Motor neurons in imdNP1182/imdNP1182 third instar larvae display a small, but statistically significant reduction in active zone density, with a similar number of type I boutons and active zones as controls. They show a similar baseline neurotransmission, with similar quantal content, mEPSP (mini excitatory postsynaptic potential) and EPSP (excitatory postsynaptic potential) amplitudes, mEPSP frequency as controls.
imdNP1182 has abnormal neurophysiology | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
imdNP1182 has abdominal segment motor neuron | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
imdNP1182 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
Motor neurons in imdNP1182, GluRIIASP16 double mutant third instar larvae have reduced mEPSP (mini excitatory postsynaptic potential) compared to single imdNP1182 (but not GluRIIASP16) mutants; reduced EPSP (excitatory postsynaptic potential) amplitudes compared to either single mutant; and reduced quantal content compared to single GluRIIASP16 (but not imdNP1182) mutants. Their capacity for long-term presynaptic homeostatic plasticity (i.e. increase in quantal content causing an increase in EPSP amplitude, approaching baseline) is completely blocked.