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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 5. Characterization of functional KOP receptors in human DRG neurons.

Figure 5.

A. Example of Ca2+ signaling in a neuron responsive to dynorphin and DAMGO, but not capsaicin. B. Both the magnitude of dynorphin-induced suppression of the evoked Ca2+ transient, and the proportion of neurons responsive to this KOP receptor agonist (inset), were concentration dependent. C. Distribution of neurons responsive to dynorphin, DAMGO, and capsaicin. D. Example of Ca2+ signaling in a neuron in which pre-application of the KOP receptor antagonist, nor-BNI was associated with the absence of a response to dynorphin. This neuron was responsive to capsaicin, however. E. Pooled data for neurons challenged with dynorphin alone or following application of nor-BNI. The proportion of neurons responsive to dynorphin (**p=0.0025, chi-square) and the magnitude of the suppression of the evoked Ca2+ transient (*p=0.027, Mann Whitney t-test) were significantly reduced by nor-BNI.