatched to the individual cases. [sent-78, score-0.663]

44 If M = 1 (single neuron case): By definition |Z|2 = 1, implying that E is constant for any θ1 , E W λ1 (1 − φ1 ) + = = σu ( cos θ1 ψ1 + λ2 = γ2 + 1 sin θ1 ) λ2 (1 − φ2 ) + 2 1/ α1 λ1 + σν 0 ψ2 + λ1 , γ2 + 1 0 2 1/ α2 λ2 + σν ET . [sent-85, score-0.185]

45 If M ≥ 2 (multiple neuron case): There always exists Z that satisfies |Z| = 0 if M ≥ 2, with which E is minimized [2]. [sent-91, score-0.123]

46 It implies that having n times the neurons is equivalent to increasing the representation SNR by the factor of n (this relation generally holds in the multiple neuron cases below). [sent-97, score-0.207]

47 If M = 1 (single neuron case): Z = Re(Z) holds iff θ1 = 0. [sent-103, score-0.087]

48 14-15) except that the direction of the representation is specified along the first eigenvector e1 , indicating that all the representational resources (namely, one neuron) are devoted to the largest data variance direction. [sent-106, score-0.088]

49 (21) γ γ ψ1 + ψ 2 ψ1 − ψ2 The existence of a root y in the domain [0, M ] depends on how γ 2 compares to the next quantity, which is a generalized form of the critical point of neural precision [2]: 2 γc = 1 M ψ1 −1 . [sent-110, score-0.136]

50 The optimal solutions are 2 E = k=1 W √ √ ( ψ1 + ψ2 )2 λk (1 − φk ) + M 2 , 2 2 γ +1 = σu V 1 2 1/ α1 λ1 + σν 0 0 2 1/ α2 λ2 + σν (26) ET , (27) where V is arbitrary up to satisfying eqn. [sent-120, score-0.122]

51 The general strategy of the proposed model is to represent the principal axis of the signal s more accurately as the signal is more degraded (by optical blur and/or sensory noise). [sent-124, score-0.768]

52 Specifically, the two neurons come to represent the identical dimension when the degradation is sufficiently large. [sent-125, score-0.136]

53 10dB 0dB -10dB blur no-blur 20dB Figure 3: Sensory noise changes the optimal linear filter. [sent-126, score-0.374]

54 The bottom row is the case where the power of the signal’s minor component is attenuated as in the optical blur (i. [sent-129, score-0.43]

55 3 Optimal receptive field populations We applied the proposed model to a natural images data set [11] to obtain the theoretically optimal population coding for mRGCs. [sent-134, score-0.699]

56 The optimal solutions were derived under the following biological constraints on the observation, or the photoreceptor response, x (Fig. [sent-135, score-0.26]

57 To model the retinal images at different retinal eccentricities, we used modulation transfer functions of the human eye [3] and cone photoreceptor densities of the human retina [1] (Fig. [sent-137, score-1.693]

58 The retinal image is further corrupted by the additive Gaussian noise to model the photon transduction noise by which the SNR of the observartion becomes smaller under dimmer illumination level [4]. [sent-139, score-0.923]

59 The information capacity of neural representations is limited by both the number of neurons and the precision of neural codes. [sent-142, score-0.347]

60 The ratio of cone photoreceptors to mRGCs in the human retina is 1 : 2 at the fovea and 23 : 2 at 40 degrees [13]. [sent-143, score-0.63]

61 We did not model neural rectification (separate on and off channels) and thus assumed the effective cell ratios as 1 : 1 and 23 : 1, respectively. [sent-144, score-0.106]

62 The optimal W can be derived with the gradient descent on E, and A can be derived from W using eqn. [sent-147, score-0.104]

63 Our initial results indicated that the optimal solutions are not unique and these solutions are equivalent in terms of MSE. [sent-153, score-0.19]

64 For the fovea, we examined 15×15 pixel image patches sampled from a large set of natural images, where each pixel corresponds to a cone photoreceptor. [sent-159, score-0.142]

65 Since the cell ratio is assumed to be 1 : 1, there were 225 model neurons in the population. [sent-160, score-0.182]

66 The precise organization of the model receptive field changes according to the SNR of the observation: as the SNR decreases, the surround inhibition gradually disappears and the center becomes larger, which serves to remove sensory noise by averaging. [sent-163, score-0.586]

67 As a population, this yields a significant overlap among adjacent receptive fields. [sent-164, score-0.33]

68 In terms of spatial-frequency, this change corresponds to a shift from band-pass to low-pass filtering, which is consistent with psychophysical measurements of the human and the macaque [17]. [sent-165, score-0.094]

69 Figure 4: The model receptive fields at the fovea under different SNRs of the observation. [sent-167, score-0.516]

70 (c) The tiling of a population of receptive fields in the visual field. [sent-170, score-0.427]

71 The ellipses show the contour of receptive fields at half the maximum. [sent-171, score-0.299]

72 (d) Spatial-frequency profiles (modulation transfer functions) of the receptive fields at different SNRs. [sent-174, score-0.339]

73 For 40 degrees retinal eccentricity, we examined 35×35 photoreceptor array that are projected to 53 model neurons (so that the cell ratio is 23 : 1). [sent-175, score-0.928]

74 The general trend of the results is the same as in the fovea except that the receptive fields are much larger. [sent-176, score-0.516]

75 This allows the fewer neurons in the population to completely tile the visual field. [sent-177, score-0.219]

76 Furthermore, the change of the receptive field with the sensory noise level is not as significant as that predicted for the fovea, suggesting that the SNR is a less significant factor when neural number is severely limited. [sent-178, score-0.585]

77 We also note that the elliptical shape of the extent of the receptive fields matches experimental observations [12]. [sent-179, score-0.299]

78 20dB -10dB Figure 5: The theoretically- derived receptive fields for 40 degrees of the retinal eccentricity. [sent-180, score-0.957]

79 Finally, we demonstrate the performance of de- blurring, de- noising, and information preservation by these receptive fields (Fig. [sent-183, score-0.299]

80 The original image is well recovered in spite of both the noisy representation (10% of the code’s variation is noise because of the 10 dB precision) and the noisy, degraded observation. [sent-185, score-0.291]

81 Note that the 40 degrees eccentricity is subject to an additional, significant dimensionality reduction, which is why the reconstruction error (e. [sent-186, score-0.246]

82 For both the fovea and 40 degrees retinal eccentricity, two sensory noise conditions are shown (20 and −10 dB). [sent-201, score-1.083]

83 The percentages indicate the average distortion in the observation or the reconstruction error, respectively, over 60,000 samples. [sent-202, score-0.106]

84 The blocking effect is caused by the implementation of the optical blur on each image patch using a matrix H instead of convolving the whole image. [sent-203, score-0.458]

85 If there 2 is no sensory noise σν = 0 and no optical blur H = IN , then φk = 1 for all k, which reduces all the optimal solutions above to those reported in [2]. [sent-205, score-0.746]

86 The optimal solution is given by the Wiener filter: s √ √ α1 λ1 αN λN 2 ,··· , ET , (29) W = Σs HT [HΣs HT + σν IN ]−1 = E diag 2 2 α1 λ1 + σν αN λN + σν E = tr[Σs ] − tr[WHΣs ] = N k=1 λk (1 − φk ), (30) (note that the diagonal matrix in eqn. [sent-207, score-0.13]

