Toxin resistance is a recurring evolutionary response by predators feeding on toxic prey. These adaptations impact physiological interaction and community ecology. Mechanisms for resistance vary depending on the predator and the nature of the toxin. Potent neurotoxins like tetrodotoxin (TTX) and saxitoxin (STX) that are highly toxic to humans and other vertebrates, target conserved voltage-gated sodium channels (NaV) of nerve and muscle, causing paralysis. The copepod Calanus finmarchicus consumes the STX-producing dinoflagellate, Alexandrium fundyense with no effect on survival. Using transcriptomic approaches to search for the mechanism that confers resistance in C. finmarchicus, we identified splice variants of NaVs that were predicted to be toxin resistant. These were co-expressed with putatively non-resistant form in all developmental stages. However its expression was unresponsive to toxin challenge nor was there any up-regulation of genes involved in multi-xenobiotic resistance (MXR) or detoxification (phases I or II). Instead, adults consistently regulated genes encoding digestive enzymes, possibly to complement channel resistance by limiting toxin assimilation via the digestive process. The nauplii, which were more susceptible to STX, did not regulate these enzymes. This study demonstrates how deep-sequencing technology can elucidate multiple mechanisms of toxin resistance concurrently, revealing the linkages between molecular/cellular adaptations and the ecology of an organism.