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The discovery of new molecules that function in neuronal communication can be viewed as a progression of steps beginning with the identification of the molecular structure, moving to the understanding of the mecha nisms mediating the synaptic action, and to the appraisal of the involve ment of the new molecules in various neuronal mechanisms, and finally reaching the evaluation of this molecule’s role in brain function and the consequences that are triggered by its abnormalities. Enkephalins have followed such a pattern, and the present publication expresses the salient points of the last two phases in this succession. Enkephalins were discovered in December 1975; in addition to pain threshold regulation, their participation in other brain functions was soon ascertained. Perhaps, there are multiple recognition sites for multiple molecular forms of endogenous enkephalins; similarly to other transmitter recognition sites, these are coupled with ionic and nucleotide amplifying systems; thus, when activated, they can modify membrane funtion and ionic permeability of membranes. The present publication probes the current status of our knowledge concerning the consequences related to abnormalities in enkephalin storage, release, and synthesis. However, since our basic understanding of enkephalins is incomplete, the views reported should be considered to be in a state of flux.
