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Cellular mechanisms governing neuronal plasticity during serotonin-induced neuromodulation and regeneration
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Modulation of neuronal activity is an important cellular correlate of behavioral plasticity. Many signals, including neurotransmitters, trophic factors, and the process of regeneration can modify the electrophysiologicai properties of neurons and neural networks underlying an animals behavior. In this thesis, electrophysiological modifications of identified buccal neuron 5.(B5) induced by the neurotransmitter serotonin (5-hydroxytryptamine; 5-HT) and axonal crush were examined using intracellular recording and pharmacological techniques. Exogenous application of serotonin (50AM), in both semi-intact ganglia and isolated cells, reduced spiking frequency of identified neuron B5. This serotonin-induced neuromodulation involved both a membrane hyperpolarization and a reduction in input resistance. Experiments examining the CAMP and arachidonic acid signal transduction pathways indicated that serotonin's modulatory effects on B5 excitability are not mediated by a CAMP cascade, but potentially via a lipoxygenase pathway of arachidonic acid metabolism. modulation of B5 neuronal excitability also occurred during regeneration following crush-axotomy. Neurons regenerating axonal arbors both in vivo and in culture, displayed a transient (<24 hr) reduction in excitability followed by a period of increasing excitability which is maintained for many days (>5 d). B5 neurons in cell culture exhibited this period of increased excitability levels only when exposed to conditioning factors released from injured neural tissue, although the identification and nature of these signals remain undefined. Temporal analyses suggest an intrinsic "window of competence" for trophic factor-induced modulation of B5 excitability post-isolation. Following the 5 day period of enhanced excitability in culture, maximum numbers of stimulus-evoked action potentials dropped to levels not significantly different than those of recently crushed or isolated neurons. Although this critical period in cell culture corresponds to neuron B5's window of competence for neurite outgrowth, changes in neuronal excitability were independent of process outgrowth state. Injury-induced neuromodulation of B5 was neither mimicked nor blocked by cAMP-dependent protein kinase A analogs. However, studies utilizing the translational inhibitor anisomycin suggest that new protein synthesis is required for the expression of these excitability changes induced by extrinsic factors.
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Achee, Nicole Louise (1995). Cellular mechanisms governing neuronal plasticity during serotonin-induced neuromodulation and regeneration. Master's thesis, Texas A&M University. Available electronically from
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