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. 2013 Feb 6;33(6):2650–2660. doi: 10.1523/JNEUROSCI.2037-12.2013

Figure 4.

Figure 4.

Postsynaptic D2R stimulation and inhibition of PKA mimic and occlude LTDGABA in a CaN-dependent manner. a, Single experiment illustrating the effect of a 10 min (see bar) bath application of 20 μm quinpirole on basal synaptic transmission and the induction of pairing-induced LTDGABA (only 5 min of the baseline before the emergence of the quinpirole-induced depression is shown in this sample experiment). Inset, Averaged IPSCs before (black) or the peak response of quinpirole (red) or 25 min after pairing (green). Calibration: 50 pA, 25 ms. b, Averaged experiments with bath application of 20 μm quinpirole (open symbols) or 20 μm quinpirole plus intra-pipette cyclosporin A (1 μm, half-filled symbols). A continuous or a brief 10 min exposure of midbrain slices to quinpirole induces a rapid rundown of IPSCs that is blocked by cyclosporin A treatment (quinpirole cells, 67 ± 1.6% of the first 5 min baseline values, F(9.6,74.9) = 9.707, p < 0.0001; quinpirole plus cyclosporine A, 95 ± 4% of the pre-quinpirole values, F(2.8,5.64) = 1.106, p = 0.417). c, Averaged LTD induction experiments with (open symbols) or without (filled symbols) quinpirole. Quinpirole-induced depression occludes pairing-induced LTDGABA (control LTD, 75 ± 0.8% of pre-pairing values, F(11,177.36) = 19.121, p < 0.0001; quinpirole, 98 ± 3.7% of pre-pairing values, F(9.4,84.7) = 0.973, p = 0.470). d, Single experiment illustrating the effect of intra-pipette PKI(6–22) on basal synaptic transmission and the induction of pairing-induced LTDGABA in the PKI(6–22)-loaded cell (only 5 min of the baseline before the emergence of the PKI(6–22)-induced depression is shown in this sample experiment). Inset, Averaged IPSCs before (black) or the peak response of PKI(6–22) (red) or 25 min after pairing (green). Calibration: 50 pA, 25 ms. e, Averaged experiments with intra-pipette 10 μm PKI(6–22) (open symbols) or intra-pipette 10 μm PKI(6–22) plus 1 μm cyclosporin A (half-filled symbols). PKI(6–22) induces a rapid rundown of IPSCs that is blocked by cyclosporin A treatment (PKI cells, 75 ± 3% of the first 5 min baseline values, F(2.03,25.5) = 70.525, p < 0.0001; PKI(6–22) plus cyclosporine A, 95 ± 4% of the first 5 min baseline values, F(3,15) = 1.634, p = 0.224). f, Averaged LTD induction experiments with (open symbols) or without (filled symbols) intra-pipette PKI(6–22). LTD induction was attempted at 30 min or later after the initiation of the whole cell recording with intra-pipette PKI. PKI(6–22)-induced depression occludes pairing-induced LTDGABA (control LTD, 71 ± 1% of pre-pairing values, F(5.27,25.35) = 7.167, p < 0.0001; PKI(6–22) cells, 90 ± 4.2% of pre-pairing values, F(1.85,7.4) = 1.899, p = 0.216). g, Averaged experiments with intra-pipette 10 μm PKI(6–22) plus quipirole (open symbols). Intra-pipette PKI(6–22) occludes quinpirole-induced depression of IPSCs (quinpirole plus PKI cells, 90 ± 3% of the pre-quinpirole values, F(3.7,7.434) = 1.127, p = 0.409).