Image Restoration

This book represents a sample of recent contributions of researchers all around the world in the field of image restoration. The book consists of 15 chapters organized in three main sections (Theory, Applications, Interdisciplinarity). Topics cover some different aspects of the theory of image restoration, but this book is also an occasion to highlight some new topics of research related to the emergence of some original imaging devices. From this arise some real challenging problems related to image reconstruction/restoration that open the way to some new fundamental scientific questions closely related with the world we interact with

Identification of the optimal parameters for electrical stimulation to generate locomotor patterns in the rat isolated spinal cord

Recently, an innovative protocol of electrical stimulation, named \u201cfictive locomotion induced stimulation\u201d (FListim), which consists of an intrinsically variable noisy waveform, has been obtained from a segment of chemically-induced fictive locomotion (FL) sampled from the ventral root (VR) of an in vitro preparation of neonatal rat spinal cord. FListim delivered at sub-threshold intensities to a dorsal root (DR) has been shown to optimally activate the central pattern generators (CPGs) for locomotion (Taccola, 2011). In an attempt to introduce novel and improved protocols of stimulation in combination with neurochemicals, the current PhD project aims to identify the features that make sub-threshold noisy waveforms effective in activating locomotor patterns. In an attempt to introduce novel and improved protocols of stimulation in combination with neurochemicals, the current PhD project aims to identify the features that make sub-threshold noisy waveforms effective in activating locomotor patterns. To reach this aim, locomotor-like patterns in response to different noisy waveforms were compared. In order to obtain a wide palette of noisy protocols electromyographic (EMG) recordings were performed from leg muscles of adult volunteers during walking. These recordings were then delivered as stimulating patterns called real locomotion-induced stimulation (ReaListim). To reach this aim, locomotor-like patterns in response to different noisy waveforms were compared. In order to obtain a wide palette of noisy protocols electromyographic (EMG) recordings were performed from leg muscles of adult volunteers during walking. These recordings were then delivered as stimulating patterns called real locomotion-induced stimulation (ReaListim). ReaListim protocols, sampled during different motor behaviours, are equally able to induce an epoch of locomotor-like oscillations. Conversely, smooth kinematic profiles and non-phasic noisy patterns such as standing and isometric contraction, are unable to activate the locomotor CPGs. The complexity of noisy waveforms was then reduced at motoneuronal level, by recording electrical activity of a single motoneuron during FL. Long-lasting episode of FL, were evoked in response to intracellular patterns delivered at sub-threshold intensities. The analysis of motoneuronal firing during FL was used to identify four recurrent frequency values that optimally activated the locomotor CPGs when applied simultaneously in a multifrequency protocol. Different permutations were tried to further simplify the multifrequency protocol while isolating the most effective components of the four identified frequencies. The simplest asynchronous paradigm that can induce locomotor-like episodes consists of a train of rectangular pulses that contain two frequencies: 35 and 172 Hz. This protocol resulted already effective at subthreshold intensity even when delivered for a very short time (500 ms). The role of oxytocin in the modulation of neuronal networks is explored here on spinal networks. Intracellular recordings demonstrate that oxytocin dosedependently depolarizes single motoneurons with the appearance of sporadic bursts with superimposed firing. By applying the selective blocker of sodium channels, tetrodotoxin (TTX), the effects of oxytocin can be completely abolished, which suggest a premotoneuronal-level origin. The neuropeptide is capable to induce VRs depolarization with superimposed synchronous bursts of activity, while reflex responses induced by single pulses are depressed depending on the stimulus strength and peptide-concentration. The disinhibited bursting evoked by the pharmacological blockade of glycine and GABAA receptors blockers, strychnine and bicuculline, respectively, is accelerated by oxytocin, an effect that is suppressed by the selective oxytocin receptor antagonist atosiban. On spinal locomotor networks oxytocin facilitates the emergence of FL episodes in response either to weak noisy waveforms protocols or to the conjoint application of NMDA and 5HT at sub-threshold concentrations, even if the periodicity of a stable FL is not significantly affected by the neuropeptide. Interestingly, the facilitation of the locomotor CPGs by oxytocin is dependent on the endogenous release of 5HT, as is demonstrated by incubation with the inhibitor of 5HT synthesis, pchlorophenilalanine (PCPA). Low-frequency trains of stereotyped pulses (0.33 and 0.67Hz) delivered with a controlled time interval (delays 0.5 to 2 s) to multiple DRs converged on spinal locomotor circuits to generate locomotor rhythm. The same finding is confirmed by the phase resetting that is induced by single afferent stimuli during a simultaneous train of pulses delivered to another DR. Staggered protocols fail to elicit FL when simultaneously applied to multiple DRs, while a multi-site randomized pulse train is still effective in eliciting locomotor-like patterns. This thesis outlines new strategies for optimizing the reactivation of spinal locomotor networks after spinal damage. Though the technology that is currently available in clinics does not allow for the delivery of highly-variable stimulating patterns, experiments reported here indicate a way to overcome these limitations. Indeed, protocols that contain few distinct frequencies that are isolated from the spectrum of noisy waves can activate the CPGs even when delivered with a multisite approach. This suggests that it may be possible to separately supply multiple trains of pulses to several cord sites using different electrostimulators. The yield of stimulation in activating locomotor circuits will be further improved by the association with the neuropeptide oxytocin

