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. 2005 Mar 23;25(12):3192–3198. doi: 10.1523/JNEUROSCI.4585-04.2005

Figure 4.

Figure 4.

Upregulation of cAMP/PKA-mediated signal transduction during morphine withdrawal is not responsible for inducing DOPr function. A, mIPSC rate and amplitude in the absence and presence of H-89. PAG slices from morphine-treated mice were preincubated in the absence of morphine for 1 h and in the presence of the PKA inhibitor H-89 (10 μm) for 30 min before commencement and throughout the course of the experiment. DELT- (300 nm) mediated inhibition of mIPSC frequency persisted in the presence of H-89 (**p < 0.01; *p < 0.05; n = 5; paired t tests in the absence and presence of DELT). B, Histogram showing the augmentation of mIPSC frequency in morphine-naive PAG neurons by forskolin (1 μm; n = 4; ***p < 0.001; paired t test). Subsequent application of DELT (1 μm) in the continued presence of forskolin did not affect the mIPSC rate, but Met-enkephalin (ME; 10 μm) did reduce the mIPSC rate. The forskolin-induced increase in mIPSC rate was abolished by previous treatment with H-89 (10 μm; p < 0.001; unpaired t test; n = 5). ICI, ICI 174864.