87 Here, we have treated the model primarily as a theory of retinal coding, but its generality would allow it to be applied to a wide range of problems in signal processing. [sent-210, score-0.689]

88 Modeling non-Gaussian signal distributions might account for coding efficiency constraints on the retinal population. [sent-213, score-0.849]

89 There have been earlier approaches to theoretically characterizing the retinal code [4, 6, 7, 8]. [sent-215, score-0.696]

90 First, it is not restricted to the so-called complete representation (M = N ) and can predict properties of mRGCs at any retinal eccentricity. [sent-217, score-0.599]

91 Second, we do not assume a single, translation invariant filter and can derive the optimal receptive fields for a neural population. [sent-218, score-0.406]

92 Third, we accurately model optical blur, retinal sampling, cell ratio, and neural precision. [sent-219, score-0.832]

93 Finally, we assumed that, as in [4, 8], the objective of the retinal coding is to form the neural code that yields the minimum MSE with linear decoding, while others assumed it to form the neural code that maximally preserves information about signal [6, 7]. [sent-220, score-1.112]

94 To the best of our knowledge, we don’t know a priori which objective should be appropriate for the retinal coding. [sent-221, score-0.57]

95 A theoretical analysis of robust coding over noisy overcomplete channels. [sent-234, score-0.293]

96 Modulation transfer of the human eye as a function of retinal eccentricity. [sent-242, score-0.695]

97 Theoretical predictions of spatiotemporal receptive fields of fly LMCs, and experimental validation. [sent-273, score-0.299]

98 Spatiochromatic receptive field properties derived from information-theoretic analyses of cone mosaic responses to natural scenes. [sent-305, score-0.399]

99 Fidelity of the ensemble code for visual motion in primate retina. [sent-318, score-0.141]

100 Sparse coding of natural images using an overcomplete set of limited capacity units. [sent-337, score-0.356]


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Author: Joseph M. Kimmel, Richard M. Salter, Peter J. Thomas

