Figure 6.

Csp is required for long-term homeostatic compensation. (A) T15 × UAS-Csp[RNAi] shows a failure to upregulate quantal content compared to its GAL4-driven UAS-Csp[RNAi] control (ns, p = 0.15). Knock down of Csp shows a slight impairment in evoked neurotransmission (EPSP) compared to control (**p < 0.01). (B) Representative electrophysiological traces show the failure of T15 × UAS-Csp[RNAi] larvae to maintain evoked potentials at control levels. (C) Homozygosity for the Csp^DG29203 allele or heterozygosity for the Csp^EY22488 allele block homeostatic upregulation of quantal content compared to their respective non-GluRIIA^SP16genetic controls (ns, p = 0.44 and p = 0.14, respectively). (D) Representative traces show a failure of homeostatic compensation for GluRIIA^SP16, Csp^DG29203. (E) Postsynaptic knock down of Csp function leaves homeostatic plasticity intact. (F) Acute homeostatic compensation is intact in Csp^DG29203 as evidenced by the elevated quantal content in response to philanthotoxin-433 (PhTox) application (**p < 0.01). (G) A doubly heterozygous combination of Csp^DG29203/+ and cac^S/+ shows a homeostatic block in the GluRIIA^SP16 background because of a failure to increase quantal content over cac^S/+; Csp^DG29203/+ controls (ns, p = 0.24). By contrast, the single heterozygous mutations retain partial homeostatic compensatory capacity. Scale bars for EPSPs (mEPSPs): 5 mV (1 mV); 50 ms (2000 ms). (ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001).