Morphine concentrations in plasma and four discrete areas of the rat brain following intravenous administration, can be described by a three-compartment open model. The pharmacokinetic behavior of morphine was the same in each of the different parts of the brain. When relating this behavior to the effects of morphine on the threshold for vocalisation and vocalisation-after-discharge, it was possible to develop a pharmacokinetic model which suggests that morphine induces its analgesic effect by a change of activities in at least two neurophysiological systems. As a result of investigations of morphine-induced changes of catecholamine turnover in different parts of the brain and of the consequences of modulating central monoaminergic activity prior to morphine administration, it was suggested that one of the two neurophysiological systems could be dopaminergic. In this system morphine increases the turnover of dopamine, most probably by releasing this transmitter from limbic structures that initiate the effect of morphine on the threshold for vocalisation-afterdischarge (the emotional component of pain reactions).