Abstract: Chemical reaction networks by which individual cells gather and process information about their chemical environments have been dubbed “signal transduction” networks. Despite this suggestive terminology, there have been few attempts to analyze chemical signaling systems with the quantitative tools of information theory. Gradient sensing in the social amoeba Dictyostelium discoideum is a well characterized signal transduction system in which a cell estimates the direction of a source of diffusing chemoattractant molecules based on the spatiotemporal sequence of ligand-receptor binding events at the cell membrane. Using Monte Carlo techniques (MCell) we construct a simulation in which a collection of individual ligand particles undergoing Brownian diffusion in a three-dimensional volume interact with receptors on the surface of a static amoeboid cell. Adapting a method for estimation of spike train entropies described by Victor (originally due to Kozachenko and Leonenko), we estimate lower bounds on the mutual information between the transmitted signal (direction of ligand source) and the received signal (spatiotemporal pattern of receptor binding/unbinding events). Hence we provide a quantitative framework for addressing the question: how much could the cell know, and when could it know it? We show that the time course of the mutual information between the cell’s surface receptors and the (unknown) gradient direction is consistent with experimentally measured cellular response times. We find that the acquisition of directional information depends strongly on the time constant at which the intracellular response is filtered. 1 Introduction: gradient sensing in eukaryotes Biochemical signal transduction networks provide the computational machinery by which neurons, amoebae or other single cells sense and react to their chemical environments. The precision of this chemical sensing is limited by fluctuations inherent in reaction and diffusion processes involving a ∗ Current address: Computational Neuroscience Graduate Program, The University of Chicago. Oberlin Center for Computation and Modeling, http://occam.oberlin.edu/. ‡ To whom correspondence should be addressed. http://www.case.edu/artsci/math/thomas/thomas.html; Oberlin College Research Associate. † finite quantity of molecules [1, 2]. The theory of communication provides a framework that makes explicit the noise dependence of chemical signaling. For example, in any reaction A + B → C, we may view the time varying reactant concentrations A(t) and B(t) as input signals to a noisy channel, and the product concentration C(t) as an output signal carrying information about A(t) and B(t). In the present study we show that the mutual information between the (known) state of the cell’s surface receptors and the (unknown) gradient direction follows a time course consistent with experimentally measured cellular response times, reinforcing earlier claims that information theory can play a role in understanding biochemical cellular communication [3, 4]. Dictyostelium is a soil dwelling amoeba that aggregates into a multicellular form in order to survive conditions of drought or starvation. During aggregation individual amoebae perform chemotaxis, or chemically guided movement, towards sources of the signaling molecule cAMP, secreted by nearby amoebae. Quantitive studies have shown that Dictyostelium amoebae can sense shallow, static gradients of cAMP over long time scales (∼30 minutes), and that gradient steepness plays a crucial role in guiding cells [5]. The chemotactic efficiency (CE), the population average of the cosine between the cell displacement directions and the true gradient direction, peaks at a cAMP concentration of 25 nanoMolar, similar to the equilibrium constant for the cAMP receptor (the Keq is the concentration of cAMP at which the receptor has a 50% chance of being bound or unbound, respectively). For smaller or larger concentrations the CE dropped rapidly. Nevertheless over long times cells were able (on average) to detect gradients as small as 2% change in [cAMP] per cell length. At an early stage of development when the pattern of chemotactic centers and spirals is still forming, individual amoebae presumably experience an inchoate barrage of weak, noisy and conflicting directional signals. When cAMP binds receptors on a cell’s surface, second messengers trigger a chain of subsequent intracellular events including a rapid spatial reorganization of proteins involved in cell motility. Advances in fluorescence microscopy have revealed that the oriented subcellular response to cAMP stimulation is already well underway within two seconds [6, 7]. In order to understand the fundamental limits to communication in this cell signaling process we abstract the problem faced by a cell to that of rapidly identifying the direction of origin of a stimulus gradient superimposed on an existing mean background concentration. We model gradient sensing as an information channel in which an input signal – the direction of a chemical source – is noisily transmitted via a gradient of diffusing signaling molecules; and the “received signal” is the spatiotemporal pattern of binding events between cAMP and the cAMP receptors [8]. We neglect downstream intracellular events, which cannot increase the mutual information between the state of the cell and the direction of the imposed extracellular gradient [9]. The analysis of any signal transmission system depends on precise representation of the noise corrupting transmitted signals. We develop a Monte Carlo simulation (MCell, [10, 11]) in which a simulated cell is exposed to a cAMP distribution that evolves from a uniform background to a gradient at low (1 nMol) average concentration. The noise inherent in the communication of a diffusionmediated signal is accurately represented by this method. Our approach bridges both the transient and the steady state regimes and allows us to estimate the amount of stimulus-related information that is in principle available to the cell through its receptors as a function of time after stimulus initiation. Other efforts to address aspects of cell signaling using the conceptual tools of information theory have considered neurotransmitter release [3] and sensing temporal signals [4], but not gradient sensing in eukaryotic cells. A typical natural habitat for social amoebae such as Dictyostelium is the complex anisotropic threedimensional matrix of the forest floor. Under experimental conditions cells typically aggregate on a flat two-dimensional surface. We approach the problem of gradient sensing on a sphere, which is both harder and more natural for the ameoba, while still simple enough for us analytically and numerically. Directional data is naturally described using unit vectors in spherical coordinates, but the ameobae receive signals as binding events involving intramembrane protein complexes, so we have developed a method for projecting the ensemble of receptor bindings onto coordinates in R3 . In loose analogy with the chemotactic efficiency [5], we compare the projected directional estimate with the true gradient direction represented as a unit vector on S2 . Consistent with observed timing of the cell’s response to cAMP stimulation, we find that the directional signal converges quickly enough for the cell to make a decision about which direction to move within the first two seconds following stimulus onset. 2 Methods 2.1 Monte Carlo simulations Using MCell and DReAMM [10, 11] we construct a spherical cell (radius R = 7.5µm, [12]) centered in a cubic volume (side length L = 30µm). N = 980 triangular tiles partition the surface (mesh generated by DOME1 ); each contained one cell surface receptor for cAMP with binding rate k+ = 4.4 × 107 sec−1 M−1 , first-order cAMP unbinding rate k− = 1.1 sec−1 [12] and Keq = k− /k+ = 25nMol cAMP. We established a baseline concentration of approximately 1nMol by releasing a cAMP bolus at time 0 inside the cube with zero-flux boundary conditions imposed on each wall. At t = 2 seconds we introduced a steady flux at the x = −L/2 wall of 1 molecule of cAMP per square micron per msec, adding signaling molecules from the left. Simultaneously, the x = +L/2 wall of the cube assumes absorbing boundary conditions. The new boundary conditions lead (at equilibrium) to a linear gradient of 2 nMol/30µm, ranging from ≈ 2.0 nMol at the flux source wall to ≈ 0 nMol at the absorbing wall (see Figure 1); the concentration profile approaches this new steady state with time constant of approximately 1.25 msec. Sampling boxes centered along the planes x = ±13.5µm measured the local concentration, allowing us to validate the expected model behavior. Figure 1: Gradient sensing simulations performed with MCell (a Monte Carlo simulator of cellular microphysiology, http://www.mcell.cnl.salk.edu/) and rendered with DReAMM (Design, Render, and Animate MCell Models, http://www.mcell.psc.edu/). The model cell comprised a sphere triangulated with 980 tiles with one cAMP receptor per tile. Cell radius R = 7.5µm; cube side L = 30µm. Left: Initial equilibrium condition, before imposition of gradient. [cAMP] ≈ 1nMol (c. 15,000 molecules in the volume outside the sphere). Right: Gradient condition after transient (c. 15,000 molecules; see Methods for details). 2.2 Analysis 2.2.1 Assumptions We make the following assumptions to simplify the analysis of the distribution of receptor activities at equilibrium, whether pre- or post-stimulus onset: 1. Independence. At equilibrium, the state of each receptor (bound vs unbound) is independent of the states of the other receptors. 