The Effects of CuSO4 on Membrane Potential and Glutamatergic Synaptic Transmission

Copper sulfate (CuSO4) is widely used in industrial and aquatic applications, yet its acute effects on membrane potential and synaptic transmission have not been fully addressed. This study investigated the effects of CuSO4 on glutamatergic neuromuscular junctions using larval Drosophila melanogaster and Red Swamp Crayfish (Procambarus clarkii) as experimental models. Intracellular electrophysiological recordings were used to measure resting membrane potential, evoked excitatory junction potentials (EJPs), and spontaneous miniature EJPs before and during acute CuSO4 exposure at multiple concentrations. In larval Drosophila, CuSO4 produced a rapid, concentration-dependent reduction in both evoked and spontaneous synaptic responses, with higher concentrations nearly abolishing neurotransmission. The co-application of glutamate and CuSO4 reduced the sustained depolarization produced by glutamate alone, suggesting antagonistic effects on glutamate receptors. CuSO4 also altered the resting membrane potential, producing significant hyperpolarization at lower concentrations. In contrast, crayfish preparations exhibited enhanced synaptic transmission, with increased EJP amplitudes at higher CuSO4 concentrations accompanied by membrane hyperpolarization. These findings demonstrate that acute CuSO4 exposure differentially affects synaptic transmission and membrane potential across model systems, indicating distinct underlying cellular mechanisms. The results suggest that CuSO4 may influence both glutamate receptor function and ion channel activity, providing insight into the neurophysiological effects of copper toxicity and establishing a foundation for future mechanistic investigations.