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. Author manuscript; available in PMC: 2011 Feb 1.
Published in final edited form as: Nat Neurosci. 2010 Jul 18;13(8):967–972. doi: 10.1038/nn.2597

Figure 5.

Figure 5

Presynaptic cannabinoid receptor activations delays the time to peak of inhibition. (a) Type I cannabinoid receptor (CB1R) agonist-sensitive inhibitory postsynaptic currents evoked by repeated 2pTeFo ChR2-photostimulation at a single location in the pyramidal layer in a GAD65-Cre mice in the presence of CB1R agonist (1 μM WIN55,212-2, blue) and following CB1R antagonist (10 μM AM251, green) application. Red tickmarks indicate the timing of the 2pTeFo photostimulation pulses at 880 nm. (b) Representative membrane potential traces of CB1R agonist-sensitive inhibitory responses evoked by burst 2pTeFo photostimulation (36 stimuli; #1 - #6 non-overlapping locations repeated six times with a 1 ms duration and a 3 ms interval, ∼40 Hz cycle) alone (lower traces) and paired with depolarizing current injections (+200 pA, upper traces), in the presence of WIN55,212-2 (1 μM, blue) and following subsequent application of AM251 (10 μM, green). Note that the timing of APs is shifted forward in the presence of CB1R agonist. Red tickmarks indicate the timing and relative intensity of the 2pTeFo photostimulation pulses at 880 nm. c, Summary data of peak phase of inhibitory responses evoked by 2pTeFo photostimulation in PV-Cre mice (open circles, n = 2) and peak phase of CB1R agonist-sensitive inhibitory responses evoked by 2pTeFo photostimulation in GAD65-Cre mice (right, solid gray circles, n = 5, black: mean ± s.e.m), in the presence of WIN55,212-2 (1 μM) and following subsequent application of AM251 (10 μM).