The findings of clinical and experimental studies conducted over the past 25 years provide extensive evidence that in both laboratory animals and man memory can be modified by treatments which affect the central nervous system. Patients with head injuries may suffer from retrograde amnesia, a loss of memory for experiences which occur just prior to the onset of the injury. Findings of laboratory studies using animal subjects indicate that retrograde amnesia can be produced by a wide variety of experimental treatments.

There are now well-established examples of carriers and pores which facilitate the transfer of ions across thin lipid membranes. In the absence of such agents, lipid bilayer membranes are extremely impermeable to the common inorganic ions. Thus, the conductance of a pure lecithin + decane or glyceryl mono-oleate + decane membrane in M/10 NaCl is less than10−9Ω −1 cm−2. However, on the addition of small lipid-soluble molecules such as valinomycin, or surface-active polypeptides such as gramicidin A, the conductance may become so high (> 10−1 ω−l cm−2) that the resistance of the membrane merges into that of the aqueous phase. This review is concerned with the extent to which we now understand how these added substances transfer ions across lipid membranes. Attention has been concentrated on the simpler systems, i.e. the lipid-soluble ions, the 1–1 carriets, a simple pore and, with some loss of simplicity, a substance which prodeces interacting pores. Only molecules of known primary structure are discussed.