Skip to main content
. Author manuscript; available in PMC: 2015 Sep 26.
Published in final edited form as: Science. 2014 Sep 26;345(6204):1616–1620. doi: 10.1126/science.1255514

Fig. 2. Pharmacology of spine enlargement induced by STDP plus DAopto with a 0.6-s delay.

Fig. 2

(A) Time courses of spine enlargement induced by STDP + DAopto with a 0.6-s delay in the absence (control, 24 spines, 7 dendrites) and presence of NMDAR antagonist (50 μM D-AP5, 22 spines, 6 dendrites), CaMKII inhibitor (3 μM KN62, 23 spines, 6 dendrites), or protein synthesis inhibitor (5 μM anisomycin, 25 spines, 6 dendrites). (B) Time courses of spine enlargement in the presence of D1R antagonist (3 μM SCH23390, 23 spines, 6 dendrites), D2R antagonist (10 μM sulpiride, 22 spines, 6 dendrites), or PKA inhibitor (10 μM PKI, in the pipette, 24 spines, 6 dendrites). (C) Time courses of spine enlargement in the presence of inhibitory (100 μM, in the pipette, 24 spines, 6 dendrites) or control peptide for DARPP-32 (100 μM, in the pipette, 24 spines, 6 dendrites). (D) Averaged volume changes in the absence and presence of the compounds. Data are presented as mean ± SEM. P = 3.4 × 10−6 with Kruskal-Wallis and *P = 0.023 (AP5), 0.023 (KN62), 0.037 (AIP) (fig. S5A), 0.023 (anisomycin), 0.035 (SCH23390), 0.023 (PKI), 0.037 (KT5720) (fig. S5A), and 0.023 (DARPP-32 inhibitory peptide) with Steel test.