The purpose of this study was to determine if resistance exercise altered peripheral BDNF concentration. Eighteen trained male subjects were split into two groups performing varied repetition ranges. DUP-HR and DUP-LR groups trained 3x/week for 8 weeks, and were equated for total volume (repetitions X sets X intensity). Plasma BDNF and interleukin-6 (IL-6) levels were measured prior to and immediately following the first exercise session of weeks 1, 2, 4 and 6. Pre-exercise levels were also assessed prior to the second and third sessions of week 1 and 6. Lastly, resting levels were measured before and after training intervention. No group differences (p>0.05) were detected for either biomarker. An acute BDNF elevation (p=0.018) was detected only in the final week of training. IL-6 elevations were detected at all acute measurements (p<0.01). BDNF and IL-6 percentage change correlated significantly (p<0.05) in week-1. No chronic alterations were observed (p>0.05). / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2015 / FAU Electronic Theses and Dissertations Collection

Out of 60 million Americans suffering from sleep disorder, an estimated 18 million have sleep apnea. According to the U.S. Department of Health & Human Services, sleep apnea is a chronic condition that disrupts a patient’s sleep. While the annual cost of treating sleep apnea patients in the United States is approximately $3.18 billion (including screening costs) it is estimated that untreated sleep apnea may cause $3.4 billion in additional medical costs. A polysomnography (PSG) is an all-night sleep study which monitors various physical functions during sleep including electrical activity of the heart, brain wave patterns, eye movement, muscle tone, body movements, and breathing. It is currently, the most accurate and sophisticated test for the diagnosis of sleep-disordered breathing (SDB), but also, the most expensive. The cost of an overnight sleep study is estimated between $900 and $3,000. In addition, the PSG is not mobile and has to be administered outside a patient’s home. The Long QT Syndrome (LQTS) is a rhythm disorder that causes erratic (unpredictable) heartbeats. The LQTS has been linked to patients with the most severe form of sleep apnea. If LQTS is left untreated, sudden cardiac death may occur. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2014. / FAU Electronic Theses and Dissertations Collection

The advent of sexual reproduction in early evolutionary history had profound effects on the evolution of animals. In most sexually reproducing species, males and females have distinct morphological and behavioral differences that are shaped by the evolutionary imperatives of each sex. Underlying the behavioral differences between males and females are distinct and measurable dimorphisms in the nervous system. These dimorphisms can arise in the form of connectivity, neurotransmitter usage, gene expression or combinations of all three. The androdioecious nematode Caenorhabditis elegans, with its stereotyped development and simple nervous system, offers a remarkably powerful system for studying the conserved mechanisms of sex determination that shape neural development. In this thesis, I present my work on the characterization of several genes that regulate the development of sexual dimorphisms in the nervous system. The first part of the thesis concerns the characterization of the gene ham-3, which codes for a subunit of the C. elegans ortholog of the SWI/SNF chromatin remodeling complex. ham-3 is required for the proper terminal differentiation of the HSN, a serotonergic neuron of the sex-specific nervous system, which it manages by regulating the expression of transcription factors required for crucial steps of migration, axon guidance and serotonergic fate adoption. The second part of the thesis concerns the investigation of sexually dimorphic pruning mechanisms. I show that unc-6/Netrin is subject to direct transcriptional repression in hermaphrodites by tra-1, the master transcriptional regulator of sexual fate determination in C. elegans. This regulation is required for the proper timing of the sexually dimorphic pruning of synapses in the tail region in hermaprhodites. In males, where unc-6 is not repressed by tra-1, unc-6 expression perdures into adulthood and the synapse is maintained. Together, these data provide insight into the ways in which conserved genetic and developmental mechanisms manage the generation differentiation, connectivity, and maintenance of sexually dimorphic nervous systems.

