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. Author manuscript; available in PMC: 2009 Jan 29.
Published in final edited form as: Brain Res. 2007 Nov 28;1191:180–191. doi: 10.1016/j.brainres.2007.11.034

Figure 3. TMEV-infection caused a significant decrease in morphine’s antinociceptive effect on thermal hyperalgesia.

Figure 3

Baseline morphine antinociception responses were determined by administering saline, 1, 2.5 or 10 mg/kg subcutaneously at day 60 PI in female (A) and male (B) TMEV-infected and uninfected controls. (C) TMEV-infected female mice exhibited thermal hyperalgesia when compared to uninfected control mice (‡ p<0.05). Morphine antinociception was determined in the chronic phase of TMEV-infection at days 90, 120, 150 and 180 PI by administering either saline or 10 mg/kg morphine subcutaneously. Uninfected control female mice exhibited significant morphine antinociception at all time points when compared to uninfected saline treated mice and TMEV infected female mice exhibited significant morphine analgesia at days 90 and 120 PI (* p<0.05). TMEV-infected female mice exhibited significantly decreased morphine analgesia when compared to uninfected controls at days 90, 120, 150 and 180 PI († p<0.05). (D) TMEV-infected male mice exhibited thermal hyperalgesia when compared to uninfected control mice (‡ p<0.05). Morphine antinociception was determined in the chronic phase of TMEV-infection at days 90, 120, 150 and 180 PI by administering either saline or 10 mg/kg morphine subcutaneously. Both TMEV-infected and uninfected control male mice exhibited significant morphine antinociception at all time points when compared to uninfected saline treated mice (* p<0.05). TMEV-infected male mice exhibited significantly decreased morphine analgesia when compared to uninfected controls at days 120, 150 and 180 PI († p<0.05).