Mutations in the PINK1 gene are responsible for typical symptoms of Parkinson's disease. Using Drosophila melanogaster mutant PINK1B9 and after PINK1 silencing with RNAi using transgenic lines, we observed defects in synapses and behavior. The lack or reduced expression of PINK1 prolonged sleep during the day (nap) and decreased the total locomotor activity during 24 h, in addition to a decrease in climbing ability and a reduced lifespan. In the brain, PINK1 mutants had a lower level of Bruchpilot (BRP), a presynaptic scaffolding protein that is crucial for neurotransmission in all type of synapses in Drosophila. In addition, other proteins that are involved in synaptic transmission; Rab5, Syntaxin and Wishful Thinking were also decreased in abundance in mutants, except Synaptotagmin. Transmission electron microscopy (TEM) also confirmed less and abnormal synaptic vesicles at tetrad synapses in the visual system of PINK1 mutants. The lower level of BRP and longer day sleep observed was also detected in white mutants, which were examined to test the effect of the\r\nwhite background on the PINK1B9 strain. The reduced locomotor activity and longer day sleep in PINK1 mutants and after decreasing the PINK1 level in neurons seem to be correlated with a decrease in mitochondria number during the day, when they normally peak, and with impaired synaptic transmission.