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
AUTHORS (7)
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.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (0)
CITATIONS (10)
EXTERNAL LINKS
PlumX Metrics
RECOMMENDATIONS
FAIR ASSESSMENT
Coming soon ....
JUPYTER LAB
Coming soon ....