Abstract: Background and Objective: Zinc (Zn2+) is essential for physiological function but excessive zinc can cause disruption to physiological processes. This study examined the impact of acute zinc overexposure on various facets of zinc exposure in both Drosophila and crawfish, as well as the role of zinc in the mechanism of neurological processes. Materials and Methods: Drosophila larvae development/survival was examined with feeding various ZnCl2 concentrations (N = 100 and t-Test). The ZnCl2 crawfish injections were observed (N = 6 and t-Test). Effects of ZnCl2 (0.1, 1 mM) at both animals’ synaptic transmission at the neuromuscular junction were observed (N = 6 per concentration and paired t-Test). Results: Increased dietary Zn2+ delayed development, decreased survival/survival time, and impaired normal Drosophila behavior. Acute Zn2+ exposure eliminated the response to sensory stimulation of crawfish, but increased activity in the muscle receptor organ. Zinc exposure also decreased heart rate (sometimes to elimination) in both Drosophila and crawfish. Excessive zinc exposure also drastically reduced excitatory junction potentials of both Drosophila and crawfish, though this activity was recovered upon removal of the zinc exposure. Conclusion: Overall, acute zinc overexposure largely disrupted neurological and cardiac function, behavior, development and survival of Drosophila and crawfish.