Homozygous recessive mutations in MYO7A cause Usher Syndrome Type 1 (UST1), characterized by profound congenital deafness and retinopathy. The mariner mutant is a zebrafish model of UST1 caused by mutations in myo7aa and exhibits deafness and circular swimming. The objective of this study is to facilitate drug screening that rescue the mutant swimming phenotype. We assessed zebrafish swimming and evaluated the efficacy of drugs by measuring average global change in body orientation (AGC). The AGC for wildtype fish was 680 +/- 130 radians/s. In contrast, the mutant fish had an AGC of 1100 +/- 300 radians/s (p<0.0001). Using a L-type calcium channel agonist, (±) Bay K 8644 the AGC was 780 +/- 200 radians/s. The drug did not have any adverse reactions on the wildtype fish. The AGC of the mutant fish incubated in 5 µM of (±) Bay K 8644 differed from the control mutant fish (p<0.0001) and did not differ from wildtype control fish (p=0.0451). We tested a second L-type calcium channel agonist, FPL 64176. Values of the AGC did not present statistical significance between the mariner mutants in the compound compared to the mutant controls. However, the pattern of swimming for the mariner mutants incubated in 0.5 µM FPL 64176 more closely resembles wildtype swimming. These preliminary studies support that using L-type calcium channels shifts swimming behavior towards wildtype swimming. This represents a significant step towards discovering compounds to treat hearing loss caused by mutations in MYO7A.