2. Linear Gradient. At equilibrium under the imposed gradient condition, the concentration of ligand molecule varies linearly with position along the gradient axis. 3. Symmetry. 1 http://nwg.phy.bnl.gov/∼bviren/uno/other/ (a) Rotational equivariance of receptor activities. In the absence of an applied gradient signal, the probability distribution describing the receptor states is equivariant with respect to arbitrary rotations of the sphere. (b) Rotational invariance of gradient direction. The imposed gradient seen by a model cell is equally likely to be coming from any direction; therefore the gradient direction vector is uniformly distributed over S2 . (c) Axial equivariance about the gradient direction. Once a gradient direction is imposed, the probability distribution describing receptor states is rotationally equivariant with respect to rotations about the axis parallel with the gradient. Berg and Purcell [1] calculate the inaccuracy in concentration estimates due to nonindependence of adjacent receptors; for our parameters (effective receptor radius = 5nm, receptor spacing ∼ 1µm) the fractional error in estimating concentration differences due to receptor nonindependence is negligible ( 10−11 ) [1, 2]. Because we fix receptors to be in 1:1 correspondence with surface tiles, spherical symmetry and uniform distribution of the receptors are only approximate. The gradient signal communicated via diffusion does not involve sharp spatial changes on the scale of the distance between nearby receptors, therefore spherical symmetry and uniform identical receptor distribution are good analytic approximations of the model configuration. By rotational equivariance we mean that combining any rotation of the sphere with a corresponding rotation of the indices labeling the N receptors, {j = 1, · · · , N }, leads to a statistically indistinguishable distribution of receptor activities. This same spherical symmetry is reflected in the a priori distribution of gradient directions, which is uniform over the sphere (with density 1/4π). Spherical symmetry is broken by the gradient signal, which fixes a preferred direction in space. About this axis however, we assume the system retains the rotational symmetry of the cylinder. 2.2.2 Mutual information of the receptors In order to quantify the directional information available to the cell from its surface receptors we construct an explicit model for the receptor states and the cell’s estimated direction. We model the receptor states via a collection of random variables {Bj } and develop an expression for the entropy of {Bj }. Then in section 2.2.3 we present a method for projecting a temporally filtered estimated direction, g , into three (rather than N ) dimensions. ˆ N Let the random variables {Bj }j=1 represent the states of the N cAMP receptors on the cell surface; Bj = 1 if the receptor is bound to a molecule of cAMP, otherwise Bj = 0. Let xj ∈ S2 represent the direction from the center of the center of the cell to the j th receptor. Invoking assumption 2 above, we take the equilibrium concentration of cAMP at x to be c(x|g) = a + b(x · g) where g ∈ S2 is a unit vector in the direction of the gradient. The parameter a is the mean concentration over the cell surface, and b = R| c| is half the drop in concentration from one extreme on the cell surface to the other. Before the stimulus begins, the gradient direction is undefined. It can be shown (see Supplemental Materials) that the entropy of receptor states given a fixed gradient direction g, H[{Bj }|g], is given by an integral over the sphere: π 2π a + b cos(θ) sin(θ) dφ dθ (as N → ∞). (1) a + b cos(θ) + Keq 4π θ=0 φ=0 On the other hand, if the gradient direction remains unspecified, the entropy of receptor states is given by H[{Bj }|g] ∼ N Φ π 2π θ=0 φ=0 H[{Bj }] ∼ N Φ a + b cos(θ) a + b cos(θ) + Keq sin(θ) dφ dθ (as N → ∞), 4π − (p log2 (p) + (1 − p) log2 (1 − p)) , 0 < p < 1 0, p = 0 or 1 binary random variable with state probabilities p and (1 − p). where Φ[p] = (2) denotes the entropy for a In both equations (1) and (2), the argument of Φ is a probability taking values 0 ≤ p ≤ 1. In (1) the values of Φ are averaged over the sphere; in (2) Φ is evaluated after averaging probabilities. Because Φ[p] is convex for 0 ≤ p ≤ 1, the integral in equation 1 cannot exceed that in equation 2. Therefore the mutual information upon receiving the signal is nonnegative (as expected): ∆ M I[{Bj }; g] = H[{Bj }] − H[{Bj }|g] ≥ 0. The analytic solution for equation (1) involves the polylogarithm function. For the parameters shown in the simulation (a = 1.078 nMol, b = .512 nMol, Keq = 25 nMol), the mutual information with 980 receptors is 2.16 bits. As one would expect, the mutual information peaks when the mean concentration is close to the Keq of the receptor, exceeding 16 bits when a = 25, b = 12.5 and Keq = 25 (nMol). 2.2.3 Dimension reduction The estimate obtained above does not give tell us how quickly the directional information available to the cell evolves over time. Direct estimate of the mutual information from stochastic simulations is impractical because the aggregate random variables occupy a 980 dimensional space that a limited number of simulation runs cannot sample adequately. Instead, we construct a deterministic function from the set of 980 time courses of the receptors, {Bj (t)}, to an aggregate directional estimate in R3 . Because of the cylindrical symmetry inherent in the system, our directional estimator g is ˆ an unbiased estimator of the true gradient direction g. The estimator g (t) may be thought of as ˆ representing a downstream chemical process that accumulates directional information and decays with some time constant τ . Let {xj }N be the spatial locations of the N receptors on the cell’s j=1 surface. Each vector is associated with a weight wj . Whenever the j th receptor binds a cAMP molecule, wj is incremented by one; otherwise wj decays with time constant τ . We construct an instantaneous estimate of the gradient direction from the linear combination of receptor positions, N gτ (t) = j=1 wj (t)xj . This procedure reflects the accumulation and reabsorption of intracellular ˆ second messengers released from the cell membrane upon receptor binding. Before the stimulus is applied, the weighted directional estimates gτ are small in absolute magniˆ tude, with direction uniformly distributed on S2 . In order to determine the information gained as the estimate vector evolves after stimulus application, we wish to determine the change in entropy in an ensemble of such estimates. As the cell gains information about the direction of the gradient signal from its receptors, the entropy of the estimate should decrease, leading to a rise in mutual information. By repeating multiple runs (M = 600) of the simulation we obtain samples from the ensemble of direction estimates, given a particular stimulus direction, g. In the method of Kozachenko and Leonenko [13], adapted for the analysis of neural spike train data by Victor [14] (“KLV method”), the cumulative distribution function is approximated directly from the observed samples, and the entropy is estimated via a change of variables transformation (see below). This method may be formulated in vector spaces Rd for d > 1 ([13]), but it is not guaranteed to be unbiased in the multivariate case [15] and has not been extended to curved manifolds such as the sphere. In the present case, however, we may exploit the symmetries inherent in the model (Assumptions 3a-3c) to reduce the empirical entropy estimation problem to one dimension. Adapting the argument in [14] to the case of spherical data from a distribution with rotational symmetry about a given axis, we obtain an estimate of the entropy based on a series of observations of the angles {θ1 , · · · , θM } between the estimates gτ and the true gradient direction g (for details, see ˆ Supplemental Materials): 1 H∼ M M log2 (λk ) + log2 (2(M − 1)) + k=1 γ + log2 (2π) + log2 (sin(θk )) loge (2) (3) ∆ (as M → ∞) where after sorting the θk in monotonic order, λk = min(|θk − θk±1 |) is the distance between each angle and its nearest neighbor in the sample, and γ is the Euler-Mascheroni constant. As shown in Figure 2, this approximation agrees with the analytic result for the uniform distribution, Hunif = log2 (4π) ≈ 3.651. 3 Results Figure 3 shows the results of M = 600 simulation runs. Panel A shows the concentration averaged across a set of 1µm3 sample boxes, four in the x = −13.5µm plane and four in the x = +13.5µm Figure 2: Monte Carlo simulation results and information analysis. A: Average concentration profiles along two planes perpendicular to the gradient, at x = ±13.5µm. B: Estimated direction vector (x, y, and z components; x = dark blue trace) gτ , τ = 500 msec. C: Entropy of the ensemble of diˆ rectional vector estimates for different values of the intracellular filtering time constant τ . Given the directions of the estimates θk , φk on each of M runs, we calculate the entropy of the ensemble using equation (3). All time constants yield uniformly distributed directional estimates in the pre-stimulus period, 0 ≤ t ≤ 2 (sec). After stimulus onset, directional estimates obtained with shorter time constants respond more quickly but achieve smaller gains in mutual information (smaller reductions in entropy). Filtering time constants τ range from lightest to darkest colors: 20, 50, 100, 200, 500, 1000, 2000 msec. plane. The initial bolus of cAMP released into the volume at t = 0 sec is not uniformly distributed, but spreads out evenly within 0.25 sec. At t = 2.0 sec the boundary conditions are changed, causing a gradient to emerge along a realistic time course. Consistent with the analytic solution for the mean concentration (not shown), the concentration