The aim of this thesis is to develop a novel technique for the estimation of firing rate dynamics from single-unit recordings of neural pulse trains. This method applies an offline digital filtering technique to extract information transmitted by a neuron in teens of a rate code. While there is increasing evidence that the traditional rate coding cannot account for all the information transmitted by a cell, and that information may also be contained in the precise timing of spikes, the firing rate signal remains the benchmark by which the vast majority of electrophysiological studies relating neural activity to functional behaviour have been interpreted. Nevertheless, there does not seem to be an agreement on a single definition of a rate code let alone a consensus on an optimal estimation method. This study raises significant concerns about the validity of some of the most common methods in systems neuroscience, and proposes a simple yet more robust alternative. This latter is based on the convolution of the spike train with an optimally designed Kaiser window. Using computer-simulated as well as experimental data obtained from single-unit recordings of vestibular canal afferents, the proposed technique is shown to consistently outperform the current methods and even to permit robust estimations under time-varying conditions. These results suggest that estimates acquired with the conventional methods are biased and hence models of neural dynamics based on these latter may not be reliable.

It has been hypothesized that head-unrestrained gaze shifts are controlled by an error signal produced by a feedback loop. It has also been hypothesized that the superior colliculus (SC) is within this feedback loop. If the feedback-to-SC hypothesis is valid, an unexpected mid-flight perturbation in gaze trajectory should be quickly followed by a concurrent change in the discharges of collicular saccade-related neurons. To verify this prediction experimentally, primate head movements were unexpectedly and briefly halted during head-unrestrained gaze shifts in the dark. Perturbed gaze shifts were composed of first a gaze saccade made when the head was immobilized by the head-brake, followed by a period where gaze was immobile, called a gaze plateau. The latter was composed of an initial period when the eyes and head were immobile, followed by a period wherein the head was released and the eyes counter-rotated to stabilize gaze. The plateau ended with a corrective gaze saccade to the goal location. In perturbed gaze shifts, there was widely distributed activity on the SC map during gaze plateaus, and there was no evidence that the initial motor program was aborted; the corrective gaze saccades were not "fresh" small stand-alone movements. Cells on the SC map responded at short latencies to head accelerations and associated gaze shift perturbations and carried a gaze position error (GPE = final - instantaneous gaze position) signal. As a large gaze shift progressed there was a caudo-rostral moving hill of activity on the SC map that encoded, not instantaneous veridical GPE, but a filtered version of it (time constant 100ms). Recordings from both the motor map and the so-called "fixation zone" in the rostral SC during perturbed head-unrestrained gaze shifts reveal gaze feedback control and a gaze feedback signal to the SC. However, these results do not prove that the SC is within the online gaze feedback loop, only that such a loop exists and that the collicular map is informed about its calculations.

What changes in our brain when we learn? This is perhaps the most intriguing question of science in this century. In an attempt to learn more about the inner workings of neural circuitry, I studied cultured 2-dimensional networks of neurons on multi-electrode arrays (MEAs). MEAs are ideal tools for studying long-term neural ensemble activity because many individual cells can be studied continuously for months, through electrical stimulation and recording. One of the most prominent patterns of activity observed in these cultures is network-wide spontaneous bursting, during which most of the active electrodes in the culture show elevated firing rates. We view the persistence of spontaneous bursting in vitro as a sign of arrested development due to deafferentation. Substituting distributed electrical stimulation for afferent input transformed the activity in dissociated cultures from bursting to more dispersed spiking, reminiscent of activity in the adult brain. Burst suppression reduced the variability in neural responses making it easier to induce and detect functional plasticity caused by tetanic stimulation. This suggests that spontaneous bursts interfere with the effects of external stimulation and that a burst-free environment leads to more stable connections and predictable effects of tetanization. Moreover, our culture models continuously receive input stimulation in the form of background electrical stimulation, and so better resemble the intact brain than isolated (non-continuously stimulated) cultures. The proportion of GABAergic neurons in the cultures was significantly increased (p<1e-2, paired t-test) after burst-quieting for 2 days, suggesting that burst suppression operated through the homeostatic control of inhibitory neurotransmitter levels. We also studied the role of spontaneous bursts as potential carriers of information in the network by clustering these spatiotemporally diverse bursts. Spontaneous burst clusters were stable over hours and tetanic stimulation significantly reorganized the distribution of the clusters. In summary, this body of work explores the rules of network-level functional plasticity and provides the input (electrical stimulation) output (spatiotemporal patterns) mappings for behavioral studies in embodied hybrid systems. The results of this study may also have clinical implications in the development of sensory prostheses and treatment of diseases of aberrant network activity such as epilepsy.

