Memory traces: how to increase and decrease their strength.

Abstract

In addition to the memory trace itself, the memory circuit may include a modulatory input that influences the strength of the memory trace. This modulatory input, which can make memory traces stronger as well as weaker, appears to be intimately associated with systems that convey the importance of the present event. A single exposure to a sufficiently salient event may activate the modulatory input to a level high enough to produce an enduring memory. Experimental investigation of this modulatory input indicates that pharmacological treatment can often be substituted for practice to strengthen the memory trace, suggesting that drugs or practice activate a common mechanism. Similarly, drugs and the UCS interact in such a way as to suggest they also act on a common mechanism to modulate retention. Dose-response curves for drug treatment or UCS amplitude versus performance are often U-shaped. Many drugs that modulate memory appear to do so through a primary site of action outside the blood-brain barrier. Our investigation of one such peripheral system, namely that for [leu]enkephalin, revealed an enzyme mechanism in plasma which may be regulatory with regard to escape performance. We suggest that investigation of the interface between the memory trace and its modulatory input may lead to understanding of how mammalian systems store information, particularly in regard to associative strength.