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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: J Neurochem. 2016 Oct 18;139(5):737–747. doi: 10.1111/jnc.13852

Fig. 2.

Fig. 2

Effects of chronic morphine on Cav-1 scaffolding generalize to sufentanil (SUF), hydrocodone (HYDRO) and oxycodone (OXY). The Triton insoluble membrane fraction was obtained from opioid naïve, acute (5 min) sufentanil-treated and chronic sufentanil-, hydrocodone- or oxycodone-treated (1 μM, 48 h) MOR-CHO, after which it was solubilized and subjected to immunoprecipitation with anti-Cav-1 antibody. MOR (A) and Gsα (B) were visualized and quantified as described for Fig. 1. All co-IPs were normalized to their corresponding directly IPed Cav-1 protein. The content of MOR or Gsα in the Cav-1 IP from opioid treated MOR-CHO is expressed as a percent of their content in Cav-1 IP obtained from opioid naïve cells (C). n=3–5; *indicates p<0.05. The ability of chronic morphine to augment Cav-1 scaffolding of MOR and Gsα generalized to sufentanil, oxycodone, and hydrocodone. Chronic, not acute, opioid exposure is a prerequisite for the observed augmented Cav-1 scaffolding, which is eliminated by concomitant exposure to naloxone (Nx).