Figure 4: The parkin mutation slows the locomotor CPG, with rescue by neuronal expression of parkin or application of DA to the CNS. (a) Recordings with a larval extensometer (i) show that (ii–iv) the frequency (controlled by the CNS) but not the amplitude (controlled by the muscle performance) is affected by the parkin mutant (parkZ3678/parkin25). The contraction frequency is rescued by expression of Drosophila wild-type parkin in the nerve (elav3e1 GAL4), but not the muscle (G14 GAL4). (b) In a semi-intact preparation, with en-passant nerve recordings, the frequency of bursting is reduced in the parkin mutant. (c) In the isolated CNS, the fictive locomotion rhythmic bursting pattern is also reduced in the parkin mutant and rescued by application of dopamine (DA, 1 mM in HL-3 saline supplemented with 3 mM ascorbic acid to reduce oxidation). Data in (a) and (b) from [23], with original recordings in (c).