Year of Graduation
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Restricted Access Thesis
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Patsy S. Dickinson
Central pattern generators (CPGs) are neural networks that generate rhythmic motor patterns. Flexibility in CPG output can be achieved via the actions of neuromodulators. Peptides, the largest class of neuromodulators, are integral for communication within neuronal systems, as well as for altering outputs of individual neurons and neuronal networks. The cardiac neuromuscular system of the American lobster, Homarus americanus, is a model CPG system for understanding the modulatory control of rhythmic motor patterns. The CPG, the cardiac ganglion (CG), consists of just nine neurons: five large motor neurons and four smaller premotor neurons.
Chapter One built upon extensive research of the rhythmic output of the Homarus cardiac neuromuscular system and examined this CPG-effector system at the neural level. Here, we asked whether the premotor and motor neurons of the CG can burst independently of one another, and if so, how these neuron types would respond to a peptide when decoupled. Here, we show that the premotor and motor neurons can establish independent bursting patterns when decoupled by a physical ligature. Myosuppressin (pQDLDHVFLRFamide), a well-characterized crustacean neuropeptide, is known to act both centrally on the CG and peripherally on the cardiac muscle. Here, we show that myosuppressin can modulate the decoupled premotor and motor neurons of the CG and suggest that these physiological responses may be due to a differential expression of five putative myosuppressin receptors across the neuron types.
Chapter Two examined how structure alters peptide function within a signaling network. Here, we assessed the role of post-translational modifications in determining the modulatory effects of myosuppressin by testing three differentially modified isoforms at various levels of the Homarus cardiac neuromuscular system. While full myosuppressin and non-cyclized myosuppressin (QDLDHVFLRFamide) both elicited similar changes in the whole heart, the cardiac periphery, the intact CG, and the physically decoupled CG neurons, non-amidated myosuppressin (pQDLDHVFLRFG) elicited markedly smaller changes in the rhythmic cardiac output at all levels. A weak correlation between the extent of whole heart modulation by non-amidated myosuppressin and modulation of the intact CG suggested that this isoform may only exert localized effects on the ganglion itself.
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