Effects of Actinomycin D on Memory and Brain RNA Synthesis in an Appetitive Learning Task

Abstract

CURRENT selectional models of learning and memory^1–3 suggest that messenger RNA (mRNA) is implicated in biochemical processes in the brain which mediate long term memory. The role assigned to mRNA in these models is that of a carrier of information to the ribosome complex from environmentally stimulated derepressed regions of the DNA molecule. The specific protein molecule or peptide thus produced is supposed to signpost or colour-code neurones in such a way that conduction of subsequent impulses, similar to that which first specified the existence of the molecule, is facilitated. The loss of RNA from such a system should prevent the production of the specific protein molecule and impair the formation of a permanent memory trace, but experiments which have attempted to prevent the synthesis of mRNA by means of actinomycin during avoidance learning have given ambiguous results^4–7. We have therefore set out to determine, in an appetitive learning situation, the time after acquisition at which actinomycin becomes effective in impairing memory, the extent of diffusion of the drug vehicle through brain tissue and the effect of the quantities of the drug used on brain RNA synthesis.