Short-Term Plasticity at the Schaffer Collateral: A New Model with Implications for Hippocampal Processing

A new mathematical model of short-term synaptic plasticity (STP) at the Schaffer collateral is introduced. Like other models of STP, the new model relates short-term synaptic plasticity to an interaction between facilitative and depressive dynamic influences. Unlike previous models, the new model successfully simulates facilitative and depressive dynamics within the framework of the synaptic vesicle cycle. The novelty of the model lies in the description of a competitive interaction between calcium-sensitive proteins for binding sites on the vesicle release machinery. By attributing specific molecular causes to observable presynaptic effects, the new model of STP can predict the effects of specific alterations to the presynaptic neurotransmitter release mechanism. This understanding will guide further experiments into presynaptic functionality, and may contribute insights into the development of pharmaceuticals that target illnesses manifesting aberrant synaptic dynamics, such as Fragile-X syndrome and schizophrenia. The new model of STP will also add realism to brain circuit models that simulate cognitive processes such as attention and memory. The hippocampal processing loop is an example of a brain circuit involved in memory formation. The hippocampus filters and organizes large amounts of spatio-temporal data in real time according to contextual significance. The role of synaptic dynamics in the hippocampal system is speculated to help keep the system close to a region of instability that increases encoding capacity and discriminating capability. In particular, synaptic dynamics at the Schaffer collateral are proposed to coordinate the output of the highly dynamic CA3 region of the hippocampus with the phase-code in the CA1 that modulates communication between the hippocampus and the neocortex

29th Annual Computational Neuroscience Meeting: CNS*2020

Meeting abstracts This publication was funded by OCNS. The Supplement Editors declare that they have no competing interests. Virtual | 18-22 July 202

Afferent information modulates spinal network activity in vitro and in preclinical animal models

