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Rieke, F.

Publications and source records attributed to Rieke, F..

6 recordsLinked to original sources

Temporal resolution of single photon responses in primate rod photoreceptors and limits imposed by cellular noise

Sensory receptor noise corrupts sensory signals, contributing to imperfect perception and dictating central processing strategies. For example, noise in rod phototransduction limits our ability to detect light and minimizing the impact of this noise requires precisely tuned nonlinear processing by the retina. But detection sensitivity is only one aspect of night vision: prompt and accurate behavior also requires that rods reliably encode the timing of photon arrivals. We show here that the temporal resolution of responses of primate rods is much finer than the duration of the light response and identify the key limiting sources of transduction noise. We also find that the thermal activation rate of rhodopsin is lower than previous estimates, implying that other noise sources are more important than previously appreciated. A model of rod single-photon responses reveals that the limiting noise relevant for behavior depends critically on how rod signals are pooled by downstream neurons.

neuroscience

Rod signaling in primate retina: range, routing and kinetics

Stimulus or context dependent routing of neural signals through parallel pathways can permit flexible processing of diverse inputs. For example, work in mouse shows that rod photoreceptor signals are routed through several retinal pathways, each specialized for different light levels. This light level-dependent routing of rod signals has been invoked to explain several human perceptual results, but it has not been tested in primate retina. Here we show, surprisingly, that rod signals traverse the primate retina almost exclusively through a single pathway, regardless of light level. Indeed, identical experiments in mouse and primate reveal large differences in how rod signals traverse the retina. These results require reevaluating human perceptual results in terms of flexible computation within this single pathway. This includes a prominent speeding of rod signals with light level - which we show is inherited directly from the rods photoreceptors themselves rather than from different pathways with different kinetics.

neuroscience

Inferring synaptic inputs from spikes with a conductance-based neural encoding model

A popular approach to the study of information processing in the nervous system is to char-acterize neural responses in terms of a cascade of linear and nonlinear stages: a linear filter to describe the neurons stimulus integration properties, followed by a rectifying nonlinearity to convert filter output to spike rate. However, real neurons integrate stimuli via the modula-tion of nonlinear excitatory and inhibitory synaptic conductances. Here we introduce a bio-physically inspired point process model with conductance-based inputs. The model provides a novel interpretation of the popular Poisson generalized linear model (GLM) as a special kind of conductance-based model, where excitatory and inhibitory conductances are modulated in a \"push-pull\" manner so that total conductance remains constant. We relax this constraint to obtain a more general and flexible \"conductance-based encoding model\" (CBEM), which can exhibit stimulus-dependent fluctuations in gain and dynamics. We fit the model to spike trains of macaque retinal ganglion cells and show that, remarkably, we can accurately infer underlying inhibitory and excitatory conductances, using comparisons to intracellularly measured conductances. Using extracellular data, we corroborate the intracellular finding that synaptic excitation temporally precedes inhibition in retina. We show that the CBEM outperforms the classic GLM at predicting retinal ganglion cell responses to full-field stimuli, generalizes better across contrast levels, and captures inhibition-dependent response properties to spatially structured stimuli. The CBEM provides a powerful tool for gaining insights into the intracellular variables governing spiking, and forges an important link between extracellular characterization methods and biophysically detailed response models.

neuroscience

Receptive field center-surround interactions mediate context-dependent spatial contrast encoding in the retina

Antagonistic receptive field surrounds are a near-universal property of early sensory processing. A key assumption in many models for retinal ganglion cell encoding is that receptive field surrounds are added only to the fully formed center signal. But anatomical and functional observations indicate that surrounds are added before the summation of signals across receptive field subunits that creates the center. Here, we show that this receptive field architecture has an important consequence for spatial contrast encoding: the surround can control sensitivity to fine spatial structure by changing the way the center integrates visual information over space. The impact of the surround is particularly prominent when center and surround signals are correlated, as they are in natural stimuli. This role of the surround differs substantially from classic center-surround models and raises the possibility that the surround plays unappreciated roles in shaping ganglion cell sensitivity to natural inputs.

neuroscience

Simulation of visual perception and learning with a retinal prosthesis

The nature of artificial vision with a retinal prosthesis, and the degree to which the brain can adapt to the unnatural input from such a device, are poorly understood. Therefore, the development of current and future devices may be aided by theory and simulations that help to infer and understand what prosthesis patients see. A biologically-informed, extensible computational framework is presented here to predict visual perception and the potential effect of learning with a subretinal prosthesis. The framework relies on optimal linear reconstruction of the stimulus from retinal responses to infer the visual information available to the patient. A simulation of the physiological optics of the eye and light responses of the major retinal neurons was used to calculate the optimal linear transformation for reconstructing natural images from retinal activity. The result was then used to reconstruct the visual stimulus during the artificial activation expected from a subretinal prosthesis in a degenerated retina, as a proxy for inferred visual perception. Several simple observations reveal the potential utility of such a simulation framework. The inferred perception obtained with prosthesis activation was substantially degraded compared to the inferred perception obtained with normal retinal responses, as expected given the limited resolution and lack of cell type specificity of the prosthesis. Consistent with clinical findings and the importance of cell type specificity, reconstruction using only ON cells, and not OFF cells, was substantially more accurate. Finally, when reconstruction was re-optimized for prosthesis stimulation, simulating the greatest potential for learning by the patient, the accuracy of inferred perception was much closer to that of healthy vision. The reconstruction approach thus provides a more complete method for exploring the potential for treating blindness with retinal prostheses than has been available previously. It may also be useful for interpreting patient data in clinical trials, and for improving prosthesis design.

neuroscience

Effective synaptic interactions in subsampled nonlinear networks with strong coupling

A major obstacle to understanding neural coding and computation is the fact that experimental recordings typically sample only a small fraction of the neurons in a circuit. Measured neural properties are skewed by interactions between recorded neurons and the \"hidden\" portion of the network. To properly interpret neural data and determine how biological structure gives rise to neural circuit function, we thus need a better understanding of the relationships between measured effective neural properties and the true underlying physiological properties. Here, we focus on how the effective spatiotemporal dynamics of the synaptic interactions between neurons are reshaped by coupling to unobserved neurons. We find that the effective interactions from a pre-synaptic neuron r' to a post-synaptic neuron r can be decomposed into a sum of the true interaction from r' to r plus corrections from every directed path from r' to r through unobserved neurons. Importantly, the resulting formula reveals when the hidden units have--or do not have--major effects on reshaping the interactions among observed neurons. As a particular example of interest, we derive a formula for the impact of hidden units in random networks with \"strong\" coupling--connection weights that scale with [Formula], where N is the network size, precisely the scaling observed in recent experiments. With this quantitative relationship between measured and true interactions, we can study how network properties shape effective interactions, which properties are relevant for neural computations, and how to manipulate effective interactions.

neuroscience