Figure 2. Scatchard plots indicate that racemic ketamine increased the K (d)(pM, -1/slope) for [(3) H]diprenorphine without affecting the Bmax(fmoles/mg protein, x-intercept) in Chinese hamster ovary (CHO) cells expressing the recombinant [micro sign](A, 100 [micro sign]M ketamine) and [small kappa, Greek](C, 50 [micro sign]M ketamine) opioid receptors. Data are from a typical paired experiment from n = 5. Dissociation time courses are shown for CHO cells expressing the recombinant [micro sign](B, 200 [micro sign]M ketamine) and [small kappa, Greek](D, 100 [micro sign]M ketamine) opioid receptors. Cells were labeled to equilibrium with 0.5 nM [(3) H]diprenorphine; then dissociation was initiated (at t = 0) with 10 [micro sign]M naloxone (N) in the absence and presence of racemic ketamine. In control cells, dissociation was not initiated. Data are mean +/− SEM (n = 6).

Figure 2. Scatchard plots indicate that racemic ketamine increased the K (d)(pM, -1/slope) for [(3) H]diprenorphine without affecting the Bmax(fmoles/mg protein, x-intercept) in Chinese hamster ovary (CHO) cells expressing the recombinant [micro sign](A, 100 [micro sign]M ketamine) and [small kappa, Greek](C, 50 [micro sign]M ketamine) opioid receptors. Data are from a typical paired experiment from n = 5. Dissociation time courses are shown for CHO cells expressing the recombinant [micro sign](B, 200 [micro sign]M ketamine) and [small kappa, Greek](D, 100 [micro sign]M ketamine) opioid receptors. Cells were labeled to equilibrium with 0.5 nM [(3) H]diprenorphine; then dissociation was initiated (at t = 0) with 10 [micro sign]M naloxone (N) in the absence and presence of racemic ketamine. In control cells, dissociation was not initiated. Data are mean +/− SEM (n = 6).

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