Context: 

Synaptic plasticity is a core mechanism responsible for neuronal functions such as long-term memory and 
learning, as when humans and animals learn, the synaptic plasticity within neuronal networks are responding to specific cues which elicit various changes in behaviour. Additionally, recent findings have suggested that activity-regulated genes (ARGs), such as Hormone receptor-like in 38 (Hr38), and dopamine-driven synaptic plasticity are equally crucial for consolidation of long-term memory, as well as the re-evaluation of learned information and the integration of various ‘internal states’. Surprisingly, ARGs are poorly studied in well used model organisms like Drosophila, thus, in the hopes of further understanding the neuronal mechanisms behind the consolidation of long-term memory (LTM), here we stimulated Drosophila neurons with appetitive conditioning to induce dopamine-driven plasticity, and then used the GAL4-UAS system, along with interference RNAs (RNAis), to knock-down and subsequently try to deduce the role of Hr38 within memory consolidation. 

Bibliography (also found in report):  

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In addition to this report I have also uploaded a report detailing this presentation, and subsequently my project in more detail, and a poster summarising the project as well. Hopefully you can find them on my profile. Thank you for reading.