| Summary: | <p> Glutamate is the most abundant excitatory neurotransmitter in the central nervous system. It is implicated in synaptic plasticity including learning and memory and long term potentiation, which are characterized by changes in the number and localization of glutamate receptors (GluRs) in the postsynaptic cell. We have found that proteins important for autophagy, a cellular process that degrades cellular components for reuse, affect the synaptic localization of GluRs at the <i>Drosophila</i> neuromuscular junction. Preliminary data indicated that mutations in atg1 and atg8a lead to a reduction in synaptic GluRs, suggesting that they either indirectly regulate GluR localization or signal independent of autophagy. The present study examined the effects of tissue specific overexpression or knockdown of atg8a to determine that atg8a is important either pre- or postsynaptically for proper GluR localization, and is possibly acting downstream of FOXO signaling. These results also indicate that atg8a may be acting independently of autophagy to determine GluR localization. </p><p>
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