The cellular underpinnings of memory deficits in Alzheimer's disease (AD) are poorly understood. We utilized the tractable neural circuits sub-serving memory in to investigate the role of impaired Ca handling in memory deficits caused by expression of human 0N4R isoform of tau which is associated with AD. Expression of tau in mushroom body neuropils, or a subset of mushroom body output neurons, led to impaired memory. By using the Ca reporter GCaMP6f, we observed changes in Ca signaling when tau was expressed in these neurons, an effect that could be blocked by the L-type Ca channel antagonist nimodipine or reversed by knock-down of the L-type channel gene. The L-type Ca channel itself is required for memory formation, however, knock-down of the L-type Ca channel in neurons overexpressing human tau resulted in flies whose memory is restored to levels equivalent to wild-type. Expression data suggest that L-type Ca channel mRNA levels are increased upon tau expression in neurons, thus contributing to the effects observed on memory and intracellular Ca homeostasis. Together, our Ca imaging and memory experiments suggest that expression of the 0N4R isoform of human tau increases the number of L-type Ca channels in the membrane resulting in changes in neuronal excitability that can be ameliorated by knockdown or pharmacological blockade of L-type Ca channels. This highlights a role for L-type Ca channels in tauopathy and their potential as a therapeutic target for AD.