Official websites use. Share sensitive information only on official, secure websites. Correspondence should be addressed to Thomas J. Carew at the above address. This heterosynaptic sharing of plasticity represents a dynamic, short-term synaptic enhancement of synaptic inputs onto a common postsynaptic target.
Our results support a model in which postsynaptic summation of IP 3 signals from suprathreshold and subthreshold inputs results in molecular coincidence detection that gives rise to a novel form of heterosynaptic plasticity. Synaptic plasticity exists in a wide range of temporal domains. Activity-dependent short-term plasticity, lasting on the order of seconds to minutes, includes paired-pulse facilitation, paired-pulse depression, and post-tetanic potentiation PTP.
Whereas long-lasting forms of plasticity, such as long-term potentiation LTP and long-term depression LTD , are generally considered to provide a means of information storage in neurons, these short-term forms of plasticity are critical for dynamic, moment-to-moment adjustments of synaptic strength during online processing of neural information.
At most synapses, PTP is typically thought to be mediated solely by presynaptic mechanisms Zucker and Regehr, Moreover, heterosynaptic sharing is facilitated by postsynaptic injection of nonhydrolyzable IP 3 and by photoactivated caged IP 3. Finally, heterosynaptic sharing is blocked by disruption of Homer-mediated protein interactions following postsynaptic injection of a synthetic peptide containing the Homer binding sequence of the Aplysia IP 3 receptor IP 3 R.
These findings provide evidence for a novel form of short-term heterosynaptic plasticity that arises from postsynaptic interactions between presynaptic inputs, and indicates that activity-dependent spread of plasticity is not limited to the long-term time domains. Moreover, this unique form of plasticity provides a mechanism for dynamic, temporally restricted amplification of synaptic inputs onto a common postsynaptic target.