The Neuregulin 1 (NRG1)-ErbB4 signalling pathway is implicated in critical processes for the development and function of neuronal circuits. Post mortem studies have reported that elevated expression of NRG1 type 1 isoform is associated with schizophrenia. Importantly previous behavioural studies in mice that overexpress the NRG1 type 1 isoform (NRG1^tg-type-I) have suggested a schizophrenia endophenotype including impairment in the hippocampus-dependent spatial working memory, prepulse inhibition (PPI) of the startle reflex and alterations in the gamma band rhythmogenesis This study aims to reveal the cellular targets of the NRG1-ErbB4 signalling pathway and putative alterations in the function of the hippocampal network in NRG1^tg-type-I mice. Immunocytochemical analysis showed that the NRG1 receptor ErbB4 is predominantly localized in interneurons comprising parvalbumin positive (PV) and cholecystokinin (CCK) expressing cells. Comparison of the density of ErbB4-positive cells between the hippocampus of wild type (WT) and NRG1^tg-type-I mice suggested that NRG1 over-expression resulted in decreased number of ErbB4 immunopositive hippocampal interneurons. This is consistent with the proposed role of the NRG1-ErbB4 signalling in the migration of GABAergic cells during neurodevelopment and with the NRG1-mediated internalisation of the ErbB4 receptors. CCK- positive cells are a major target of NRG1-ErbB4 signalling, and therefore the NMDA receptor and AMPA receptor components of glutamatergic transmission were analysed in this population of cells by performing whole cell recordings of evoked and miniature excitatory post synaptic currents. Glutamatergic neurotransmission in CCK-positive cells was found to be compromised in the hippocampus of NRG1^tg-type-I mice. This change was attributed to hypofunction of NMDA receptors but not AMPA receptors post-synaptically. Next, the inhibitory output of CCK-positive cells to pyramidal cells was examined. Analysis of the optogenetically elicited inhibitory post synaptic currents (IPSCs) did not reveal any changes in the properties of the GABAergic synapse formed by these cells due to NRG1 over-expression Finally, the effects of this NMDA receptor hypofunction in the recurrent inhibition were analysed by performing whole cell recordings during the gamma relevant optogenetic entrainment of the hippocampal network. It was found that the disynaptic inhibition, a key synaptic interaction for the generation of gamma oscillations, depends on the NMDA receptors and was altered in the hippocampus of NRG1^tg-type-I mice. Together these data point out a key modulatory role of the NRG1-ErbB4 signalling in the neurodevelopment of cortical microcircuits and a link between ErbB4 and NMDA receptor function with a possible association to schizophrenia pathogenesis.

A current challenge in neuroscience and systems biology is to better understand properties that allow organisms to exhibit and sustain appropriate behaviours despite the effects of perturbations (behavioural robustness). There are still significant theoretical difficulties in this endeavour, mainly due to the context-dependent nature of the problem. Biological robustness, in general, is considered in the literature as a property that emerges from the internal structure of organisms, rather than being a dynamical phenomenon involving agent-internal controls, the organism body, and the environment. Our hypothesis is that the capacity for behavioural robustness is rooted in dynamical processes that are distributed between agent ‘brain', body, and environment, rather than warranted exclusively by organisms' internal mechanisms. Distribution is operationally defined here based on perturbation analyses. Evolutionary Robotics (ER) techniques are used here to construct four computational models to study behavioural robustness from a systemic perspective. Dynamical systems theory provides the conceptual framework for these investigations. The first model evolves situated agents in a goalseeking scenario in the presence of neural noise perturbations. Results suggest that evolution implicitly selects neural systems that are noise-resistant during coupling behaviour by concentrating search in regions of the fitness landscape that retain functionality for goal approaching. The second model evolves situated, dynamically limited agents exhibiting minimalcognitive behaviour (categorization task). Results indicate a small but significant tendency toward better performance under most types of perturbations by agents showing further cognitivebehavioural dependency on their environments. The third model evolves experience-dependent robust behaviour in embodied, one-legged walking agents. Evidence suggests that robustness is rooted in both internal and external dynamics, but robust motion emerges always from the systemin-coupling. The fourth model implements a historically dependent, mobile-object tracking task under sensorimotor perturbations. Results indicate two different modes of distribution, one in which inner controls necessarily depend on a set of specific environmental factors to exhibit behaviour, then these controls will be more vulnerable to perturbations on that set, and another for which these factors are equally sufficient for behaviours. Vulnerability to perturbations depends on the particular distribution. In contrast to most existing approaches to the study of robustness, this thesis argues that behavioural robustness is better understood in the context of agent-environment dynamical couplings, not in terms of internal mechanisms. Such couplings, however, are not always the full determinants of robustness. Challenges and limitations of our approach are also identified for future studies.

