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. Author manuscript; available in PMC: 2016 Jan 13.
Published in final edited form as: Cell Rep. 2014 Dec 31;10(2):162–169. doi: 10.1016/j.celrep.2014.12.016

Figure 4. Heterosynaptic spine shrinkage requires signaling through calcineurin, IP3Rs, and group I mGluRs, but not CaMKII.

Figure 4

(A) Images of dendrites from EGFP-transfected neurons exposed to multiple HFU (yellow crosses) in the presence of inhibitors of CaMKII (KN62, 10 μM), calcineurin (FK506, 2 μM), IP3Rs (Xesto C, 1 μM), or group I mGluRs (MPEP, 15 μM and CPCCOEt, 45 μM).

(B) Inhibition of CaMKII with KN62 blocked structural potentiation of stimulated spines (black bar; 13 cells; p = 0.067) but did not block heterosynaptic shrinkage (red bar; 13 spines; p < 0.01). In contrast, inhibition of calcineurin with FK506 (blue bar; 13 spines, p < 0.05), IP3Rs with Xesto C (blue bar; 11 spines, p = 0.58), or group I mGluRs with MPEP and CPCCOEt (blue bar; 10 spines, p = 0.51) blocked heterosynaptic shrinkage without affecting HFU-induced spine enlargement (black bars; FK506, 13 cells, p < 0.01; Xesto C, 11 cells, p < 0.01; MPEP and CPCCOEt, 10 cells, p < 0.05), which was not different from that observed without drug (far left black bar; vs. FK506, p = 0.24; vs. Xesto C, p = 0.66; vs. MPEP and CPCCOEt, p = 0.49). “No drug” data from Fig. 1B.