Lambert-Eaton Myasthenic Syndrome (LEMS) is a neuromuscular disorder characterized by muscle weakness in which the motor nerve has difficulty releasing enough neurotransmitter to cause muscle contraction. Through clinical trials, 3,4-diaminopyridine (DAP) has been shown to successfully treat LEMS by increasing muscle contraction and strength. However, the precise effect of DAP on synaptic facilitation (an increase in transmitter release seen during high frequency stimulation) is not well understood. Here a well described neuromuscular synaptic preparation and a selective neurotoxin is used to model LEMS. Using the cutaneous pectoris muscle of the leopard frog (Rana pipiens), the electrical response of muscle cells to various frequencies of synaptic stimuli was measured using intracellular recording methods. The amplitude of muscle cell response to the nerve stimuli was used as an assay of neurotransmitter release in both LEMS-like and control (low calcium) conditions. The data indicate that, as expected, DAP increases the amount of neurotransmitter released in both control and LEMS conditions, but decreases the degree of facilitation in both conditions. The preliminary results are not sufficient to determine whether DAP causes a higher level of facilitation in LEMS conditions than in the control (low calcium) conditions. The collected data are a foundation for the continued studies on the mechanism of action of DAP, and the functional arrangement of synaptic proteins in a model synapse.