The Journal of Neuroscience, February 1, 2006, ():
Presynaptic, Activity-Dependent Modulation of Cannabinoid Type 1 Receptor-Mediated Inhibition of GABA Release
J. Neurosci. Földy et al.
26: 1465
Supplemental data
Files in this Data Supplement:
- supplemental material
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Supplementary Figure 1. Anatomical and immunocytochemical identification of the recorded presynaptic interneurons in CA1. A, Example of a visualized basket cell (camera lucida drawing, based on intracellular filling with biocytin), with the soma located in the stratum radiatum (Str. Rad.). Note the axonal arbor within or close to the pyramidal cell layer (Str. Pyr.; the initial segment is located to the right of the soma, and is indicated with a thick line; Str. Oriens: Stratum oriens). B, The immunochemical identification of the biocytin-filled interneuron shown in A revealed the presence of cholecystokinin (CCK), but the cell was immunonegative for parvalbumin.
- supplemental material
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Supplementary Figure 2. Antagonism by AM251 of the WIN- and DSI-induced suppression of eIPSCs, and the course of the recovery from CB1 agonist-induced suppression of GABA-release. A, The CB1 antagonist AM251 (10 μM) reversed the blockade of eIPSCs by WIN55,212-2 (WIN; 5μM; presynaptic firing rate: 10Hz). B, Course of the recovery from the WIN-induced blockade of GABA-release (Control: n=11 pairs; WIN: n=9 pairs; bin size: 5 action potentials; “Normalized eIPSCs (%)” includes failures; presynaptic firing frequency: 40Hz). Note that the full recovery from WIN-inhibition took place in about 25 action potentials at 40Hz. C, The CB1 antagonist AM251 (10μM) abolished DSI (traces shown are from the same cell pair; n=4 pairs; presynaptic firing frequency: 10Hz).