approaches equilibrium more rapidly near the absorbing wall (descending trace) than at the imposed flux wall (ascending trace). Panel B shows the evolution of a directional estimate vector gτ for a single run, with τ = 500 ˆ msec. During uniform conditions all vectors fluctuate near the origin. After gradient onset the variance increases and the x component (dark trace) becomes biased towards the gradient source (g = [−1, 0, 0]) while the y and z components still have a mean of zero. Across all 600 runs the mean of the y and z components remains close to zero, while the mean of the x component systematically departs from zero shortly after stimulus onset (not shown). Hence the directional estimator is unbiased (as required by symmetry). See Supplemental Materials for the population average of g . ˆ Panel C shows the time course of the entropy of the ensemble of normalized directional estimate vectors gτ /|ˆτ | over M = 600 simulations, for intracellular filtering time constants ranging from 20 ˆ g msec to 2000 msec (light to dark shading), calculated using equation (3). Following stimulus onset, entropy decreases steadily, showing an increase in information available to the amoeba about the direction of the stimulus; the mutual information at a given point in time is the difference between the entropy at that time and before stimulus onset. For a cell with roughly 1000 receptors the mutual information has increased at most by ∼ 2 bits of information by one second (for τ = 500 msec), and at most by ∼ 3 bits of information by two seconds (for τ =1000 or 2000 msec), under our stimulation protocol. A one bit reduction in uncertainty is equivalent to identifying the correct value of the x component (positive versus negative) when the stimulus direction is aligned along the x-axis. Alternatively, note that a one bit reduction results in going from the uniform distribution on the sphere to the uniform distribution on one hemisphere. For τ ≤ 100 msec, the weighted average with decay time τ never gains more than one bit of information about the stimulus direction, even at long times. This observation suggestions that signaling must involve some chemical components with lifetimes longer than 100 msec. The τ = 200 msec filter saturates after about one second, at ∼ 1 bit of information gain. Longer lived second messengers would respond more slowly to changes from the background stimulus distribution, but would provide better more informative estimates over time. The τ = 500 msec estimate gains roughly two bits of information within 1.5 seconds, but not much more over time. Heuristically, we may think of a two bit gain in information as corresponding to the change from a uniform distribution to one covering uniformly covering one quarter of S2 , i.e. all points within π/3 of the true direction. Within two seconds the τ = 1000 msec and τ = 2000 msec weighted averages have each gained approximately three bits of information, equivalent to a uniform distribution covering all points with 0.23π or 41o of the true direction. 4 Discussion & conclusions Clearly there is an opportunity for more precise control of experimental conditions to deepen our understanding of spatio-temporal information processing at the membranes of gradient-sensitive cells. Efforts in this direction are now using microfluidic technology to create carefully regulated spatial profiles for probing cellular responses [16]. Our results suggest that molecular processes relevant to these responses must have lasting effects ≥ 100 msec. We use a static, immobile cell. Could cell motion relative to the medium increase sensitivity to changes in the gradient? No: the Dictyostelium velocity required to affect concentration perception is on order 1cm sec−1 [1], whereas reported velocities are on the order µm sec−1 [5]. The chemotactic response mechanism is known to begin modifying the cell membrane on the edge facing up the gradient within two seconds after stimulus initiation [7, 6], suggesting that the cell strikes a balance between gathering data and deciding quickly. Indeed, our results show that the reported activation of the G-protein signaling system on the leading edge of a chemotactically responsive cell [7] rises at roughly the same rate as the available chemotactic information. Results such as these ([7, 6]) are obtained by introducing a pipette into the medium near the amoeba; the magnitude and time course of cAMP release are not precisely known, and when estimated the cAMP concentration at the cell surface is over 25 nMol by a full order of magnitude. Thomson and Kristan [17] show that for discrete probability distributions and for continuous distributions over linear spaces, stimulus discriminability may be better quantified using ideal observer analysis (mean squared error, for continuous variables) than information theory. The machinery of mean squared error (variance, expectation) do not carry over to the case of directional data without fundamental modifications [18]; in particular the notion of mean squared error is best represented by the mean resultant length 0 ≤ ρ ≤ 1, the expected length of the vector average of a collection of unit vectors representing samples from directional data. A resultant with length ρ ≈ 1 corresponds to a highly focused probability density function on the sphere. In addition to measuring the mutual information between the gradient direction and an intracellular estimate of direction, we also calculated the time evolution of ρ (see Supplemental Materials.) We find that ρ rapidly approaches 1 and can exceed 0.9, depending on τ . We found that in this case at least the behavior of the mean resultant length and the mutual information are very similar; there is no evidence of discrepancies of the sort described in [17]. We have shown that the mutual information between an arbitrarily oriented stimulus and the directional signal available at the cell’s receptors evolves with a time course consistent with observed reaction times of Dictyostelium amoeba. Our results reinforce earlier claims that information theory can play a role in understanding biochemical cellular communication. Acknowledgments MCell simulations were run on the Oberlin College Beowulf Cluster, supported by NSF grant CHE0420717. References [1] Howard C. Berg and Edward M. Purcell. Physics of chemoreception. Biophysical Journal, 20:193, 1977. [2] William Bialek and Sima Setayeshgar. Physical limits to biochemical signaling. PNAS, 102(29):10040– 10045, July 19 2005. [3] S. Qazi, A. Beltukov, and B.A. Trimmer. Simulation modeling of ligand receptor interactions at nonequilibrium conditions: processing of noisy inputs by ionotropic receptors. Math Biosci., 187(1):93–110, Jan 2004. [4] D. J. Spencer, S. K. Hampton, P. Park, J. P. Zurkus, and P. J. Thomas. The diffusion-limited biochemical signal-relay channel. In S. Thrun, L. Saul, and B. Sch¨ lkopf, editors, Advances in Neural Information o Processing Systems 16. MIT Press, Cambridge, MA, 2004. [5] P.R. Fisher, R. Merkl, and G. Gerisch. Quantitative analysis of cell motility and chemotaxis in Dictyostelium discoideum by using an image processing system and a novel chemotaxis chamber providing stationary chemical gradients. J. Cell Biology, 108:973–984, March 1989. [6] Carole A. Parent, Brenda J. Blacklock, Wendy M. Froehlich, Douglas B. Murphy, and Peter N. Devreotes. G protein signaling events are activated at the leading edge of chemotactic cells. Cell, 95:81–91, 2 October 1998. [7] Xuehua Xu, Martin Meier-Schellersheim, Xuanmao Jiao, Lauren E. Nelson, and Tian Jin. Quantitative imaging of single live cells reveals spatiotemporal dynamics of multistep signaling events of chemoattractant gradient sensing in dictyostelium. Molecular Biology of the Cell, 16:676–688, February 2005. [8] Jan Wouter-Rappel, Peter. J Thomas, Herbert Levine, and William F. Loomis. Establishing direction during chemotaxis in eukaryotic cells. Biophys. J., 83:1361–1367, 2002. [9] T.M. Cover and J.A. Thomas. Elements of Information Theory. John Wiley, New York, 1990. [10] J. R. Stiles, D. Van Helden, T. M. Bartol, E.E. Salpeter, and M. M. Salpeter. Miniature endplate current rise times less than 100 microseconds from improved dual recordings can be modeled with passive acetylcholine diffusion from a synaptic vesicle. Proc. Natl. Acad. Sci. U.S.A., 93(12):5747–52, Jun 11 1996. [11] J. R. Stiles and T. M. Bartol. Computational Neuroscience: Realistic Modeling for Experimentalists, chapter Monte Carlo methods for realistic simulation of synaptic microphysiology using MCell, pages 87–127. CRC Press, Boca Raton, FL, 2001. [12] M. Ueda, Y. Sako, T. Tanaka, P. Devreotes, and T. Yanagida. Single-molecule analysis of chemotactic signaling in Dictyostelium cells. Science, 294:864–867, October 2001. [13] L.F. Kozachenko and N.N. Leonenko. Probl. Peredachi Inf. [Probl. Inf. Transm.], 23(9):95, 1987. [14] Jonathan D. Victor. Binless strategies for estimation of information from neural data. Physical Review E, 66:051903, Nov 11 2002. [15] Marc M. Van Hulle. Edgeworth approximation of multivariate differential entropy. Neural Computation, 17:1903–1910, 2005. [16] Loling Song, Sharvari M. Nadkarnia, Hendrik U. B¨ dekera, Carsten Beta, Albert Bae, Carl Franck, o Wouter-Jan Rappel, William F. Loomis, and Eberhard Bodenschatz. Dictyostelium discoideum chemotaxis: Threshold for directed motion. Euro. J. Cell Bio, 85(9-10):981–9, 2006. [17] Eric E. Thomson and William B. Kristan. Quantifying stimulus discriminability: A comparison of information theory and ideal observer analysis. Neural Computation, 17:741–778, 2005. [18] Kanti V. Mardia and Peter E. Jupp. Directional Statistics. John Wiley & Sons, West Sussex, England, 2000.

