Fig. 9
Homeostatic control of postsynaptic GluR abundance is induced and expressed following hypo-innervation in hiw mutants. a Schematic illustrating a hiw-mutant NMJ and a hypo-innervated hiw-mutant muscle 7 NMJ (hiw M7 hypo: hiwΔN; tubP>stop>Gal4, UAS-FLP, UAS-CD8-GFP/UAS-FasII-PEST+; H94-Gal4, nSyb-Gal80). Representative mEPSP and EPSP traces of the indicated genotypes are shown below. Quantification of mEPSP amplitude (b), EPSP amplitude (c), and quantal content (d) in the indicated genotypes demonstrates a homeostatic increase in mEPSP amplitude maintains baseline synaptic strength despite a reduction in quantal content in hiw M7 hypo. e Representative images of muscle 7 larval NMJs in hiw and hiw M7 hypo immunostained with antibodies that recognize vGlut and the neuronal membrane (HRP). Note the reduced innervation of boutons onto muscle 7 in the hiw M7 hypo condition. Right: Representative GluRIIA staining of the indicated genotypes. An upregulation in GluRIIA levels is observed specifically on hiw M7 hypo NMJs. Quantification of bouton numbers (f) and GluRIIA puncta intensity (g) in the indicated genotypes. h Schematic illustrating injury-related adaptations to synaptic function and homeostatic plasticity. Activation of presynaptic DLK signaling induces a reduction in GluR levels. This diminished state of synaptic strength is achieved through a silencing of PHP signaling upstream of Tor activity, and stabilized by GluR scaling. Error bars indicate ± SEM followed by an unpaired t-test. *p ≤ 0.05; **p 0.01; NS not significant, p > 0.05
