Calcium permeability-enhancing mutations in GluRIIC suppress sustained presynaptic homeostatic plasticity triggered by loss of GluRIIA.

Restoring synaptic calcium influx in Drosophila NMJ GluRIIA -/- larvae using pore-mutant glutamate receptor transgenes blocks sustained presynaptic homeostatic plasticity.

• Why it matters: The trigger for sustained PHP is unclear, even though many manipulations reduce calcium influx and quantal size.
• What they did: The authors expressed a glutamate receptor transgene with pore mutations that largely restore calcium influx in GluRIIA -/- larvae without affecting quantal size, then assessed PHP and synaptic structure.
• The result: When calcium influx is restored, PHP is blocked with no detectable synaptic structural changes, indicating reduced synaptic calcium influx is necessary for triggering and/or maintaining sustained PHP at the NMJ.