Epilepsy is a neurological disorder characterized by recurring, unpredictable seizures. Its disease burden is high, seeing as it ranks fourth in the world’s neurological disorders burden following: tension-type headaches, migraines, and Alzheimer’s disease. The commonly used antiepileptic drug levetiracetam (Keppra) reducing epileptic seizures; however, the exact mechanism is not known. Some studies suggest sodium and/or potassium ionic channels are directly altered, reducing membrane excitability while others suggest it interacts with SV2 protein to alter synaptotagmin’s (a calcium sensor protein) action in the presynaptic nerve terminal and reduce excitability. The glutamatergic synapses at crayfish and larval Drosophila neuromuscular junctions (NMJs) were used to assess the drug’s action. The evoked excitatory junction potentials (EJPs) of the crayfish NMJ were enhanced by exposure to 1 mM, but not lower doses within 20 min of stimulation after static incubation for 10 min. However, no significant alterations were noted in the amplitude of the EJPs at the Drosophila NMJ for 1 mM over 20 min while stimulating the NMJ at 5 Hz. The crayfish model and the effects of levetiracetam was used as an authentic undergraduate research experience (ACURE) in a neurophysiology teaching laboratory with 16 students. It appears levetiracetam acts differently in different animal models or varied experimental conditions are required to note its effects.