In the article “Persistent, Exocytosis-Independent Silencing of Release Sites Underlies Homosynaptic Depression at Sensory Synapses in Aplysia,” by Tony D. Gover, Xue-Ying Jiang, and Thomas W. Abrams, which appeared on pages 1942–1955 of the March 1, 2002 issue, the text contained in rows 1 and 2 of the second and fourth columns of “Table1. Alternative mechanisms of HSD” printed incorrectly. The correct version of Table 1 is printed here.
Table 1.
Alternative mechanisms of HSD
| HSD is consequence of exocytosis event | HSD is consequence of presynaptic spike (independent of release) | ||||
|---|---|---|---|---|---|
| HSD results from decrease in: | HSD results from decrease in: | ||||
| Initially strong and weak synapses differ in: | Number of readily releasable vesicles (n) | Release probability of individual vesicles (Pves) | Number of functional release sites (Nsite) | Release probability of individual vesicles (Pves) | Number of functional release sites (Nsite) |
| Number of readily releasable vesicles (n) | HSD is strength dependent1-a | HSD is strength dependent | HSD is strength dependent | HSD is strength dependent | HSD is strength independent1-b |
| Release probability of individual vesicles (Pves) | HSD is strength dependent | HSD is strength dependent | HSD is strength dependent | HSD is strength dependent | HSD is strength independent |
| Number of active zones (Nsite)1-c | Nonphysiological | Nonphysiological | Nonphysiological | Nonphysiological | Nonphysiological |
Indicates that HSD depends on initial strength of synaptic connections.
Indicates that HSD develops independently of initial strength of synaptic connections.
Not tested in simulations because paired-pulse ratio data indicate that strong and weak synapses differ in the properties of their individual release sites (not only in number of release sites).