The metabotropic glutamate receptor, mGluR5, is densely expressed in brain regions involved in incentive learning processes. There is considerable evidence to suggest that following exposure to addictive drugs such as cocaine, adaptations in these brain areas may underlie the development and maintenance of behavioural responses related to addictive processes. The present thesis examines the role of mGluR5 in both incentive learning processes and some behavioural and neurobiological effects of cocaine. First, using a novel mutant mouse line in which mGluR5 is selectively knocked down in cells that express dopamine D1 receptors (D1R), I argue that this mGluR5 population is critically important for specific incentive learning processes. By blocking mGluR5 in wild-type mice with a selective antagonist, I then propose mGluR5 as necessary for the acquisition, but not the expression of an incentive association. Next, I present data showing that mGluR5 on dopaminoceptive neurons are not necessary for the „conditioned rewarding‟ properties of cocaine, measured in the conditioned place preference model, but do contribute to the psychomotor activating effects of cocaine. Finally, I present an immunohistochemistry study that examines cocaine-induced activation of the extracellular-signal related kinase (ERK) pathway. In the mGluR5 knock-down mice, activation of the ERK pathway in the striatum is disrupted following an acute injection of cocaine. Given the importance of the ERK pathway in establishing and maintaining long term memories, I propose that disruption of this pathway could contribute, in part, to some findings reported in the present thesis. Taken together, this thesis will argue that signalling through mGluR5 on D1R expressing neurons is important for the formation of incentive associations, and may contribute to neural adaptations necessary for the development and maintenance of behavioural responses related to addictive processes.

Oscillatory neural activity is closely related to cognition and behaviour, with synchronisation mechanisms playing a key role in the integration and functional organization of different cortical areas. Nevertheless, its informational content and relationship with behaviour - and hence cognition - are still to be fully understood. This thesis is concerned with better understanding the role of neuronal oscillations and information dynamics towards the generation of embodied cognitive behaviours and with investigating the efficacy of such systems as practical robot controllers. To this end, we develop a novel model based on the Kuramoto model of coupled phase oscillators and perform three minimally cognitive evolutionary robotics experiments. The analyses focus both on a behavioural level description, investigating the robot's trajectories, and on a mechanism level description, exploring the variables' dynamics and the information transfer properties within and between the agent's body and the environment. The first experiment demonstrates that in an active categorical perception task under normal and inverted vision, networks with a definite, but not too strong, propensity for synchronisation are more able to reconfigure, to organise themselves functionally, and to adapt to different behavioural conditions. The second experiment relates assembly constitution and phase reorganisation dynamics to performance in supervised and unsupervised learning tasks. We demonstrate that assembly dynamics facilitate the evolutionary process, can account for varying degrees of stimuli modulation of the sensorimotor interactions, and can contribute to solving different tasks leaving aside other plasticity mechanisms. The third experiment explores an associative learning task considering a more realistic connectivity pattern between neurons. We demonstrate that networks with travelling waves as a default solution perform poorly compared to networks that are normally synchronised in the absence of stimuli. Overall, this thesis shows that neural synchronisation dynamics, when suitably flexible and reconfigurable, produce an asymmetric flow of information and can generate minimally cognitive embodied behaviours.