Primary afferents are responsible for the transmission of peripheral sensory information to the spinal cord. Spinal circuits involved in sensory processing and in motor activity are directly modulated by incoming input conveyed by afferent fibres. Current neurorehabilitation exploits primary afferent information to induce plastic changes within lesioned spinal circuitries. Plasticity and neuromodulation promoted by activity-based interventions are suggested to support both the functional recovery of locomotion and pain relief in subjects with sensorimotor disorders. The present study was aimed at assessing spinal modifications mediated by afferent information. At the beginning of my PhD project, I adopted a simplified in vitro model of isolated spinal cord from the newborn rat. In this preparation, dorsal root (DR) fibres were repetitively activated by delivering trains of electrical stimuli. Responses of dorsal sensory-related and ventral motor-related circuits were assessed by extracellular recordings. I demonstrated that electrostimulation protocols able to activate the spinal CPG for locomotion, induced primary afferent hyperexcitability, as well. Thus, evidence of incoming signals in modulating spinal circuits was provided. Furthermore, a robust sensorimotor interplay was reported to take place within the spinal cord. I further investigated hyperexcitability conditions in a new in vivo model of peripheral neuropathic pain. Adult rats underwent a surgical procedure where the common peroneal nerve was crushed using a calibrated nerve clamp (modified spared nerve injury, mSNI). Thus, primary afferents of the common peroneal nerve were activated through the application of a noxious compression, which presumably elicited ectopic activity constitutively generated in the periphery. One week after surgery, animals were classified into two groups, with (mSNI+) and without (mSNI-) tactile hypersensitivity, based on behavioral tests assessing paw withdrawal threshold. Interestingly, the efficiency of the mSNI in inducing tactile hypersensitivity was halved with respect to the classical SNI model. Moreover, mSNI animals with tactile hypersensitivity (mSNI+) showed an extensive neuroinflammation within the dorsal horn, with activated microglia and astrocytes being significantly increased with respect to mSNI animals without tactile hypersensitivity (mSNI-) and to sham-operated animals. Lastly, RGS4 (regulator of G protein signaling 4) was reported to be enhanced in lumbar dorsal root ganglia (DRGs) and dorsal horn ipsilaterally to the lesion in mSNI+ animals. Thus, a new molecular marker was demonstrated to be involved in tactile hypersensitivity in our preclinical model of mSNI. Lastly, we developed a novel in vitro model of newborn rat, where hindlimbs were functionally connected to a partially dissected spinal cord and passively-driven by a robotic device (Bipedal Induced Kinetic Exercise, BIKE). I aimed at studying whether spinal activity was influenced by afferent signals evoked during passive cycling. I first demonstrated that BIKE could actually evoke an afferent feedback from the periphery. Then, I determined that spinal circuitries were differentially affected by training sessions of different duration. On one side, a short exercise session could not directly activate the locomotor CPG, but was able to transiently facilitate an electrically-induced locomotor-like activity. Moreover, no changes in reflex or spontaneous activity of dorsal and ventral networks were promoted by a short training. On the other side, a long BIKE session caused a loss in facilitation of spinal locomotor networks and a depression in the area of motor reflexes. Furthermore, activity in dorsal circuits was long-term enhanced, with a significant increase in both electrically-evoked and spontaneous antidromic discharges. Thus, the persistence of training-mediated effects was different, with spinal locomotor circuits being only transiently modulated, whereas dorsal activity being strongly and stably enhanced. Motoneurons were also affected by a prolonged training, showing a reduction in membrane resistance and an increase in the frequency of post-synaptic currents (PSCs), with both fast- and slow-decaying synaptic inputs being augmented. Changes in synaptic transmission onto the motoneuron were suggested to be responsible for network effects mediated by passive training. In conclusion, I demonstrated that afferent information might induce changes within the spinal cord, involving both neuronal and glial cells. In particular, spinal networks are affected by incoming peripheral signals, which mediate synaptic, cellular and molecular modifications. Moreover, a strong interplay between dorsal and ventral spinal circuits was also reported. A full comprehension of basic mechanisms underlying sensory-mediated spinal plasticity and bidirectional interactions between functionally different spinal networks might lead to the development of neurorehabilitation strategies which simultaneously promote locomotor recovery and pain relief

対属性仮説に基づく結合問題の解決と多次元情報統合過程のモデル化

科学研究費助成事業 研究成果報告書：挑戦的萌芽研究2014-2017課題番号 : 2659017

Modelling human choices: MADeM and decision‑making

Research supported by FAPESP 2015/50122-0 and DFG-GRTK 1740/2. RP and AR are also part of the Research, Innovation and Dissemination Center for Neuromathematics FAPESP grant (2013/07699-0). RP is supported by a FAPESP scholarship (2013/25667-8). ACR is partially supported by a CNPq fellowship (grant 306251/2014-0)