A Novel Postsynaptic Mechanism for Heterosynaptic Sharing of Short-Term Plasticity

Time Factors Sensory Receptor Cells 4 Intracellular Space Presynaptic Terminals Sequence Homology In Vitro Techniques Receptors, Metabotropic Glutamate Medical and Health Sciences 03 medical and health sciences Homer Scaffolding Proteins Receptors Aplysia Metabotropic Glutamate Animals Inositol 1,4,5-Trisphosphate Receptors Invertebrate Amino Acid Sequence 5-Trisphosphate Receptors Motor Neurons 0303 health sciences Neurology & Neurosurgery Neuronal Plasticity Sequence Homology, Amino Acid Psychology and Cognitive Sciences Neurosciences Excitatory Postsynaptic Potentials Inositol 1 Ganglia, Invertebrate Amino Acid Synapses Ganglia Calcium Carrier Proteins
DOI: 10.1523/jneurosci.4767-09.2010 Publication Date: 2010-07-23T15:33:58Z
ABSTRACT
Postsynaptic release of Ca(2+) from intracellular stores is an important means of cellular signaling that mediates numerous forms of synaptic plasticity. Previous studies have identified a postsynaptic intracellular Ca(2+) requirement for a form of short-term plasticity, post-tetanic potentiation (PTP) at sensory neuron (SN)-motor neuron synapses in Aplysia. Here, we show that postsynaptic IP(3)-mediated Ca(2+) release in response to a presynaptic tetanus in an SN that induces PTP can confer transient plasticity onto a neighboring SN synapse receiving subthreshold activation. This heterosynaptic sharing of plasticity represents a dynamic, short-term synaptic enhancement of synaptic inputs onto a common postsynaptic target. Heterosynaptic sharing is blocked by postsynaptic disruption of Ca(2+)- and IP(3)-mediated signaling, and, conversely, it is mimicked by postsynaptic injection of nonhydrolyzable IP(3), and by photolysis of caged IP(3) in the MN. The molecular mechanism for heterosynaptic sharing involves metabotropic glutamate receptors and Homer-dependent interactions, indicating that Homer can facilitate the integration of Ca(2+)-dependent plasticity at neighboring postsynaptic sites and provides a postsynaptic mechanism for the spread of plasticity induced by presynaptic activation. 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.
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