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Larisch, R.

Publications and source records attributed to Larisch, R..

3 recordsLinked to original sources

A systematic analysis of the joint effects of ganglion cells, lagged LGN cells, and intercortical inhibition on spatiotemporal processing and direction selectivity

Simple cells in the visual cortex process spatial as well as temporal information of the visual stream and enable the perception of motion information. Previous work suggests that the direction selectivity of V1 simple cells is associated with a temporal offset in the thalamocortical input stream through lagged and non-lagged cells of the lateral geniculate nucleus (LGN), but alternatively, it may also result from intercortical inhibition. While there exists a large corpus of models for spatiotemporal receptive fields, the majority of them built-in the spatiotemporal dynamics by utilizing a combination of spatial and temporal functions and thus, do not explain the emergence of spatiotemporal dynamics on basis of network dynamics emerging in the retina and the LGN. In order to better comprehend the emergence of spatiotemporal processing and direction selectivity, we used a spiking neural network to implement the visual pathway from the retina to the primary visual cortex. By varying different functional parts in our network, we demonstrate how the direction selectivity of simple cells emerges through the interplay between two components: tuned intercortical inhibition and a temporal offset in the feedforward path through lagged LGN cells. We observe that direction-selective simple cells are linked to a particular spiking pattern in a local excitatory-inhibitory circuit: If the stimulus moves in the non-preferred direction of a simple cell, inhibitory neurons with a different spatial position or tuning spike earlier, preventing the simple cell to spike. However, in the preferred direction, these inhibitory cells spike later, enabling the simple cell to spike.

neuroscience↗

The control of plastic inhibition over excitatory synaptic plasticity leads to the joint emergence of sensory coding and contrast invariance.

Visual stimuli are represented by a highly efficient code in the primary visual cortex, but the development of this code is still unclear. Two distinct factors control coding efficiency: Representational efficiency, which is determined by neuronal tuning diversity, and metabolic efficiency, which is influenced by neuronal gain. How these determinants of coding efficiency are shaped during development, supported by excitatory and inhibitory plasticity, is only partially understood. We investigate a fully plastic spiking network of the primary visual cortex, building on phenomenological plasticity rules. Our results suggest that inhibitory plasticity is key to the emergence of tuning diversity and accurate input encoding. We show that inhibitory feedback (random and specific) increases the metabolic efficiency by implementing a gain control mechanism. Interestingly, this led to the spontaneous emergence of contrast-invariant tuning curves. Our findings highlight that (1) interneuron plasticity is key to the development of tuning diversity and (2) that efficient sensory representations are an emergent property of the resulting network.

neuroscience↗

TRPV5, TRPV6, TRPM6, and TRPM7 do not contribute to hair-cell mechanotransduction

The hair-cell mechanotransduction channel remains unidentified. We tested whether four transient receptor channel (TRP) family members, TRPV5, TRPV6, TRPM6, and TRPM7, participated in transduction. Using cysteine-substitution mouse knock-ins and methanethiosulfonate reagents selective for those alleles, we found that inhibition of TRPV5 or TRPV6 had no effect on transduction in mouse cochlear hair cells. TRPM6 and TRPM7 each interacted with the tip-link component PCDH15 in cultured eukaryotic cells, which suggested they could participate in transduction. Cochlear hair cell transduction was insensitive to shRNA knockdown of Trpm6 or Trpm7, however, and was not affected by manipulations of Mg2+, which normally perturbs TRPM6 and TRPM7. To definitively examine the role of these two channels in transduction, we showed that deletion of either or both of their genes selectively in hair cells had no effect on auditory function. We suggest that TRPV5, TRPV6, TRPM6, and TRPM7 are unlikely to be the pore-forming subunit of the hair-cell transduction channel.

neuroscience↗