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. Author manuscript; available in PMC: 2014 Apr 24.
Published in final edited form as: Neuroscience. 2012 Jul 13;222:181–190. doi: 10.1016/j.neuroscience.2012.07.010

Figure 2.

Figure 2

The mu opioid specific agonist DAMGO significantly inhibited ST-EPSCs. A. Representative traces of a pair of ST-EPSCs (an average of 10 sweeps is shown, stimulated 20 ms apart) showing inhibition by 10 nM DAMGO and reversal by the opioid anatagonist naloxone (10 uM). B. Dose Response curve for DAMGO’s inhibition of the ST-EPSCs. 10nM, 30nM and 100nM DAMGO all significantly inhibited the amplitude of the ST-EPSC (p<0.001, One way ANOVA). C. Bar graph showing the paired pulse ratio (PPR) under control conditions, in100nM DAMGO and in 100nM DAMGO + 10uM naloxone. The PPR was significantly increased by DAMGO, an effect reversed by naloxone (p<0.05, One way ANOVA). D+N = DAMGO + Naloxone. D. Bar graph showing the average inhibition of the ST-EPSC by opioid agonists and blockade by opioid antagonists. Shown are Met-Enk (10uM), DAMGO (100nM, D), the delta receptor selective agonist DPDPE (1 uM, DP), the kappa selective agonist U50,488 (1 uM, U) and blockade of the effect by the non-specific opioid antagonist, naloxone (10uM) and the mu opioid receptor specific antagonist CTOP (1uM); Both Met-Enk and DAMGO significantly inhibited the control EPSC amplitude by an average of 82 4% and 73 6% respectively (p<0.005, Paired Student t test), all other treatments did not have significant effects compared to control.