Word recognition is based on the complex interplay of bottom up processing of acoustic input and corresponding top-down processing based on linguistic redundancies (i.e., contextual cues). Friedrich and Kotz (2007) investigated the timeline of integrating top-down and bottom-up processes among young adults with normal hearing using sentences presented in quiet. As a follow-up study, also with young adults with normal hearing (Experiment 1 of this dissertation), we used sentences embedded in multi-talker background noise and found similar results to Friedrich and Kotz (2007); but, with the use of principal component analysis (PCA) unveiled additional effects of phonological and semantic integration of spoken sentences presented in background noise. These past studies provide evidence of the time course of bottom-up and top-down mechanisms among young adult listeners in quiet and in noise; however, it is unknown if a similar pattern would be present among older adult listeners, which was the primary goal of the dissertation. In Experiment 2, we aimed to elucidate the time-course, and behavioral and neural correlates of word recognition primed by speech-in-noise in older adults with near normal hearing (i.e., thresholds ≤ 25 dB-HL through 3000 Hz and minimal high frequency hearing loss). Older adults often report difficulty understanding speech in the presence of background noise. Degradation in peripheral and central auditory processing along with age-related cognitive decline has been hypothesized as reasons why older adults struggle in the presence of noise.

Biological responses to orthodontic forces involve various cell types, these include fibroblasts, endothelial cells, blood vessels and sensory nerves in the periodontal ligament as well as osteoblasts, osteoclasts and cementoblasts in roots and bone surfaces. Neurotrophins are believed to interact with these cells to initiate the process of bone resorption particularly during orthodontic tooth movement. Neuropeptides released from sensory neurons have been shown to modulate the tissue inflammatory responses. In addition, neurotrophins, including nerve growth factor (NGF), play an important role in neural cell differentiation and survival. The exact localization and function of neurotrophins and neurotrophic receptors in the dento-alveolar complex remains unclear. Moreover, the identity and distribution of structures expressing neurotrophins and neurotrophic receptors has yet to be fully determined. It is reasonable to propose that periodontal ligament and alveolar bone remodelling may be influenced by NGF. In addition, anti-NGF may block neurochemical changes and, hence, inhibit orthodontic tooth movement. The aims of this research were to investigate the cells responsible for NGF secretion within the periodontal ligament (PDL), pulp and bone, and the effect that anti-NGF might have on orthodontic tooth movement. 28, 8 week-old, male Sprague-Dawley rats were randomly divided into control and experimental groups. Fourteen experimental animals had anti-NGF injected paradentally. Animals were sacrificed at 7 and 14 days. Sections from an earlier study were examined and stained using TRAP for osteoclast identification and analysed histomorphometrically to enable comparisons between control and experimental groups. The findings of this investigation indicated that injections of anti-NGF did not significantly affect the rate of tooth movement with the use of different tooth movement measurement methods. TRAP staining proved to be a useful and reliable marker of osteoclasts. TRAP-positive osteoclastic cells were detected in both anti-NGF and control groups. However, the TRAP-positive cells were not stained intensely with NGF immunolabelling. On the other hand, cells that were stained intensely with NGF, were TRAP-negative. The results suggested that both sympathetic and nociceptive nerves might function in counter balance to modulate bone resorption, and osteoclasts might not be directly responsible for NGF secretion within the PDL and bone. Further studies to determine the effect of NGF on tooth movement are warranted to more clearly identify the NGF expressing cells within the rat dento-alveolar complex and possible role played by NGF in orthodontic tooth movement. / http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1297498 / Thesis (D.Clin.Dent.)-- School of Dentistry, 2007

<p>Skin temperature is detected through signals in unmyelinated C-fibers and thin myelinated Aδ-fibers in the peripheral and central nervous system. Disorders in thin nerve fibres are important and not rare but difficult to diagnose by the most common neurophysiological methods. In this pilot study different methods for quantitative sensory testing, QST, were compared to give some ideas about which method could be the most efficient to use in order to point out injuries of the sensory system in clinical practice. The comparison was made between Békésy (separate warmand cold thresholds) and Marstock test (combined warm and cold thresholds). The study also included the test persons estimations of the difficulty to perform the tests.</p><p>The study showed that there was no practical difference between the tests and that the test persons estimations did not show any indications that the methods differed in rating of difficulty. Our study did not give reason to stop measuring warm and cold detection thresholds separately, which is the international standard and have some theoretical advantages. We also compared detection thresholds for hand and foot, warmth and cold and for both slow and fast temperature changes to enlighten factors that could affect our measuring data.</p>