Intracellular recordings of neurally evoked excitatory junction potentials were made from the hermit crab neuromuscular junction and the effects of a series of putative antagonists, including the phosphonic amino acids, were examined for their effectiveness. The most potent antagonists were (+/-)2-amino-5-phosphonohexanoic acid and (+/-) 2-amino-5-phosphonovaleric acid while glutamate diethyl ester, DL-alpha-aminoadipate, 2-amino-7-phosphonoheptanoic acid and gamma-D-glutamylglycine were less effective. None of the compounds produced a change in membrane input resistance, but pyridine-2,5-dicarboxylic acid depolarized the muscle membrane and this probably accounted for its apparent antagonist properties. All the compounds readily and reversibly, but not competitively, antagonized the ionophoretic L-glutamate-induced depolarization. Since none of the compounds was capable of producing complete antagonism it is concluded that a more potent and competitive antagonist is required.