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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Nat Neurosci. 2013 Mar 17;16(4):456–463. doi: 10.1038/nn.3353

Figure 4. Inhibiting CaMKII or preventing CaMKII autophosphorylation at Thr286 enhances endocannabinoid-mediated retrograde transmission in striatal MSNs.

Figure 4

(a,b) DSE is significantly enhanced in D2(−) MSNs from T286A-KI (KI) mice (gray) relative to WT (black), and when the CaMKII inhibitory peptide AIP (10 μM; white) is included in the patch pipette (WT 74±2%, n=15 cells from 4 mice; KI 65±2%, n=10 cells from 4 mice; AIP 61±2%, n=9 cells from 3 mice; 1-way ANOVA: F(2,31)=8.30, p=0.0013; Bonferroni’s post-test: WT vs. KI t31=2.764, *p<0.05; WT vs. AIP t31=3.830, **p<0.01). (c,d) In D2(+) MSNs, DSE was similar in WT and T286A-KI MSNs (gray), but loading AIP in WT cells significantly enhanced DSE (WT 67±2%, n=15 cells from 4 mice; KI 69±2%, n=11 cells from 5 mice; AIP 53±5%, n=7 cells from 3 mice. 1-way ANOVA: F2,30=8.769, p=0.001. Bonferroni’s post-test: WT vs. KI t30=0.5626, p>0.05. WT vs. AIP t30=3.654, **p<0.01). (e, f) Pretreatment of slices with DHPG (10 μM) enhanced DSE in D2(−) MSNs and prevented differences between WT and T286A-KI mice with 10 s depolarization (WT 57±3%, n=7 cells from 3 mice; KI 54±1, n=9 cells from 3 mice; unpaired two-tailed t-test, p>0.05). (g, h) Addition of DHPG also enhanced DSE in D2(+) MSNs but did not reveal differences between WT and T286A-KI mice with 10 s depolarization (WT 57±3%, n=7 cells from 4 mice; KI 53±2, n=8 cells from 4 mice; unpaired two-tailed t-test, p>0.05). Representative traces are shown for each condition. Calibration bars 20 ms × 150 pA.