Genetic Dissection of the Neural Circuitry Underlying Memory Stability in Drosophila: A Dissertation
AuthorsKeene, Alex Carl
Faculty AdvisorScott Waddell Ph.D.
Document TypeDoctoral Dissertation
Dorsal Paired Medial neurons
Animal Experimentation and Research
MetadataShow full item record
AbstractUnderstanding how memory is formed requires looking beyond the genes involved to the neural circuitry and temporal aspects of memory. In this dissertation I have focused my investigation on Dorsal Paired Medial (DPM) neurons, two modulatory neurons essential for memory in Drosophila. DPM neurons highly express the amnesiac (amn) gene, which encodes for a putative pre-pro-neuropeptide. amn function in DPM neurons is required for memory. Here I provide evidence that DPM neurons are cholinergic and that acetylcholine (ACh) and AMN act as co-transmitters essential for DPM function. In order to investigate the temporal requirements of DPM output I blocked transmitter release during discrete intervals in the memory process using shibirets1 and tested flies for shock and sugar-reinforced memory. These experiments demonstrated that stable memory requires persistent transmitter release from DPM neurons. Furthermore these results suggest AMN and DPM neurons act as general stabilizers of mushroom body dependent memory. To further investigate the neural circuitry underlying DPM function I disrupted DPM projections onto the mushroom body lobes by ectopically expressing DScam17-2::GFP in DPM neurons. Flies with DPM neurons that predominantly project to the mushroom body α´/β´ lobes exhibit normal memory, and blocking transmitter release from the mushroom body prime lobes neurons themselves abolishes memory indicating DPM neuron-mushroom body α´/β´ neuron interaction that are critical for memory. Taken together, the experimental evidence presented here are used to provide a rudimentary model of the neural circuitry involved in memory stability, where DPM neurons form a recurrent feedback loop with the mushroom body α´/β´ lobe neurons and act to stabilize odorspecific conditioned memories at Kenyon cell synapses.
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/31562
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