Rotter, S. | Search bioRxiv

bioRxiv2018

Propagation of orientation selectivity in a spiking network model of layered primary visual cortex

We studied the propagation of orientation selectivity over layers in a model of rodent primary visual cortex in terms of the underlying connectivity. While significant progress has been made in measuring the activity in the different sub-populations as well as the connectivity between those in experiments, a comprehensive theoretical explanation of how network structure and its dynamics are related is still missing. We suggest a model of layered mouse visual cortex by extending the model suggested by Potjans and Diesmann (2014) with thalamic input that has an orientation bias according to Sadeh et al. (2014). We then studied the response properties of the network to such non-homogeneous input. We found that, without further assumptions, the connectivity derived from experimental data leads to layer-specific distributions of orientation selectivity very similar to what has been observed in mouse experiments. Interestingly, the network settles in a dynamical operating point, in which the efficacy of the different projections and their contribution to orientation tuning deviate strongly from the expectations based on the underlying anatomical connectivity. To understand the processes that shape the observed dynamics, it is essential to perform the analysis of the microcircuit on the system level. With that perspective, we find in particular that the difference in tuning of L2/3 and L4 neurons is an immediate, albeit unexpected consequence of the specific network connectivity. Furthermore, we introduce a novel method for predicting the effects of optogenetic stimulation of specific neuronal sub-populations and demonstrate its power in network simulations.\n\nSignificance StatementUnderstanding the precise roles of neuronal sub-populations in shaping the activity of neuronal networks is a fundamental objective of neuroscience research. To this end, our work makes three important contributions. First, we show that the experimentally extracted connectivity suffices to explain the degree of selectivity of sub-populations in mouse visual cortex to visual stimulation. Second, we introduce a novel system-level approach for the analysis of input-output relations of recurrent networks, which lead to distinct activity patterns. Third, we present a method for the design of optogenetic experiments that can be used to devise specific stimuli which result in a desired and predictable change of neuronal activity.

neuroscience↗

bioRxiv2018

Transmission of motor signals from the basal ganglia to the thalamus: effect of correlations, sensory responses, and excitation

Movement-related decreases in firing rate have been observed in basal ganglia output neurons. They may transmit motor signals to the thalamus, but the effect of these firing rate decreases on downstream neurons in the motor thalamus is not known. One possibility is that they lead to thalamic post-inhibitory rebound spikes. However, it has also been argued that the physiological conditions permitting rebound spiking are pathological, and primarily present in Parkinsons disease. As in Parkinsons disease neural activity becomes pathologically correlated, we investigated the impact of correlations in basal ganglia output on the transmission of motor signals using a Hodgkin-Huxley model of thalamocortical neurons. We found that such correlations disrupt the transmission of motor signals via rebound spikes by decreasing the signal-to-noise ratio and increasing the trial-to-trial variability. We further examined the role of sensory responses in basal ganglia output neurons and the effect of cortical excitation of motor thalamus in modulating rebound spiking. Interestingly, both could either promote or suppress the generation of rebound spikes depending on their timing relative to the motor signal. Finally, we determined parameter regimes, such as levels of excitation, under which rebound spiking is feasible in the model, and confirmed that the conditions for rebound spiking are primarily given in pathological regimes. However, we also identified specific conditions in the model that would allow rebound spiking to occur in healthy animals in a small subset of thalamic neurons. Overall, our model provides novel insights into differences between normal and pathological transmission of motor signals.

neuroscience↗