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. Author manuscript; available in PMC: 2008 Apr 1.

Published in final edited form as: Neuropharmacology. 2007 Jan 20;52(5):1244–1255. doi: 10.1016/j.neuropharm.2007.01.004

CB₁ receptor (A, top) and mu opioid receptor (B, bottom) activity of CC12. Frozen sections from globus pallidus (top) or thalamus (bottom) were incubated as described in the presence of ³⁵S-GTPγS, candidate antagonists, and increasing concentrations of either the CB₁ agonist WIN55,212-2 (WIN, top, abscissa), or the mu agonist DAMGO (bottom, abscissa). A) Specific binding of ³⁵S-GTPγS (μCi, mean ± SEM) is shown for the number of brain sections given in parentheses. B) In the thalamic sections, binding was normalized to 30 μM responses for each dose-response curve (n=5-6). For each antagonist/receptor combination, the dose ratio (shifted EC₅₀/control EC₅₀) is given along with the calculated K_d values. SR141716A (SR) and naloxone (NLX) were used as reference antagonists.

CB₁ receptor (A, top) and mu opioid receptor (B, bottom) activity of CC12. Frozen sections from globus pallidus (top) or thalamus (bottom) were incubated as described in the presence of ³⁵S-GTPγS, candidate antagonists, and increasing concentrations of either the CB₁ agonist WIN55,212-2 (WIN, top, abscissa), or the mu agonist DAMGO (bottom, abscissa). A) Specific binding of ³⁵S-GTPγS (μCi, mean ± SEM) is shown for the number of brain sections given in parentheses. B) In the thalamic sections, binding was normalized to 30 μM responses for each dose-response curve (n=5-6). For each antagonist/receptor combination, the dose ratio (shifted EC₅₀/control EC₅₀) is given along with the calculated K_d values. SR141716A (SR) and naloxone (NLX) were used as reference antagonists.