Evidence suggests that inhibition of long duration (ILD)in burst-firing cell R 15 is mediated by dopamine (DA). Current-voltage (IV) relationship studies using voltage-clamp techniques have shown that burst-firing inhibition is due to a reduction of the depolarization-activated inward current which underlies bursting. This effect is clearly seen as a diminution of the region of negative slope conductance (NSC) of the IV relationship, and can be produced by a spontaneous ILD, by bath or iontophoretic application of DA, or by stimulation of the left pleural-visceral connective. Bath application of increasing concentrations (100-500 μM) of d-amphetamine or β-phenethylamine (PEA) produces a gradual loss of the region of NSC that is similar to the effect of bath applied DA. Dihydroergotamine (DHET, 0.1 μM) blocks the effects of bath applied DA and the gradual loss of the region of NSC produced by AMPH and PEA. In addition, the higher doses of AMPH and PEA also induce post-synaptic currents (PSCs) which resemble spontaneous ILDs and further decrease the region of NSC. These PSCs, however, are not blocked by DHET. These experiments suggest that AMPH and PEA may induce ILDs in R 15 which are mediated by a neurotransmitter other than DA.