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. Author manuscript; available in PMC: 2014 Jul 8.
Published in final edited form as: Biol Psychiatry. 2011 Sep 1;71(3):232–238. doi: 10.1016/j.biopsych.2011.07.015

Figure 3.

Figure 3

Both delta opioid receptor (DOR) and mu opioid receptor (MOR) are required for the ethanol-induced increase in potency of DOR-selective agonists. (A) Ethanol-drinking wild-type, C57BL/6 mice (n = 8–10) were injected intrathecally with agonist (deltorphin II [1 nmol], [D-Pen2,D-Pen5]-Enkephalin [DPDPE] [1 nmol], SNC80 [30 nmol], or DAMGO [30 pmol]) and antinociception was measured using a radiant tail-flick assay. Involvement of MOR and DOR was determined by co-injection with either the MOR-selective antagonist CTAP (.2 nmol) or the DOR-selective antagonist Naltriben (.5 nmol), respectively. Significance between groups was determined by analysis of variance followed by a Newman-Keuls post hoc analysis. (B) Naïve or ethanol-drinking C57BL/6 DOR knockout (KO) mice (n = 8–10) were injected intrathecally with agonist (deltorphin II [1 nmol], DPDPE [1 nmol], or SNC80 [30 nmol]) and thermal antinociception was measured. (C) Naïve or ethanol-drinking C57BL/6 MOR KO mice (n = 8–9) were injected intrathecally with agonist (deltorphin II [4 nmol], DPDPE [4 nmol], SNC80 [30 nmol], or DAMGO [30 pmol]) and antinociception was measured. Data are represented as the percentage maximal possible effect, which is defined as [(measurement – baseline)/(cutoff – baseline)]*100. *p < .05; ***p < .001. Delt II, deltorphin II; EtOH, ethanol; MPE, maximal possible effect; NTB, Naltriben.