Information recovery from rank-order encoded images

The time to detection of a visual stimulus by the primate eye is recorded at 100 – 150ms. This near instantaneous recognition is in spite of the considerable processing required by the several stages of the visual pathway to recognise and react to a visual scene. How this is achieved is still a matter of speculation. Rank-order codes have been proposed as a means of encoding by the primate eye in the rapid transmission of the initial burst of information from the sensory neurons to the brain. We study the efficiency of rank-order codes in encoding perceptually-important information in an image. VanRullen and Thorpe built a model of the ganglion cell layers of the retina to simulate and study the viability of rank-order as a means of encoding by retinal neurons. We validate their model and quantify the information retrieved from rank-order encoded images in terms of the visually-important information recovered. Towards this goal, we apply the ‘perceptual information preservation algorithm’, proposed by Petrovic and Xydeas after slight modification. We observe a low information recovery due to losses suffered during the rank-order encoding and decoding processes. We propose to minimise these losses to recover maximum information in minimum time from rank-order encoded images. We first maximise information recovery by using the pseudo-inverse of the filter-bank matrix to minimise losses during rankorder decoding. We then apply the biological principle of lateral inhibition to minimise losses during rank-order encoding. In doing so, we propose the Filteroverlap Correction algorithm. To test the perfomance of rank-order codes in a biologically realistic model, we design and simulate a model of the foveal-pit ganglion cells of the retina keeping close to biological parameters. We use this as a rank-order encoder and analyse its performance relative to VanRullen and Thorpe’s retinal model

In vivo imaging reveals transient microglia recruitment and functional recovery of photoreceptor signaling after injury.

Microglia respond to damage and microenvironmental changes within the central nervous system by morphologically transforming and migrating to the lesion, but the real-time behavior of populations of these resident immune cells and the neurons they support have seldom been observed simultaneously. Here, we have used in vivo high-resolution optical coherence tomography (OCT) and scanning laser ophthalmoscopy with and without adaptive optics to quantify the 3D distribution and dynamics of microglia in the living retina before and after local damage to photoreceptors. Following photoreceptor injury, microglia migrated both laterally and vertically through the retina over many hours, forming a tight cluster within the area of visible damage that resolved over 2 wk. In vivo OCT optophysiological assessment revealed that the photoreceptors occupying the damaged region lost all light-driven signaling during the period of microglia recruitment. Remarkably, photoreceptors recovered function to near-baseline levels after the microglia had departed the injury locus. These results demonstrate the spatiotemporal dynamics of microglia engagement and restoration of neuronal function during tissue remodeling and highlight the need for mechanistic studies that consider the temporal and structural dynamics of neuron-microglia interactions in vivo

Roadmap on semiconductor-cell biointerfaces.

This roadmap outlines the role semiconductor-based materials play in understanding the complex biophysical dynamics at multiple length scales, as well as the design and implementation of next-generation electronic, optoelectronic, and mechanical devices for biointerfaces. The roadmap emphasizes the advantages of semiconductor building blocks in interfacing, monitoring, and manipulating the activity of biological components, and discusses the possibility of using active semiconductor-cell interfaces for discovering new signaling processes in the biological world

Correlated disorder in myelinated axons orientational geometry and structure

While the ultrastructure of the myelin has been considered to be a quasi-crystalline stable system, nowadays its multiscale complex dynamics appears to play a key role for its functionality, degeneration and repair processes following neurological diseases and trauma. In this work, we have investigated the axons interactions associated to the nerve functionality, measuring the spatial distribution of the orientational fluctuations of axons in a Xenopus Laevis sciatic nerve. At this aim, we have used Scanning micro X-ray Diffraction (SmXRD), a non-invasive already applied to other heterogeneous systems presenting complex geometries from microscale to nanoscale. We have found that the orientational spatial fluctuations of fresh axons show a correlated disorder described by Levy flight distribution. Thus, we have studied how this correlated disorder evolves during the degeneration of the nerve. Our results show that the spatial distribution of axons orientational fluctuations in unfresh, aged nerve loose the correlated disorder assuming a randomly disordered behaviour. This work allows a deeper understanding of nerve states and paves the way to study other materials and biomaterials with the same technique to detect and to characterize their states and supramolecular structure, associated with dynamic structural changes at the nanoscale and mesoscale.Comment: 9 pages, 4 figure

A Pipeline for Volume Electron Microscopy of the Caenorhabditis elegans Nervous System.

