Prolonged, bright luminescent glows in Porichthys photophores are elicited by administration of 2,4-dinitrophenol (DNP) and potassium cyanide (KCN). Ultrastructural alterations of varicose nerve endings precede photocyte changes during such luminescent activity. Common alterations of nerve profiles include mitochondrial disruptions, flattening and depletion of synaptic vesicles, formation of large vacuolar cisternae, and invaginations in the contour of axolemma. Protracted luminescent activity in response to DNP results in depletion of photocyte vesicle material while vesicle and ER membranes accumulate and coil inside coalesced vesicle pools, and photocyte microvilli disappear completely. Although similar photocyte alterations are initially observed in KCN treated luminescing photophores, the early extinction of the response to KCN is related to deleterious, irreversible effects of this chemical on photocytes. These observations, along with some pharmacological manipulations, indicate that at least DNP acts initially and primarily on neural structures, probably the mitochondria, to induced transmitter release and consequent photocyte activity. Based on this and earlier studies, a chain of subcellular events leading to light emission of Porichthys photophores is proposed and discussed.