Thesis (M.Sc.)--Memorial University of Newfoundland, 2003. / Bibliography: leaves 110-138. Also available online.

Thesis (Ph. D.)--University of Washington, 2006. / Vita. Includes bibliographical references (leaves 126-139).

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / Typescript. Vita. Includes bibliographical references (leaves 166-187). Also available on the Internet.

Foram enfocadas neste presente estudo, 3 raças de cães, ou seja, Boxer, Dobermann e Rottweiler, com tipos constitucionais e aptidões funcionais característicos e distintos entre si, sendo coletados 4 encéfalos de cada raça. Dos encéfalos foram retirados fragmentos das diferentes áreas do córtex cerebral, que foram preparados segundo técnica histológica convencional e corados por violeta cresil modificada. Através de contagem visual-manual, foram buscados dados comparativos, entre áreas cerebrais versus raça associando tipos constitucionais versus aptidão funcional. As lâminas foram analisadas com auxílio do Axióscopio Zeiss®, acoplado ao programa de análise de imagens KS-400 versão 2.0 Kontron - Zeiss®. Os fatores raças, áreas e hemisférios cerebrais podem ser variáveis dependentes entre si, pois foram encontradas diferenças estatisticamente significativas em valores correspondentes à média de corpos de neurônios das áreas estudadas nas diferentes raças, bem como entre os hemisférios cerebrais. / They had been focused in this present study three dog breeds: Boxer, Dobermann e Rottweiler, with types constitutional and aptitudes functional characteristic and between itself, being collected 4 brains of each race. Of the brians they had been removed slices of the different areas of the brain cortex, that they had been prepared second conventional histological technique and stained by modified violet cresil. Through counting appearance-manual, comparative data were reached, mainly between brain areas versus breed associating types constitutional and aptitudes functional. The slices were analyzed with aid of Axióscopio Zeiss® connected to the program of analysis of images KS-400 version 2.0 Kontron - Zeiss®. The factors races, areas and brain hemispheres can be changeable dependents between itself, therefore estatisticament significant differences in corresponding values to the average of bodies of neurons of the areas studied in the different races had been found, as well as between the brain hemispheres.

The electrophysiological properties of somatic and dendritic membranes of CA1 pyramidal neurons were investigated using the rat in vitro hippocampal slice preparation. A comprehensive analysis of extracellular field potentials, current-source density (CSD) and intracellular activity has served to identify the site of origin of action potential (AP) discharge in CA1 pyramidal neurons. 1) Action potential discharge of CA1 pyramidal cells was evoked by suprathreshold stimulation of the alveus (antidromic) or afferent synaptic inputs in stratum oriens (SO) or stratum radiatum (SR). Laminar profiles of the "stimulus evoked" extracellular field potentials were recorded at 25µm intervals along the dendro-somatic axis of the pyramidal cell and a 1-dimensional CSD analysis applied. 2) The shortest latency population spike response and current sink was recorded in stratum pyramidale or the proximal stratum oriens, a region corresponding to somata and axon hillocks of CA1 pyramidal neurons. A biphasic positive/negative spike potential (current source/sink) was recorded in dendritic regions, with both components increasing in peak latency through the dendritic field with distance from the border of stratum pyramidale. 3) A comparative intracellular analysis of evoked activity in somatic and dendritic membranes revealed a basic similarity in the pattern of AP discharge at all levels of the dendro-somatic axis. Stimulation of the alveus, SO, or SR evoked a single spike while injection of depolarizing current evoked a repetitive train of spikes grouped for comparative purposes into three basic patterns of AP discharge. 4) Both current and stimulus evoked intracellular spikes displayed a progressive decline in amplitude and increase in halfwidth with distance from the border of stratum pyramidale. 5) The only consistent voltage threshold for intracellular spike discharge was found in the region of the cell body, with no apparent threshold for spike activation in dendritic locations. 6) Stimulus evoked intradendritic spikes were evoked beyond the peak of the population spike recorded in stratum pyramidale, and aligned with the biphasic extradendritic field potential shown through laminar profile analysis to conduct with increasing latency from the cell body layer. The evoked characteristics of action potential discharge in CA1 pyramidal cells are interpreted to indicate the initial generation of a spike in the region of the soma-axon hillock and a subsequent retrograde spike invasion of dendritic arborizations. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

