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. Author manuscript; available in PMC: 2021 Jul 1.
Published in final edited form as: Pain. 2020 Jul;161(7):1636–1649. doi: 10.1097/j.pain.0000000000001846

Figure 3. Characterization of DOP receptor agonist, SNC80, in human DRG neurons.

Figure 3.

A. Example of a neuron pre-treated (for 30 min) with the PTEN inhibitor, bpV(Phen), that was responsive to SNC80 (1 μM), DAMGO (1 μM), and capsaicin (500 nM). B. Without pretreatment with bpV(Phen), very few neurons were responsive to SNC80 at a concentration of 1 μM. However, the fractional inhibition and percentage of responsive neurons (inset) increased as the concentration of SNC80 was increased to 3 and 10 μM. C. Pooled data of neurons pre-treated with bpV(Phen) or vehicle that were subsequently challenged with 1 μM SCN80 (p=0.026, chi-square). D. Distribution of vehicle and bpV(Phen) treated neurons that were responsive to SNC80, DAMGO, and/or capsaicin. In this and subsequent figures, each spoke in the wheel represents a single neuron. Of note, the vehicle wheel includes the 2/15 neurons responsive to SNC80 when challenged with the agonist alone, as well as the 2/2 neurons responsive to SNC80 when challenged with the agonist following application of naltrindole. E. Example of a neuron challenged with SCN80 following application of the DOP receptor antagonist naltrindole. The neuron was subsequently challenged with DAMGO and capsaicin. Note the inhibition associated with naltrindole alone. F. Pooled data of bpV(Phen) treated neurons that were subsequently challenged with SCN80 alone or following the application of naltrindole. While there was no significant influence of naltrindole on the percentage of neurons responsive to SNC80 (p=0.24, chi-square), the attenuation of the magnitude of the suppression of the evoked transient was significant (t=2.97, df=17, **p=0.01, unpaired t-test).