Proper development of a mature neural circuit is crucial for function. Abnormal development of neural circuitry can lead to pervasive neurological disorders, such as Alzeimer's Disease, Parkinson's Disease, or Huntington's Disease. Although the underlying mechanisms causing these diseases are not yet clear, previous work has illuminated factors that are critical for proper growth and maintenance of the neural circuitry. Recent studies have shown the importance of dopamine action in the development of the stomatogastric feeding circuit in Drosophila melanogaster larvae. The complexity of the neuronal architecture of this circuit has been correlated with its functional output, feeding. While dopamine does not directly modulate feeding behavior, it does adopt a trophic role during neuronal development. Other research has shown a potential neuroprotective role of nicotinamide mononucleotide adenylyltransferase (NMNAT) in lesioned neural fibers. The exact mechanism of NMNAT's action is still largely unknown, but there is evidence to suggest that it aids in mitochondrial stability in these fibers. This mitochondrial stability has been associated with proper function of dopaminergic neurons. We are interested in the potential protective effects of overexpression of NMNAT in dopamine deficient animals. We reduced neuronal synthesis of dopamine through targeted knockdowns of tyrosine hydroxylase, the rate-limiting enzyme in dopamine synthesis , using RNAi technology. Elucidation of NMNAT's actions in dopaminergic neurons will not only give insight on its mechanism of action, but also provide potential therapeutic targets for degenerative diseases.

Effects of NMNAT expression on stomatogastric circuit development in dopamine deficient <i>Drosophila melanogaster</i> larvae

247th National Meeting (2014)

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Effects of NMNAT expression on stomatogastric circuit development in dopamine deficient Drosophila melanogaster larvae