Thesis (Ph. D.)--Mechanical Engineering, Georgia Institute of Technology, 2008. / Committee Chair: Steve M. Potter; Committee Member: Eric Schumacher; Committee Member: Robert J. Butera; Committee Member: Stephan P. DeWeerth; Committee Member: Thomas D. DeMarse.

Dissertation (Ph.D.)--University of South Florida, 2008. / Title from PDF of title page. Document formatted into pages; contains 140 pages. Includes vita. Includes bibliographical references.

Thesis (Ph. D.)--University of Alabama at Birmingham, 2008. / Title from first page of PDF file (viewed Sept. 22, 2008). Includes bibliographical references.

Thesis (Ph. D.)--University of Washington, 1999. / Vita. Includes bibliographical references (leaves 78-82).

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Este estudo teve como objetivo investigar a influência de diferentes estágios de severidade da neuropatia diabética na velocidade de condução das fibras musculares estimada em quatro músculos do membro inferior durante contrações isométricas, utilizando-se eletromiografia de superfície. Oitenta e cinco adultos foram estudados: 16 indivíduos não diabéticos e 69 diabéticos classificados em quatro estágios de neuropatia definidos por um sistema fuzzy: ausente (n=26), leve (n=21), moderada (n=11) e grave (n=11). As velocidades de condução médias das fibras musculares do tibial anterior, gastrocnêmico medial, vasto lateral e bíceps femoral foram avaliadas utilizando uma matriz linear de eletrodos de superfície e foram comparadas entre os grupos estudados por meio de ANOVAs (p < 0,05). As velocidades de condução diminuíram significativamente no grupo com neuropatia moderada para o vasto lateral em relação aos outros grupos (18 a 21% de decréscimo), e foram menores em todos os grupos com diabetes para o tibial anterior em relação ao grupo controle (15 a 20% de decréscimo). Não só a localização anatômica distal do músculo afetou a velocidade de condução, mas também a proporção do tipo de fibras musculares, uma vez que o tibial anterior, com maior proporção de fibras do tipo I, estava com sua velocidade de condução alterada já no grupo ausente, enquanto o vasto lateral, com maior proporção de fibras do tipo II, estava com sua velocidade de condução alterada em estágios mais tardios da doença. De forma geral, os músculos do membro inferior têm diferentes suscetibilidades aos efeitos do diabetes mellitus e da neuropatia e mostram uma redução da velocidade de condução conforme a neuropatia progride / This study aimed at investigating the influence of different stages of diabetic neuropathy in the muscle fiber conduction velocities estimated in four lower limb mucles during isometric maximal voluntary contraction using surface electromyography. Eighty-five adults were studied: 16 non-diabetic individuals and 69 diabetic patients classified into four neuropathy stages, defined by a fuzzy system: absent (n=26), mild (n=21), moderate (n=11) and severe (n=11). Average muscle fiber conduction velocities of gastrocnemius medialis, tibialis anterior, vastus lateralis and biceps femoris were assessed using linear array electrodes, and the studied groups were compared by ANOVAs (p < 0.05). Conduction velocities were significantly decreased in the moderate neuropathy group for the vastus lateralis compared to other groups (from 18 to 21% decrease), and were decreased in all diabetic groups for the tibialis anterior (from 15 to 20% from control group). Not only the distal anatomical localization of the muscle affects the conduction velocity, but also the proportion of muscle fiber type, where the tibialis anterior, with greater type I fiber proportion, is affected already at the absent group while the vastus lateralis with greater type II fiber proportion is affected in later stages of the disease. Generally, the muscles of the lower limb have different responsiveness to the effects of diabetes mellitus and neuropathy and show a reduction in the conduction velocity as the neuropathy progresses