Long-Term Potentiation (LTP) refers to the way in which certain neurons, especially those in the hippocampus, become much more sensitive to weak stimuli after being exposed to a strong (“potentiating”) stimulus. After repeated exposure to strong stimuli, this increased sensitivity can last for weeks or months. Because of this, LTP is believed to be relevant to the formation of long-term memory. If so, it is of great value to the field of cognitive science, since it provides a clear example of how a relatively simple behavior of neurons can be relevant to much more complex brain-processes. LTP is used by proponents of connectionist models, such as Elman, to explain how their models might actually be implemented in the brain.

LTP - Long Term Potentiation

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.

Log in or register to write something here or to contact authors.