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Abstract: Adaptively optimizing experiments can significantly reduce the number of trials needed to characterize neural responses using parametric statistical models. However, the potential for these methods has been limited to date by severe computational challenges: choosing the stimulus which will provide the most information about the (typically high-dimensional) model parameters requires evaluating a high-dimensional integration and optimization in near-real time. Here we present a fast algorithm for choosing the optimal (most informative) stimulus based on a Fisher approximation of the Shannon information and specialized numerical linear algebra techniques. This algorithm requires only low-rank matrix manipulations and a one-dimensional linesearch to choose the stimulus and is therefore efficient even for high-dimensional stimulus and parameter spaces; for example, we require just 15 milliseconds on a desktop computer to optimize a 100-dimensional stimulus. Our algorithm therefore makes real-time adaptive experimental design feasible. Simulation results show that model parameters can be estimated much more efficiently using these adaptive techniques than by using random (nonadaptive) stimuli. Finally, we generalize the algorithm to efficiently handle both fast adaptation due to spike-history effects and slow, non-systematic drifts in the model parameters. Maximizing the efficiency of data collection is important in any experimental setting. In neurophysiology experiments, minimizing the number of trials needed to characterize a neural system is essential for maintaining the viability of a preparation and ensuring robust results. As a result, various approaches have been developed to optimize neurophysiology experiments online in order to choose the “best” stimuli given prior knowledge of the system and the observed history of the cell’s responses. The “best” stimulus can be defined a number of different ways depending on the experimental objectives. One reasonable choice, if we are interested in finding a neuron’s “preferred stimulus,” is the stimulus which maximizes the firing rate of the neuron [1, 2, 3, 4]. Alternatively, when investigating the coding properties of sensory cells it makes sense to define the optimal stimulus in terms of the mutual information between the stimulus and response [5]. Here we take a system identification approach: we define the optimal stimulus as the one which tells us the most about how a neural system responds to its inputs [6, 7]. We consider neural systems in † ‡ http://www.prism.gatech.edu/∼gtg120z http://www.stat.columbia.edu/∼liam which the probability p(rt |{xt , xt−1 , ..., xt−tk }, {rt−1 , . . . , rt−ta }) of the neural response rt given the current and past stimuli {xt , xt−1 , ..., xt−tk }, and the observed recent history of the neuron’s activity, {rt−1 , . . . , rt−ta }, can be described by a model p(rt |{xt }, {rt−1 }, θ), specified by a finite vector of parameters θ. Since we estimate these parameters from experimental trials, we want to choose our stimuli so as to minimize the number of trials needed to robustly estimate θ. Two inconvenient facts make it difficult to realize this goal in a computationally efficient manner: 1) model complexity — we typically need a large number of parameters to accurately model a system’s response p(rt |{xt }, {rt−1 }, θ); and 2) stimulus complexity — we are typically interested in neural responses to stimuli xt which are themselves very high-dimensional (e.g., spatiotemporal movies if we are dealing with visual neurons). In particular, it is computationally challenging to 1) update our a posteriori beliefs about the model parameters p(θ|{rt }, {xt }) given new stimulus-response data, and 2) find the optimal stimulus quickly enough to be useful in an online experimental context. In this work we present methods for solving these problems using generalized linear models (GLM) for the input-output relationship p(rt |{xt }, {rt−1 }, θ) and certain Gaussian approximations of the posterior distribution of the model parameters. Our emphasis is on finding solutions which scale well in high dimensions. We solve problem (1) by using efficient rank-one update methods to update the Gaussian approximation to the posterior, and problem (2) by a reduction to a highly tractable onedimensional optimization problem. Simulation results show that the resulting algorithm produces a set of stimulus-response pairs which is much more informative than the set produced by random sampling. Moreover, the algorithm is efficient enough that it could feasibly run in real-time. Neural systems are highly adaptive and more generally nonstatic. A robust approach to optimal experimental design must be able to cope with changes in θ. We emphasize that the model framework analyzed here can account for three key types of changes: stimulus adaptation, spike rate adaptation, and random non-systematic changes. Adaptation which is completely stimulus dependent can be accounted for by including enough stimulus history terms in the model p(rt |{xt , ..., xt−tk }, {rt−1 , ..., rt−ta }). Spike-rate adaptation effects, and more generally spike history-dependent effects, are accounted for explicitly in the model (1) below. Finally, we consider slow, non-systematic changes which could potentially be due to changes in the health, arousal, or attentive state of the preparation. Methods We model a neuron as a point process whose conditional intensity function (instantaneous firing rate) is given as the output of a generalized linear model (GLM) [8, 9]. This model class has been discussed extensively elsewhere; briefly, this class is fairly natural from a physiological point of view [10], with close connections to biophysical models such as the integrate-and-fire cell [9], and has been applied in a wide variety of experimental settings [11, 12, 13, 14]. The model is summarized as: tk λt = E(rt ) = f ta aj rt−j ki,t−l xi,t−l + i l=1 (1) j=1 In the above summation the filter coefficients ki,t−l capture the dependence of the neuron’s instantaneous firing rate λt on the ith component of the vector stimulus at time t − l, xt−l ; the model therefore allows for spatiotemporal receptive fields. For convenience, we arrange all the stimulus coefficients in a vector, k, which allows for a uniform treatment of the spatial and temporal components of the receptive field. The coefficients aj model the dependence on the observed recent activity r at time t − j (these terms may reflect e.g. refractory effects, burstiness, firing-rate adaptation, etc., depending on the value of the vector a [9]). For convenience we denote the unknown parameter vector as θ = {k; a}. The experimental objective is the estimation of the unknown filter coefficients, θ, given knowledge of the stimuli, xt , and the resulting responses rt . We chose the nonlinear stage of the GLM, the link function f (), to be the exponential function for simplicity. This choice ensures that the log likelihood of the observed data is a concave function of θ [9]. Representing and updating the posterior. As emphasized above, our first key task is to efficiently update the posterior distribution of θ after t trials, p(θt |xt , rt ), as new stimulus-response pairs are trial 100 trial 500 trial 2500 trial 5000 θ true 1 info. max. trial 0 0 random −1 (a) random info. max. 2000 Time(Seconds) Entropy 1500 1000 500 0 −500 0 1000 2000 3000 Iteration (b) 4000 5000 0.1 total time diagonalization posterior update 1d line Search 0.01 0.001 0 200 400 Dimensionality 600 (c) Figure 1: A) Plots of the estimated receptive field for a simulated visual neuron. The neuron’s receptive field θ has the Gabor structure shown in the last panel (spike history effects were set to zero for simplicity here, a = 0). The estimate of θ is taken as the mean of the posterior, µt . The images compare the accuracy of the estimates using information maximizing stimuli and random stimuli. B) Plots of the posterior entropies for θ in these two cases; note that the information-maximizing stimuli constrain the posterior of θ much more effectively than