Retrograde endocannabinoid signaling at striatal synapses requires a regulated postsynaptic release step

Adermark and Lovinger. 10.1073/pnas.0706873104.

Supporting Information

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SI Figure 4
SI Figure 5
SI Figure 6




SI Figure 4

Fig. 4. Holding potential and AEA release. (a) AEA-induced depression during paired-pulse stimulation was independent of postsynaptic holding potential. Example traces show EPSCs induced by paired-pulse stimulation in MSNs clamped at -70 mV. (b) Single-pulse stimulation was insufficient to induce a depression in EPSC amplitude in cells clamped at -50 mV, but a small rundown was observed in cells clamped at -70 mV or loaded with AEA- and CsCl-based internal solution. Example traces show baseline EPSCs (black) in MSNs clamped at -70 mV after 30-35 min of single-pulse stimulation (gray). EPSC amplitude data are mean ± SEM. (Calibration bars, 25 msec and 100 pA.)





SI Figure 5

Fig. 5. Evoked IPSCs are GABAergic. IPSCs were completely abolished by 50 mM picrotoxin. Example traces show baseline IPSC (black) and at t = 20-25 min (gray). IPSC amplitude data are mean ± SEM (n = 3 cells). (Calibration bars, 25 msec and 100 pA.)





SI Figure 6

Fig. 6. NO synthesis and group I mGluRs are not involved in eCB mobilization at inhibitory synapses. Blockade of NO synthesis with 100 mM L-NAME or mGluRs with MPEP and CPCCOEt did not prevent AEA-induced depression. Example traces show IPSCs at baseline and after 20-25 min of paired-pulse stimulation in an MPEP- and CPCCOEt-treated slice. IPSC amplitude data are mean+/- SEM. (Calibration bars, 25 msec and 100 pA.)