Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE) are two related forms of short‐term synaptic plasticity of GABAergic and glutamatergic transmission, respectively. They are induced by calcium concentration increases in postsynaptic cells and are mediated by the release of a retrograde messenger, which reversibly inhibits afferent synapses via presynaptic mechanisms. We review here: The evidence accumulated during the 1990s that has led to the conclusion that DSI/DSE rely on retrograde signaling. The more recent research that has led to the identification of endocannabinoids as the retrograde messengers responsible for DSI/DSE. The possible mechanisms by which presynaptic type 1 cannabinoid receptors reduce synaptic efficacy during DSI/DSE. The possible modes of induction of DSI/DSE by physiological activity patterns, and the partially conflicting evaluations of the calcium concentration increases required for cannabinoid synthesis. Finally, the relation between DSI/DSE and other forms of long‐ and short‐term synaptic inhibition, which were more recently associated with the production of endocannabinoids by postsynaptic cells. British Journal of Pharmacology (2004) 142, 9–19. doi:10.1038/sj.bjp.0705726