Abstract
The N-methyl-D-aspartate subtype of glutamate receptor (NMDAR) and its downstream signalling pathways play a crucial role in the regulation of synaptic function and plasticity in the mammalian brain. It also regulates behavioural plasticity as early studies molecules (dunce, rutabaga et al.) for various forms in relation to learning and memory. Similarly, previous studies have identified the functional NMDA-type receptor and suggested it is required synaptic and behavioural plasticity in invertebrates. Here we prepare the antibody to examine the Drosophila NMDAR1 expression level in different developmental stages to determine when the nervous system begins to express NMDAR1. By disruption of the Drosophila NMDAR1 (DrNR1) gene, we demonstrate NMDAR is required for adult learning and the consolidation of long-term memory (LTM). By acute disruption of DrNR1 with the induction of antisense mRNA, learning acquisition and LTM are diminished or abolished. Thus, my data suggest that the requirement of NMDAR for behavioural plasticity and the consolidation of LTM by NMDAR-dependent mechanism are conserved in Drosophila. For future study to understand the NMDAR1 effect in learning and memory, we have constructed the UAS-NR1 and UAS-NR1RNAi lines. These flies will be used to investigate whether the protein level of NR1 can also enhance or abolish learning and memory or not.