Where does potentiation collide?

In pharmacology and toxicology, potentiation describes a combined effect in which one agent increases the action of another beyond what either produces alone, a departure from simple additivity that must be judged against a defined no-interaction baseline. Bliss's 1939 analysis of poisons applied jointly set out how to define and test for such joint action, separating independent, additive, and synergistic effects. The referent is an enhanced pharmacological response from a combination, a construct about drug interaction, not the lasting synaptic strengthening that neuroscience calls by the same word.[1]

Unit

The excess combined effect of agents relative to an additivity baseline

Recovery means

Not applicable

Measured by

Tested with isobolograms or combination indices comparing the observed joint effect to predicted additivity

In neuroscience, long-term potentiation is a persistent increase in synaptic strength that follows brief high-frequency stimulation of a pathway, so that the same input later evokes a larger response. Bliss and Lømo's 1973 recordings in the rabbit hippocampus showed that a few seconds of tetanic stimulation potentiated transmission for hours, a finding taken as a cellular substrate of learning and memory. The referent is an enduring, activity-dependent change in a synapse's efficacy, measured electrophysiologically, and distinct from the drug-interaction meaning of potentiation.[2]

Unit

The size and duration of the increase in synaptic response after conditioning stimulation

Recovery means

Not applicable

Measured by

Quantified by the rise in evoked field-potential or EPSP slope after a tetanus, tracked over time