This project applies principles from the field of Computational Neuroscience to Robotics research, in particular to develop systems inspired by how nature manages to solve sensorimotor coordination tasks. The overall aim has been to build a self-organising sensorimotor system using biologically inspired techniques based upon human cortical development which can in the future be implemented in neuromorphic hardware. This can then deliver the benefits of low power consumption and real time operation but with flexible learning onboard autonomous robots. A core principle is the Self-Organising Feature Map which is based upon the theory of how 2D maps develop in real cortex to represent complex information from the environment. A framework for developing feature maps for both motor and visual directional selectivity representing eight different directions of motion is described as well as how they can be coupled together to make a basic visuomotor system. In contrast to many previous works which use artificially generated visual inputs (for example, image sequences of oriented moving bars or mathematically generated Gaussian bars) a novel feature of the current work is that the visual input is generated by a DVS 128 silicon retina camera which is a neuromorphic device and produces spike events in a frame-free way. One of the main contributions of this work has been to develop a method of autonomous regulation of the map development process which adapts the learning dependent upon input activity. The main results show that distinct directionally selective maps for both the motor and visual modalities are produced under a range of experimental scenarios. The adaptive learning process successfully controls the rate of learning in both motor and visual map development and is used to indicate when sufficient patterns have been presented, thus avoiding the need to define in advance the quantity and range of training data. The coupling training experiments show that the visual input learns to modulate the original motor map response, creating a new visual-motor topological map.

This thesis is composed of two chapters. Chapter one reviews what is known about adaptive plasticity in response to predators, describes the physiological systems involved in such plasticity, and outlines the evolutionary consequences of adaptive plasticity. Chapter two describes a scientific experiment that investigates how malathion may impact adaptive plasticity in the Sierran Treefrog, Pseudacris sierra. Anuran tadpoles suffer high mortality rates due to predation. In response to strong selective forces relating to these high predation rates, tadpoles evolved the ability to adaptively respond to predators through morphological and behavioral plasticity. The morphological and behavioral responses are varied and depend on the hunting strategy of the predator, and the adaptive responses may be influenced by other biotic and abiotic factors. Tadpoles detect alarm cues released from tadpoles being eaten and kairomones that are released by predators. Tadpoles respond to these signals by changing tail and body shape along with a reduction of activity level, which enables tadpoles to escape predators more effectively. These changes in morphology can occur within a week, and behavioral changes can occur within 15 minutes. The adaptive responses are critical for increasing survival rates of tadpoles to metamorphosis and may have important evolutionary consequences for anurans. Amphibians are in decline worldwide, and pollutants are considered to be a major contributor to these declines. Every year 5.2 billion pounds of active ingredients of pesticides are applied worldwide, and these application rates have led to ubiquitous low-level contamination of aquatic ecosystems. How low-level contamination of pesticides directly and indirectly affect how tadpoles respond to their predators is poorly understood. One potential indirect effect of pesticides is the inhibition of adaptive plasticity. Pesticides have been shown to modulate corticosterone levels in tadpoles. Corticosterone is the most likely mediator of the physiological response that results in adaptive morphological change. If the physiological system of tadpoles relies on corticosterone as the mediator of adaptive response, and pesticides can modulate corticosteone levels, then pesticides may inhibit or negatively impact adaptive responses to important biotic factors, like predators. Pesticides have been shown to weaken immune systems, affect developmental and physiological pathways that lead to malformations, and cause direct mortality in anurans. Little research has investigated the effect of pesticides on adaptive morphological and behavioral plasticity in response to predators. Adaptive phenotypic responses to predators increase survival rates to metamorphosis and are important in stabilizing amphibian populations through time. If pesticides influence the ecological interactions of tadpoles and their predators, this could play a part in amphibian declines. In the experiment explained in Chapter two, I tested the hypothesis that malathion at a concentration of 0.1 mg/L inhibits anti-predator morphological and behavioral responses of Pseudacris sierra to the predatory dragonfly larvae Anax junius. The results of this experiment show that malathion alone caused the tail muscle depth to increase to the same magnitude as tadpoles that only experienced a predator’s presence. Malathion also caused a significant increase in tail depth, demonstrating that malathion directly causes morphological change. The experiment did not support the hypothesis that malathion inhibits adaptive plasticity, and malathion had no impact on behavioral plasticity. The results from this experiment give evidence that an ecologically relevant concentration of malathion can influence morphological components that are critical in escaping depredation events, which could affect predator-prey interactions.

