SUMMARY

Long-term potentiation (LTP) continues to be the most intensely studied model of neuroplasticity, and is viewed by many as a substrate of learning. Other potential roles of LTP, however, have not received widespread discussion in the field. In this chapter, we will evaluate the LTP phenomena, discuss the putative connection to learning, and expand the discussion to include the participation of LTP and kindling in some forms of neuronal pathology. The available evidence appears to support a role for LTP in a continuum of events reflecting different levels of neural activity ranging from long-term depression (LTD) through LTP and kindling and culminating in cellular degeneration. In place of LTP as the substrate of learning at a neuronal level, we outline a model in which multiple levels of neural organization exert mutual control such that activity and modifiability at any level are controlled by those levels above and below.

Introduction

It is now over a quarter of a century since long-term potentiation (LTP) was first described (Bliss and Lomo, 1973). Initially it was viewed, rightly with great excitement, as an interesting phenomenon possibly linked to learning. Now it is frequently declared in unqualified terms to be the “cellular basis of learning and/or memory” (e.g., “LTP is a learning mechanism,” Fanselow, 1997) and its study virtually dominates the field of neuronal plasticity. Those new to the neurosciences would be forgiven for assuming that this transition occurred because the relationship between LTP and learning or memory had been experimentally demonstrated.