do random stimuli. C) A plot of the timing of the three steps performed on each iteration as a function of the dimensionality of θ. The timing for each step was well-fit by a polynomial of degree 2 for the diagonalization, posterior update and total time, and degree 1 for the line search. The times are an average over many iterations. The error-bars for the total time indicate ±1 std. observed. (We use xt and rt to abbreviate the sequences {xt , . . . , x0 } and {rt , . . . , r0 }.) To solve this problem, we approximate this posterior as a Gaussian; this approximation may be justified by the fact that the posterior is the product of two smooth, log-concave terms, the GLM likelihood function and the prior (which we assume to be Gaussian, for simplicity). Furthermore, the main theorem of [7] indicates that a Gaussian approximation of the posterior will be asymptotically accurate. We use a Laplace approximation to construct the Gaussian approximation of the posterior, p(θt |xt , rt ): we set µt to the peak of the posterior (i.e. the maximum a posteriori (MAP) estimate of θ), and the covariance matrix Ct to the negative inverse of the Hessian of the log posterior at µt . In general, computing these terms directly requires O(td2 + d3 ) time (where d = dim(θ); the time-complexity increases with t because to compute the posterior we must form a product of t likelihood terms, and the d3 term is due to the inverse of the Hessian matrix), which is unfortunately too slow when t or d becomes large. Therefore we further approximate p(θt−1 |xt−1 , rt−1 ) as Gaussian; to see how this simplifies matters, we use Bayes to write out the posterior: 1 −1 log p(θ|rt , xt ) = − (θ − µt−1 )T Ct−1 (θ − µt−1 ) + − exp {xt ; rt−1 }T θ 2 + rt {xt ; rt−1 }T θ + const d log p(θ|rt , xt ) −1 = −(θ − µt−1 )T Ct−1 + (2) − exp({xt ; rt−1 }T θ) + rt {xt ; rt−1 }T dθ d2 log p(θ|rt , xt ) −1 = −Ct−1 − exp({xt ; rt−1 }T θ){xt ; rt−1 }{xt ; rt−1 }T dθi dθj (3) Now, to update µt we only need to find the peak of a one-dimensional function (as opposed to a d-dimensional function); this follows by noting that that the likelihood only varies along a single direction, {xt ; rt−1 }, as a function of θ. At the peak of the posterior, µt , the first term in the gradient must be parallel to {xt ; rt−1 } because the gradient is zero. Since Ct−1 is non-singular, µt − µt−1 must be parallel to Ct−1 {xt ; rt−1 }. Therefore we just need to solve a one dimensional problem now to determine how much the mean changes in the direction Ct−1 {xt ; rt−1 }; this requires only O(d2 ) time. Moreover, from the second derivative term above it is clear that computing Ct requires just a rank-one matrix update of Ct−1 , which can be evaluated in O(d2 ) time via the Woodbury matrix lemma. Thus this Gaussian approximation of p(θt−1 |xt−1 , rt−1 ) provides a large gain in efficiency; our simulations (data not shown) showed that, despite this improved efficiency, the loss in accuracy due to this approximation was minimal. Deriving the (approximately) optimal stimulus. To simplify the derivation of our maximization strategy, we start by considering models in which the firing rate does not depend on past spiking, so θ = {k}. To choose the optimal stimulus for trial t + 1, we want to maximize the conditional mutual information I(θ; rt+1 |xt+1 , xt , rt ) = H(θ|xt , rt ) − H(θ|xt+1 , rt+1 ) (4) with respect to the stimulus xt+1 . The first term does not depend on xt+1 , so maximizing the information requires minimizing the conditional entropy H(θ|xt+1 , rt+1 ) = p(rt+1 |xt+1 ) −p(θ|rt+1 , xt+1 ) log p(θ|rt+1 , xt+1 )dθ = Ert+1 |xt+1 log det[Ct+1 ] + const. rt+1 (5) We do not average the entropy of p(θ|rt+1 , xt+1 ) over xt+1 because we are only interested in the conditional entropy for the particular xt+1 which will be presented next. The equality above is due to our Gaussian approximation of p(θ|xt+1 , rt+1 ). Therefore, we need to minimize Ert+1 |xt+1 log det[Ct+1 ] with respect to xt+1 . Since we set Ct+1 to be the negative inverse Hessian of the log-posterior, we have: −1 Ct+1 = Ct + Jobs (rt+1 , xt+1 ) −1 , (6) Jobs is the observed Fisher information. Jobs (rt+1 , xt+1 ) = −∂ 2 log p(rt+1 |ε = xt θ)/∂ε2 xt+1 xt t+1 t+1 (7) Here we use the fact that for the GLM, the likelihood depends only on the dot product, ε = xt θ. t+1 We can use the Woodbury lemma to evaluate the inverse: Ct+1 = Ct I + D(rt+1 , ε)(1 − D(rt+1 , ε)xt Ct xt+1 )−1 xt+1 xt Ct t+1 t+1 (8) where D(rt+1 , ε) = ∂ 2 log p(rt+1 |ε)/∂ε2 . Using some basic matrix identities, log det[Ct+1 ] = log det[Ct ] − log(1 − D(rt+1 , ε)xt Ct xt+1 ) t+1 = log det[Ct ] + D(rt+1 , ε)xt Ct xt+1 t+1 + o(D(rt+1 , ε)xt Ct xt+1 ) t+1 (9) (10) Ignoring the higher order terms, we need to minimize Ert+1 |xt+1 D(rt+1 , ε)xt Ct xt+1 . In our case, t+1 with f (θt xt+1 ) = exp(θt xt+1 ), we can use the moment-generating function of the multivariate Trial info. max. i.i.d 2 400 −10−4 0 0.05 −10−1 −2 ai 800 2 0 −2 −7 −10 i i.i.d k info. max. 1 1 50 i 1 50 i 1 10 1 i (a) i 100 0 −0.05 10 1 1 (b) i 10 (c) Figure 2: A comparison of parameter estimates using information-maximizing versus random stimuli for a model neuron whose conditional intensity depends on both the stimulus and the spike history. The images in the top row of A and B show the MAP estimate of θ after each trial as a row in the image. Intensity indicates the value of the coefficients. The true value of θ is shown in the second row of images. A) The estimated stimulus coefficients, k. B) The estimated spike history coefficients, a. C) The final estimates of the parameters after 800 trials: dashed black line shows true values, dark gray is estimate using information maximizing stimuli, and light gray is estimate using random stimuli. Using our algorithm improved the estimates of k and a. Gaussian p(θ|xt , rt ) to evaluate this expectation. After some algebra, we find that to maximize I(θ; rt+1 |xt+1 , xt , rt ), we need to maximize 1 F (xt+1 ) = exp(xT µt ) exp( xT Ct xt+1 )xT Ct xt+1 . t+1 t+1 2 t+1 (11) Computing the optimal stimulus. For the GLM the most informative stimulus is undefined, since increasing the stimulus power ||xt+1 ||2 increases the informativeness of any putatively “optimal” stimulus. To obtain a well-posed problem, we optimize the stimulus under the usual power constraint ||xt+1 ||2 ≤ e < ∞. We maximize Eqn. 11 under this constraint using Lagrange multipliers and an eigendecomposition to reduce our original d-dimensional optimization problem to a onedimensional problem. Expressing Eqn. 11 in terms of the eigenvectors of Ct yields: 1 2 2 F (xt+1 ) = exp( u i yi + ci yi ) ci yi (12) 2 i i i = g( 2 ci yi ) ui yi )h( i (13) i where ui and yi represent the projection of µt and xt+1 onto the ith eigenvector and ci is the corresponding eigenvalue. To simplify notation we also introduce the functions g() and h() which are monotonically strictly increasing functions implicitly defined by Eqn. 12. We maximize F (xt+1 ) by breaking the problem into an inner and outer problem by fixing the value of i ui yi and maximizing h() subject to that constraint. A single line search over all possible values of i ui yi will then find the global maximum of F (.). This approach is summarized by the equation: max F (y) = max g(b) · y:||y||2 =e b max y:||y||2 =e,y t u=b 2 ci yi ) h( i Since h() is increasing, to solve the inner problem we only need to solve: 2 ci yi max y:||y||2 =e,y t u=b (14) i This last expression is a quadratic function with quadratic and linear constraints and we can solve it using the Lagrange method for constrained optimization. The result is an explicit system of 1 true θ random info. max. info. max. no diffusion 1 0.8 0.6 trial 0.4 0.2 400 0 −0.2 −0.4 800 1 100 θi 1 θi 100 1 θi 100 1 θ i 100 −0.6 random info. max. θ true θ i 1 0 −1 Entropy θ i 1 0 −1 random info. max. 250 200 i 1 θ Trial 400 Trial 200 Trial 0 (a) 0 −1 20 40 (b) i 60 80 100 150 0 200 400 600 Iteration 800 (c) Figure 3: Estimating the receptive field when θ is not constant. A) The posterior means µt and true θt plotted after each trial. θ was 100 dimensional, with its components following a Gabor function. To simulate nonsystematic