No Arabic abstract
Thalamic relay cells fire action potentials that transmit information from retina to cortex. The amount of information that spike trains encode is usually estimated from the precision of spike timing with respect to the stimulus. Sensory input, however, is only one factor that influences neural activity. For example, intrinsic dynamics, such as oscillations of networks of neurons, also modulate firing pattern. Here, we asked if retinal oscillations might help to convey information to neurons downstream. Specifically, we made whole-cell recordings from relay cells to reveal retinal inputs (EPSPs) and thalamic outputs (spikes) and analyzed these events with information theory. Our results show that thalamic spike trains operate as two multiplexed channels. One channel, which occupies a low frequency band (<30 Hz), is encoded by average firing rate with respect to the stimulus and carries information about local changes in the image over time. The other operates in the gamma frequency band (40-80 Hz) and is encoded by spike time relative to the retinal oscillations. Because these oscillations involve extensive areas of the retina, it is likely that the second channel transmits information about global features of the visual scene. At times, the second channel conveyed even more information than the first.
It has been hypothesized that Gamma cortical oscillations play important roles in numerous cognitive processes and may involve psychiatric conditions including anxiety, schizophrenia, and autism. Gamma rhythms are commonly observed in many brain regions during both waking and sleep states, yet their functions and mechanisms remain a matter of debate. Spatiotemporal Gamma oscillations can explain neuronal representation, computation, and the shaping of communication among cortical neurons, even neurological and neuropsychiatric disorders in neo-cortex. In this study, the neural network dynamics and spatiotemporal behavior in the cerebral cortex are examined during Gamma brain activity. We have directly observed the Gamma oscillations on visual processing as spatiotemporal waves induced by targeted optogenetics stimulation. We have experimentally demonstrated the constant optogenetics stimulation based on the ChR2 opsin under the control of the CaMKII{alpha} promotor, which can induce sustained narrowband Gamma oscillations in the visual cortex of rats during their comatose states. The injections of the viral vector [LentiVirus CaMKII{alpha} ChR2] was performed at two different depths, 200 and 500 mu m. Finally, we computationally analyze our results via Wilson-Cowan model.
Primary visual cortex (V1) is the first stage of cortical image processing, and a major effort in systems neuroscience is devoted to understanding how it encodes information about visual stimuli. Within V1, many neurons respond selectively to edges of a given preferred orientation: these are known as simple or complex cells, and they are well-studied. Other neurons respond to localized center-surround image features. Still others respond selectively to certain image stimuli, but the specific features that excite them are unknown. Moreover, even for the simple and complex cells-- the best-understood V1 neurons-- it is challenging to predict how they will respond to natural image stimuli. Thus, there are important gaps in our understanding of how V1 encodes images. To fill this gap, we train deep convolutional neural networks to predict the firing rates of V1 neurons in response to natural image stimuli, and find that 15% of these neurons are within 10% of their theoretical limit of predictability. For these well predicted neurons, we invert the predictor network to identify the image features (receptive fields) that cause the V1 neurons to spike. In addition to those with previously-characterized receptive fields (Gabor wavelet and center-surround), we identify neurons that respond predictably to higher-level textural image features that are not localized to any particular region of the image.
It has been hypothesized that neural activities in the primary visual cortex (V1) represent a saliency map of the visual field to exogenously guide attention. This hypothesis has so far provided only qualitative predictions and their confirmations. We report this hypothesis first quantitative prediction, derived without free parameters, and its confirmation by human behavioral data. The hypothesis provides a direct link between V1 neural responses to a visual location and the saliency of that location to guide attention exogenously. In a visual input containing many bars, one of them saliently different from all the other bars which are identical to each other, saliency at the singletons location can be measured by the shortness of the reaction time in a visual search task to find the singleton. The hypothesis predicts quantitatively the whole distribution of the reaction times to find a singleton unique in color, orientation, and motion direction from the reaction times to find other types of singletons. The predicted distribution matches the experimentally observed distribution in all six human observers. A requirement for this successful prediction is a data-motivated assumption that V1 lacks neurons tuned simultaneously to color, orientation, and motion direction of visual inputs. Since evidence suggests that extrastriate cortices do have such neurons, we discuss the possibility that the extrastriate cortices play no role in guiding exogenous attention so that they can be devoted to other functional roles like visual decoding or endogenous attention.
Neural computation is associated with the emergence, reconfiguration and dissolution of cell assemblies in the context of varying oscillatory states. Here, we describe the complex spatio-temporal dynamics of cell assemblies through temporal network formalism. We use a sliding window approach to extract sequences of networks of information sharing among single units in hippocampus and enthorinal cortex during anesthesia and study how global and node-wise functional connectivity properties evolve along time. First, we find that information sharing networks display, at any time, a core-periphery structure in which an integrated core of more tightly functionally interconnected units link to more loosely connected network leaves. However the units participating to the core or to the periphery substantially change across time-windows. Second, we find that discrete network states can be defined on top of this continuously ongoing liquid core-periphery reorganization. Switching between network states results in a more abrupt modification of the units belonging to the core and is only loosely linked to transitions between global oscillatory states. Third, we characterize different styles of temporal connectivity that cells can exhibit within each state of the sharing network. While inhibitory cells tend to be central, we show that, otherwise, anatomical localization only poorly influences the patterns of temporal connectivity of the different cells. Cells can also change temporal connectivity style when the network changes state. Altogether, these findings reveal that the sharing of information mediated by the intrinsic dynamics of hippocampal and enthorinal cortex cell assemblies have a rich spatiotemporal structure, which could not have been identified by more conventional time- or state-averaged analyses of functional connectivity.
Visually induced neuronal activity in V1 displays a marked gamma-band component which is modulated by stimulus properties. It has been argued that synchronized oscillations contribute to these gamma-band activity [... however,] even when oscillations are observed, they undergo temporal decorrelation over very few cycles. This is not easily accounted for in previous network modeling of gamma oscillations. We argue here that interactions between cortical layers can be responsible for this fast decorrelation. We study a model of a V1 hypercolumn, embedding a simplified description of the multi-layered structure of the cortex. When the stimulus contrast is low, the induced activity is only weakly synchronous and the network resonates transiently without developing collective oscillations. When the contrast is high, on the other hand, the induced activity undergoes synchronous oscillations with an irregular spatiotemporal structure expressing a synchronous chaotic state. As a consequence the population activity undergoes fast temporal decorrelation, with concomitant rapid damping of the oscillations in LFPs autocorrelograms and peak broadening in LFPs power spectra. [...] Finally, we argue that the mechanism underlying the emergence of synchronous chaos in our model is in fact very general. It stems from the fact that gamma oscillations induced by local delayed inhibition tend to develop chaos when coupled by sufficiently strong excitation.