Previously, we have shown that 17beta-oestradiol (E(2)) induces an increase in firing activity and modifies the pattern of intracellular calcium ([Ca(2+)](i)) oscillations with a latency < 1 min in primate luteinising hormone-releasing hormone (LHRH) neurones. A recent study also indicates that E(2), the nuclear membrane impermeable oestrogen, oestrogen-dendrimer conjugate, and the plasma membrane impermeable oestrogen, E(2)-BSA conjugate, all similarly stimulated LHRH release within 10 min of exposure in primate LHRH neurones, indicating that the rapid action of E(2) is caused by membrane signalling. The results from a series of studies further suggest that the rapid action of E(2) in primate LHRH neurones appears to be mediated by GPR30. Although the oestrogen receptor antagonist, ICI 182, 780, neither blocked the E(2)-induced LHRH release nor the E(2)-induced changes in [Ca(2+)](i) oscillations, E(2) application to cells treated with pertussis toxin failed to result in these changes in primate LHRH neurones. Moreover, knockdown of GPR30 in primate LHRH neurones by transfection with human small interference RNA for GPR30 completely abrogated the E(2)-induced changes in [Ca(2+)](i) oscillations, whereas transfection with control siRNA did not. Finally, the GPR30 agonist, G1, resulted in changes in [Ca(2+)](i) oscillations similar to those observed with E(2). In this review, we discuss the possible role of G-protein coupled receptors in the rapid action of oestrogen in neuronal cells.