In 1978, we published two reviews on pain control mechanisms in the central nervous system. One concentrated on brainstem control of spinal nociceptive neurons (Fields & Basbaum 1978). The other focused on those pain control systems which use endogenous opioid compounds and presumably mediate the analgesic action of exogenous opiate analgesics (Basbaum & Fields 1978). Since those reviews were published, information in both areas has grown rapidly. For example, it is now known that there are at least three families of endogenous opioid peptides (endorphins), each having a different precursor and a differential distribution in the eNS. In addition, knowledge of the immunohistochemistry and pharmacology of the brainstem and spinal neurons involved in pain transmission and modulation has expanded. Finally, much more is known about the circuitry underlying both the transmission and control of pain. These new observations make revisions necessary in the mechanisms proposed to account for the analgesic action of exogenous opiates and electrical brain stimulation. In this paper we review the new information, concentrating on those studies that necessitate changes in the original model. I