Postsynaptic depolarization requirements for LTP and LTD: a critique of spike timing-dependent plasticity.
Long-term potentiation and long-term depression require postsynaptic depolarization, which many current models attribute to backpropagating action potentials. New experimental work suggests, however, that other mechanisms can lead to dendritic depolarization, and that backpropagating action potentials may be neither necessary nor sufficient for synaptic plasticity in vivo.
Lisman
John
J
Volen Center for Complex Systems, Biology Department, Brandeis University, 415 South Street, Waltham, Massachusetts 02454, USA. Lisman@brandeis.edu
Spruston
Nelson
N
D000200:Action Potentials; D000818:Animals; D003712:Dendrites / Q000502:physiology; D004594:Electrophysiology; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D006801:Humans; D017774:Long-Term Potentiation / Q000502:physiology*; D036881:Long-Term Synaptic Depression / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D011930:Reaction Time / Q000502:physiology; D013569:Synapses / Q000502:physiology*