The "connectome," a comprehensive wiring diagram of synaptic connectivity, is achieved through volume electron microscopy (vEM) analysis of an entire nervous system and all associated non-neuronal tissues. White et al. (1986) pioneered the fully manual reconstruction of a connectome using Caenorhabditis elegans. Recent advances in vEM allow mapping new C. elegans connectomes with increased throughput, and reduced subjectivity. Current vEM studies aim to not only fill the remaining gaps in the original connectome, but also address fundamental questions including how the connectome changes during development, the nature of individuality, sexual dimorphism, and how genetic and environmental factors regulate connectivity. Here we describe our current vEM pipeline and projected improvements for the study of the C. elegans nervous system and beyond

A simple rule for axon outgrowth and synaptic competition generates realistic connection lengths and filling fractions

Neural connectivity at the cellular and mesoscopic level appears very specific and is presumed to arise from highly specific developmental mechanisms. However, there are general shared features of connectivity in systems as different as the networks formed by individual neurons in Caenorhabditis elegans or in rat visual cortex and the mesoscopic circuitry of cortical areas in the mouse, macaque, and human brain. In all these systems, connection length distributions have very similar shapes, with an initial large peak and a long flat tail representing the admixture of long-distance connections to mostly short-distance connections. Furthermore, not all potentially possible synapses are formed, and only a fraction of axons (called filling fraction) establish synapses with spatially neighboring neurons. We explored what aspects of these connectivity patterns can be explained simply by random axonal outgrowth. We found that random axonal growth away from the soma can already reproduce the known distance distribution of connections. We also observed that experimentally observed filling fractions can be generated by competition for available space at the target neurons--a model markedly different from previous explanations. These findings may serve as a baseline model for the development of connectivity that can be further refined by more specific mechanisms.Comment: 31 pages (incl. supplementary information); Cerebral Cortex Advance Access published online on May 12, 200

The Lymnaea Cardioexcitatory Peptide (LyCEP) Receptor: A G-Protein–Coupled Receptor for a Novel Member of the RFamide Neuropeptide Family

A novel G-protein–coupled receptor (GRL106) resembling neuropeptide Y and tachykinin receptors was cloned from the molluscLymnaea stagnalis. Application of a peptide extract from the Lymnaea brain to Xenopus oocytes expressing GRL106 activated a calcium-dependent chloride channel. Using this response as a bioassay, we purified the ligand for GRL106,Lymnaea cardioexcitatory peptide (LyCEP), an RFamide-type decapeptide (TPHWRPQGRF-NH2) displaying significant similarity to the Achatina cardioexcitatory peptide (ACEP-1) as well as to the recently identified family of mammalian prolactin-releasing peptides. In the Lymnaeabrain, the cells that produce egg-laying hormone are the predominant site of GRL106 gene expression and appear to be innervated by LyCEP-containing fibers. Indeed, LyCEP application transiently hyperpolarizes isolated egg-laying hormone cells. In theLymnaea pericardium, LyCEP-containing fibers end blindly at the pericardial lumen, and the heart is stimulated by LyCEPin vitro. These data confirm that LyCEP is an RFamide ligand for GRL10

Immune or genetic-mediated disruption of CASPR2 causes pain hypersensitivity due to enhanced primary afferent excitability

Human autoantibodies to contactin-associated protein-like 2 (CASPR2) are often associated with neuropathic pain, and CASPR2 mutations have been linked to autism spectrum disorders, in which sensory dysfunction is increasingly recognized. Human CASPR2 autoantibodies, when injected into mice, were peripherally restricted and resulted in mechanical pain-related hypersensitivity in the absence of neural injury. We therefore investigated the mechanism by which CASPR2 modulates nociceptive function. Mice lacking CASPR2 (Cntnap2 ) demonstrated enhanced pain-related hypersensitivity to noxious mechanical stimuli, heat, and algogens. Both primary afferent excitability and subsequent nociceptive transmission within the dorsal horn were increased in Cntnap2 mice. Either immune or genetic-mediated ablation of CASPR2 enhanced the excitability of DRG neurons in a cell-autonomous fashion through regulation of Kv1 channel expression at the soma membrane. This is the first example of passive transfer of an autoimmune peripheral neuropathic pain disorder and demonstrates that CASPR2 has a key role in regulating cell-intrinsic dorsal root ganglion (DRG) neuron excitability