changes in the response function, the center of the Gabor function was moved according to a random walk in between trials. We modeled the changes in θ as a random walk with a white covariance matrix, Q, with variance .01. In addition to the results for random and information-maximizing stimuli, we also show the µt given stimuli chosen to maximize the information under the (mistaken) assumption that θ was constant. Each row of the images plots θ using intensity to indicate the value of the different components. B) Details of the posterior means µt on selected trials. C) Plots of the posterior entropies as a function of trial number; once again, we see that information-maximizing stimuli constrain the posterior of θt more effectively. equations for the optimal yi as a function of the Lagrange multiplier λ1 . ui e yi (λ1 ) = ||y||2 2(ci − λ1 ) (15) Thus to find the global optimum we simply vary λ1 (this is equivalent to performing a search over b), and compute the corresponding y(λ1 ). For each value of λ1 we compute F (y(λ1 )) and choose the stimulus y(λ1 ) which maximizes F (). It is possible to show (details omitted) that the maximum of F () must occur on the interval λ1 ≥ c0 , where c0 is the largest eigenvalue. This restriction on the optimal λ1 makes the implementation of the linesearch significantly faster and more stable. To summarize, updating the posterior and finding the optimal stimulus requires three steps: 1) a rankone matrix update and one-dimensional search to compute µt and Ct ; 2) an eigendecomposition of Ct ; 3) a one-dimensional search over λ1 ≥ c0 to compute the optimal stimulus. The most expensive step here is the eigendecomposition of Ct ; in principle this step is O(d3 ), while the other steps, as discussed above, are O(d2 ). Here our Gaussian approximation of p(θt−1 |xt−1 , rt−1 ) is once again quite useful: recall that in this setting Ct is just a rank-one modification of Ct−1 , and there exist efficient algorithms for rank-one eigendecomposition updates [15]. While the worst-case running time of this rank-one modification of the eigendecomposition is still O(d3 ), we found the average running time in our case to be O(d2 ) (Fig. 1(c)), due to deflation which reduces the cost of matrix multiplications associated with finding the eigenvectors of repeated eigenvalues. Therefore the total time complexity of our algorithm is empirically O(d2 ) on average. Spike history terms. The preceding derivation ignored the spike-history components of the GLM model; that is, we fixed a = 0 in equation (1). Incorporating spike history terms only affects the optimization step of our algorithm; updating the posterior of θ = {k; a} proceeds exactly as before. The derivation of the optimization strategy proceeds in a similar fashion and leads to an analogous optimization strategy, albeit with a few slight differences in detail which we omit due to space constraints. The main difference is that instead of maximizing the quadratic expression in Eqn. 14 to find the maximum of h(), we need to maximize a quadratic expression which includes a linear term due to the correlation between the stimulus coefficients, k, and the spike history coefficients,a. The results of our simulations with spike history terms are shown in Fig. 2. Dynamic θ. In addition to fast changes due to adaptation and spike-history effects, animal preparations often change slowly and nonsystematically over the course of an experiment [16]. We model these effects by letting θ experience diffusion: θt+1 = θt + wt (16) Here wt is a normally distributed random variable with mean zero and known covariance matrix Q. This means that p(θt+1 |xt , rt ) is Gaussian with mean µt and covariance Ct + Q. To update the posterior and choose the optimal stimulus, we use the same procedure as described above1 . Results Our first simulation considered the use of our algorithm for learning the receptive field of a visually sensitive neuron. We took the neuron’s receptive field to be a Gabor function, as a proxy model of a V1 simple cell. We generated synthetic responses by sampling Eqn. 1 with θ set to a 25x33 Gabor function. We used this synthetic data to compare how well θ could be estimated using information maximizing stimuli compared to using random stimuli. The stimuli were 2-d images which were rasterized in order to express x as a vector. The plots of the posterior means µt in Fig. 1 (recall these are equivalent to the MAP estimate of θ) show that the information maximizing strategy converges an order of magnitude more rapidly to the true θ. These results are supported by the conclusion of [7] that the information maximization strategy is asymptotically never worse than using random stimuli and is in general more efficient. The running time for each step of the algorithm as a function of the dimensionality of θ is plotted in Fig. 1(c). These results were obtained on a machine with a dual core Intel 2.80GHz XEON processor running Matlab. The solid lines indicate fitted polynomials of degree 1 for the 1d line search and degree 2 for the remaining curves; the total running time for each trial scaled as O(d2 ), as predicted. When θ was less than 200 dimensions, the total running time was roughly 50 ms (and for dim(θ) ≈ 100, the runtime was close to 15 ms), well within the range of tolerable latencies for many experiments. In Fig. 2 we apply our algorithm to characterize the receptive field of a neuron whose response depends on its past spiking. Here, the stimulus coefficients k were chosen to follow a sine-wave; 1 The one difference is that the covariance matrix of p(θt+1 |xt+1 , rt+1 ) is in general no longer just a rankone modification of the covariance matrix of p(θt |xt , rt ); thus, we cannot use the rank-one update to compute the eigendecomposition. However, it is often reasonable to take Q to be white, Q = cI; in this case the eigenvectors of Ct + Q are those of Ct and the eigenvalues are ci + c where ci is the ith eigenvalue of Ct ; thus in this case, our methods may be applied without modification. the spike history coefficients a were inhibitory and followed an exponential function. When choosing stimuli we updated the posterior for the full θ = {k; a} simultaneously and maximized the information about both the stimulus coefficients and the spike history coefficients. The information maximizing strategy outperformed random sampling for estimating both the spike history and stimulus coefficients. Our final set of results, Fig. 3, considers a neuron whose receptive field drifts non-systematically with time. We take the receptive field to be a Gabor function whose center moves according to a random walk (we have in mind a slow random drift of eye position during a visual experiment). The results demonstrate the feasibility of the information-maximization strategy in the presence of nonstationary response properties θ, and emphasize the superiority of adaptive methods in this context. Conclusion We have developed an efficient implementation of an algorithm for online optimization of neurophysiology experiments based on information-theoretic criterion. Reasonable approximations based on a GLM framework allow the algorithm to run in near-real time even for high dimensional parameter and stimulus spaces, and in the presence of spike-rate adaptation and time-varying neural response properties. Despite these approximations the algorithm consistently provides significant improvements over random sampling; indeed, the differences in efficiency are large enough that the information-optimization strategy may permit robust system identification in cases where it is simply not otherwise feasible to estimate the neuron’s parameters using random stimuli. Thus, in a sense, the proposed stimulus-optimization technique significantly extends the reach and power of classical neurophysiology methods. Acknowledgments JL is supported by the Computational Science Graduate Fellowship Program administered by the DOE under contract DE-FG02-97ER25308 and by the NSF IGERT Program in Hybrid Neural Microsystems at Georgia Tech via grant number DGE-0333411. 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