The distribution of cocaine- and amphetamine-regulated transcript-like immunoreactivity (CART-LI) was investigated in the rat spinal cords with the use of an antiserum against the CART peptide fragment 55-102. CART-LI fibers were concentrated in the superficial layers of the dorsal horn of all segments. In addition to CART-LI fibers, intensely labeled somata were detected in the intermediolateral cell column (IML) and other sympathetic preganglionic nuclei of the thoracolumbar segments. In the lumbosacral segments, CART-LI fibers but not somata were seen in the sacral parasympathetic nucleus. Double-labeling the spinal sections with choline acetyltransferase (ChAT)-antisera and CART-antisera revealed that the large majority of ChAT-positive somata in the sympathetic preganglionic nuclei were CART-positive, whereas ChAT-positive somata in the parasympathetic preganglionic nuclei were CART-negative. Our results show that CART-LI is selectively expressed in a population of sympathetic preganglionic neurons (SPNs), but not in parasympathetic preganglionic neurons (PPNs) of the rat.

Activity plays diverse roles in shaping neuronal development and function. These roles range from aiding in synaptic refinement to triggering cell death during traumatic brain injury. Though the importance of activity-dependent mechanisms is widely recognized, the genetic underpinnings of these processes have not been fully described. In this thesis, I use the motor circuit of Caenorhabditis elegans as a model system to explore the functional and morphological consequences of modulating neuronal activity. First, I used a gain-of-function ionotropic receptor to hyperactivate motor neurons and asked how increased excitation affects neuronal function. Through this work, I identified a cell death pathway triggered by excess activation of motor neurons. I also showed that suppression of cell body death failed to block motor axon destabilization, providing evidence that death of the cell body and of motor axons can be genetically separated. Secondly, I removed excitatory drive from a simple neural circuit and asked how loss of excitatory activity alters circuit development and function. I identified excitatory motor neurons as master regulators of inhibitory synaptic connectivity. Additionally, I was able to identify previously undescribed activity-dependent mechanisms for regulating inhibitory synapses in both developing and mature neural circuits. Finally, I show data to implicate the highly conserved genes neurexin and neuroligin in determining inhibitory synapse connectivity. Collectively this work has lent insight into activity-dependent mechanisms in place to regulate neuronal development and function, a core function of neurobiology that is relevant to the study of a wide range of neurological disorders.

Indiana University-Purdue University Indianapolis (IUPUI) / Although paclitaxel is a commonly used anti-neoplastic agent for the treatment of solid tumors, therapy often results in a number of side effects, the most debilitating of which is peripheral neuropathy. Peripheral neuropathy is defined as a pathology of peripheral nerves, and, depending on the type of nerves damaged, the neuropathy can be classified as sensory, motor, or autonomic neuropathy. In the case of peripheral neuropathy induced by paclitaxel, the symptoms are experienced in the extremities and are sensory in nature. Patients undergoing chemotherapy with paclitaxel often report sensory disturbances such as burning, tingling, numbness, a diminished sensation to pain and temperature, loss of vibration sense, loss of proprioception, and loss of deep tendon reflexes. Electrophysiological abnormalities including decreased sensory nerve action potential amplitude and conduction confirm damage to large myelinated fibers. However, the involvement of damage to small diameter sensory neurons in the etiology of paclitaxel – induced peripheral neuropathy is still controversial. Therefore, experiments were performed to determine if paclitaxel alters the function of small diameter sensory neurons and to examine the mechanisms responsible for the change in function. vi Sensory neuron mediated vasodilatation in paclitaxel – injected animals was examined as an indirect measure of calcitonin gene related peptide (CGRP) release and therefore of sensory neuron function. CGRP release was also directly measured from central terminals in the spinal cord. To examine mechanisms of paclitaxel – induced sensory neuron damage, CGRP release and neurite length was examined in paclitaxel – treated sensory neurons in culture. The results demonstrate that (1) paclitaxel decreases the ability of small diameter sensory neurons to produce an increase in blood flow in the skin; (2) paclitaxel alters the release of CGRP from the small diameter sensory neurons; (3) paclitaxel causes the neuronal processes of isolated sensory neurons to degenerate. This dissertation provides novel information showing that paclitaxel alters the function of small diameter sensory neurons and thus provides a better understanding of the mechanisms mediating the sensory disturbances characteristic of peripheral neuropathy resulting from chemotherapy with paclitaxel.

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