We present a kinetic model that can account for several experimental findings on short- and long-term potentiation (STP and LTP) and their pharmacological modulation. The model, which is consistent with Hebb's postulate, uses the hypothesis that part of the origin of LTP may be a consequence of an increased release of neurotransmitter due to a retrograde signal. The operation of the model is expressed by a set of irreversible reactions, each of which should be thought of as equivalent to a set of more complex reactions. We show that a retrograde signal alone is not sufficient to maintain LTP unless long-term change of the rate constant of some of the reactions is caused by high-frequency stimulation. Pharmacological manipulation of LTP is interpreted as modifications of the rate constants of one or more of the reactions that express a given mechanism. The model, because of its simplicity, can be useful to test more specific mechanisms by expanding one or more reactions as suggested by new experimental evidence.

This content is only available as a PDF.
You do not currently have access to this content.