AbstractPGE1elicited a slow, dose‐dependent membrane depolarization with an increase in membrane conductance in the somatic cell hybrid TCX11. The ED50was 1‐2 × 10−8M with maximal responses at 1‐5 × 10−7M. Dopamine (DA) reversed the effect of PGE1and caused the membrane potential and resistance to return to control levels. Chronic exposure of cells (measured in minutes) to DA alone would not cause this hyperpolarization. 5‐HT was also tested and failed to consistently reverse the PGE1effects. Chlorpromazine antagonized the effects of DA on the PGE1response. The electrophysiological results reported here using TCX11 cells are discussed in light of previously reported biochemical results describing interactions of PGE1and DA, and the electrophysiological effect