Abstract
Synaptic plasticity is the foremost candidate mechanism to explain the rapid acquisition of memories. In the mammalian brain, the NMDA subclass of glutamate receptors plays a central role in the induction of several forms of use-dependent plasticity. The finding that modifications in synaptic strength are largely expressed by receptors of the AMPA subclass has focused attention on molecular mechanisms that affect their function and targeting. Receptor plasticity has also been reported in pathological situations, notably in animal and human forms of epilepsy. Which of these changes are causally implicated in the generation of seizures, and which may be compensatory or neuroprotective adaptations, has not been fully resolved.