Abstract
Postsynaptic compartments can be specifically modulated during various forms of synaptic plasticity, but it is unclear whether this precision is shared at presynaptic terminals. Presynaptic homeostatic plasticity (PHP) stabilizes neurotransmission at the Drosophila neuromuscular junction, where a retrograde enhancement of presynaptic neurotransmitter release compensates for diminished postsynaptic receptor functionality. To test the specificity of PHP induction and expression, we have developed a genetic manipulation to reduce postsynaptic receptor expression at one of the two muscles innervated by a single motor neuron. We find that PHP can be induced and expressed at a subset of synapses, over both acute and chronic time scales, without influencing transmission at adjacent release sites. Further, homeostatic modulations to CaMKII, vesicle pools, and functional release sites are compartmentalized and do not spread to neighboring pre- or post-synaptic structures. Thus, both PHP induction and expression mechanisms are locally transmitted and restricted to specific synaptic compartments.
Highlights
Synaptic strength can be modulated with a remarkable degree of specificity to enable the flexibility necessary for learning and memory, where compartmentalized changes in dendritic spines tune responses to neurotransmitter release during information transfer in the nervous system
We have developed a manipulation that enables the loss of glutamate receptors (GluRs) on only one of the two postsynaptic targets innervated by a Type Ib motor neuron at the Drosophila neuromuscular junction (NMJ)
GluRs are dynamically trafficked in postsynaptic compartments where they mediate the synapse-specific expression of Hebbian plasticity such as LTP (Herring and Nicoll, 2016; Matsuzaki et al, 2004)
Summary
Synaptic strength can be modulated with a remarkable degree of specificity to enable the flexibility necessary for learning and memory, where compartmentalized changes in dendritic spines tune responses to neurotransmitter release during information transfer in the nervous system. Such plasticity mechanisms require compartmentalized trafficking and insertion of glutamate receptors (GluRs) into postsynaptic densities at specific locations in response to correlated activity (Herring and Nicoll, 2016; Malinow, 2003). How presynaptic terminals are modulated by Hebbian and homeostatic
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