An increasing amount of attention is devoted to studying the impact of non-native animal species on native species. Among other causes of ecosystem degradation, such as climate change, polution and habitat conversion, biological invasion is considered as one of the main causes of the decrease in biological diversity all over the world. In order to detect possible predation event, tadpoles use not only visual and mechanical stimuli, but also chemical one. The tadpoles respond to the certain chemicals to be a part of predator's secretions. In aquatic systems, chemical cues are a major source of information through which animals are able to assess the current state of their environment to gain information about local predation risk. Prey use chemicals released by predators to mediate a range of behavioural, morphological and life-history antipredator defences. Tadpoles swim significatnly less and also on a less direct trajectory in the presence of chemical cues released by a turtle Trachemys scripta. This article is focused on the influence of mentioned constraints on the dynamics and the time dynamics of the larval growth of Rana temporaria. The influence was judged by the impact on the tadpole's development. We anticipated a behavioral response to the predator, which would lead to various growth reactions during larval growth, the resulting body size after metamorphosis, but also in the development time of larval stage. The results indicate that tadpoles of Rana temporaria changed behaviour in the presence of Trachemys scripta. Tadpoles in the permanent presence of the turtle grew faster, metamorphosed earlier and the resulting size after metamorphosis was smaller than of the tadpoles who developed without presence of the predator. Mentioned reactions may affect the survival and fitness of a metamorphosed individual.

La préhension modifiée après tétraplégie repose sur la ténodèse. Ses caractéristiques cinématiques sont : un transport poignet fléchi, étendant les doigts puis une saisie poignet étendu, fléchissant les doigts et produisant les prises palmaires et latérales passives. Les deux phases de la préhension sont réalisées successivement après tétraplégie contrairement au maintien du couplage des deux phases du sujet sain. Les caractéristiques cinématiques des autres mouvements du membre supérieur en chaîne cinétique ouverte sont la conservation des invariants de précision et d'économie pour la programmation des gestes malgré la réduction du nombre de degrés disponibles après tétraplégie mais au détriment d'une réduction de la vitesse d'exécution. Le temps de mouvement augmente probablement pour maintenir la précision finale ou consécutivement au déficit moteur. L'extension du coude sans triceps repose sur l'augmentation des mouvements des articulations proximales de l'épaule. Cependant cette compensation est incomplète comme l'atteste la réduction de l'espace de capture supérieur où le déficit moteur des muscles agonistes, synergiques stabilisateurs de la scapulothoracique et du coude mais également la raideur et les douleurs de l'épaule sont impliqués. L'imagerie motrice (i) améliore la préhension par ténodèse, (ii) conduit une plasticité d'adaptation, (iii) améliore qualité et structure temporelle de l'imagerie. Ainsi, la préhension gagne en reproductibilité avec une réduction de la variabilité du temps de mouvement. L'extension du poignet augmente lors de la saisie attestant le renforcement du mécanisme de compensation par ténodèse pour réaliser les prises. L'imagerie motrice favorise une plasticité cérébrale adaptative avec réduction des activations des cortex prémoteur et moteur primaire anormalement augmentées après tétraplégie. Enfin, les hauts scores de vivacité sont associés à une imagerie ralentie révélant un contrôle de la qualité de la représentation mentale au détriment de sa structure temporelle. Après imagerie, la qualité de la reconstruction mentale se renforce et la structure temporelle s'améliore / Tetraplegia alters active prehension which relies on tenodesis. Its kinematic characteristics are flexion of the wrist during transport and extension of the wrist during grasping eliciting lateral and palmar grips. Transport and grasping are two consecutive movements as opposed to healthy reach-to-grasp where transport and grasping are coupled. Others open chain upper limb movements showed that despite the degrees of freedom reduction, the central nervous system still plan movements using kinematic invariants like endmovements accuracy and movement economy but at the cost of velocity that decrease. The increase of movement time can be due to the requierement of endmovement accuracy, motor deficit like inability to generate cocontraction at the elbow level being due to triceps paralysis. Despite triceps brachii paralysis, shoulder movements trigger elbow extension. However, this compensation is incomplete as shown by the decrease of superior maximal reaching. This could be due to the deficit of agonist muscles along with proximal and distal synergic stabilizer, shoulder range of motion decrease and shoulder pain. Motor imagery results in (i) prehension improvement attesting that the compensation is strengthened (ii) cortical adaptive plasticity (iii) increase in quality and temporal structure of mental reconstruction. Thereby, consistency of prehension increases as shown by the reduction of movement time variability. Wrist extension increased during grasping attesting a strengthening of tenodesis compensatory mechanism to produce grips. Motor imagery elicited adaptive brain plasticity with reduction of premotor and primary motor cortex activations that are abnormally increased after tetraplegia. Finally, motor imagery control is based on movement quality to the detriment of temporal structure. In response to motor imagery, movement quality is further enhanced and temporal structure is improved. Thereby, prehension is improved in response to motor imagery. Thus, corrective and adaptive plasticity could be promoted

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