A long-term increase in synaptic efficiency caused by high-frequency stimulation to afferent fibers. In mammals it is essential to short term memory in the hippocampus as well as more permenant memory storage.
Originally postulated by Donald Hebb, LTP occurs at the NMDA receptor. It occurs when depolarization of the cell membrane opens the NMDA receptor allowing it to expel a magnesium molecule that typically resides in its ion channel. This allows further depolarization of the neuron, allowing it to fire more readily.
This increase in firing causes proteins to collect at the site of activation and flag it for further synapse development. This process can take several days, and is the important link between Long Term Potentiation and the Hebb Postulate.
A number of drugs act on the NMDA receptor. PCP becomes lodged in the receptor much the same way magnesium does, except PCP cannot be expelled by depolarization and effectively renders the receptor disfunctional. DXM, the active ingredient in Robotussin, and Ketamine also effect this receptor, though only temporarily. Since they interfere with associative memory formation, these drugs are known as Dissociative Drugs.