LTP--a structural model to explain the inconsistencies.

Abstract

One of the major controversies in neuroscience concerns whether the expression of long-term potentiation (LTP) is a pre- or postsynaptic phenomenon, with apparently contradictory data being the norm. The model that is outlined in this article combines anatomical and electrophysiological evidence to allow apparently contradictory data to be compatible. Development of LTP involves both influx of Ca2+ through NMDA receptors, and activation of another factor, perhaps the metabotropic glutamate receptor. These two processes might result, respectively, in the insertion of activation of additional postsynaptic receptors, and the growth of microfilaments that could split simple synapses into perforated synapses, consisting of multiple active zones. Whether the latter occurred, and at what rate, would be likely to depend on multiple factors, such as temperature, the metabolic state of the cell, buffering of Ca2+, and the concentration of factors such as nitric oxide. These subtle experimental variables would thus determine whether the dominant effect observed was pre- or postsynaptic.