LTP - A STRUCTURAL MODEL TO EXPLAIN THE INCONSISTENCIES

One of the major controversies in neuroscience concerns whether the ex pression of longterm potentiation (LTP) is a pre- or postsynaptic phen omenon, with apparently contradictory data being the norm, The model t hat is outlined in this article combines anatomical and electrophysiol ogical evidence to allow apparently contradictory data to be compatibl e. Development of LTP involves both influx of Ca2+ through NMDA recept ors, and activation of another factor, perhaps the metabotropic glutam ate receptor, These two processes might result, respectively, in the i nsertion or activation of additional postsynaptic receptors, and the g rowth of microfilaments that could split simple synapses into perforat ed synapses, consisting of multiple active zones, Whether the latter o ccurred, and at what rate, would be likely to depend on multiple facto rs, such as temperature, the metabolic state of the cell, buffering of Ca2+, and the concentration of factors such as nitric oxide, These su btle experimental variables would thus determine whether the dominant effect observed was pre- or postsynaptic.