The N2cc component as an electrophysiological marker of space-based and feature-based attentional target selection processes in touch

An electrophysiological correlate of attentional target selection processes in touch (N2cc component) has recently been discovered in lateralized tactile working memory experiments. This tactile N2cc emerges at the same time as the visual N2pc component, but has a different modality-specific topography over central somatosensory areas. Here, we investigated links between N2cc components and the space-based versus feature-based attentional selection of task-relevant tactile stimuli. On each trial, a pair of tactile items was presented simultaneously to one finger on the left and right hand. Target stimuli were defined by their location (e.g., left index finger; Spatial Attention Task), by a non-spatial feature (continuous versus pulsed; Feature-based Attention Task), or by a combination of spatial and non-spatial features (Conjunction Task). Reliable N2cc components were observed in all three tasks. They emerged considerably earlier in the Spatial Attention Task than in the Feature-based Attention Task, suggesting that space-based selection mechanisms in touch operate faster than feature-guided mechanisms. The temporal pattern of N2cc components observed in the Conjunction Task revealed that space-based and feature-based attention both contributed to target selection, which was initially driven primarily by spatial location. Overall, these findings establish the N2cc component as a new electrophysiological marker of the selective attentional processing of task-relevant stimuli in touch

Wallerian-Like Degeneration of Central Neurons After Synchronized and Geometrically Registered Mass Axotomy in a Three-Compartmental Microfluidic Chip

Degeneration of central axons may occur following injury or due to various diseases and it involves complex molecular mechanisms that need to be elucidated. Existing in vitro axotomy models are difficult to perform, and they provide limited information on the localization of events along the axon. We present here a novel experimental model system, based on microfluidic isolation, which consists of three distinct compartments, interconnected by parallel microchannels allowing axon outgrowth. Neurons cultured in one compartment successfully elongated their axons to cross a short central compartment and invade the outermost compartment. This design provides an interesting model system for studying axonal degeneration and death mechanisms, with a previously impossible spatial and temporal control on specific molecular pathways. We provide a proof-of-concept of the system by reporting its application to a well-characterized experimental paradigm, axotomy-induced Wallerian degeneration in primary central neurons. Using this model, we applied localized central axotomy by a brief, isolated flux of detergent. We report that mouse embryonic cortical neurons exhibit rapid Wallerian-like distal degeneration but no somatic death following central axotomy. Distal axons show progressive degeneration leading to axonal beading and cytoskeletal fragmentation within a few hours after axotomy. Degeneration is asynchronous, reminiscent of in vivo Wallerian degeneration. Axonal cytoskeletal fragmentation is significantly delayed with nicotinamide adenine dinucleotide pretreatment, but it does not change when distal calpain or caspase activity is inhibited. These findings, consistent with previous experiments in vivo, confirm the power and biological relevance of this microfluidic architecture