Role of μ-opioid receptor in parafascicular nucleus of thalamus on morphine-induced antinociception in a rat model of acute trigeminal pain

Abstract

The parafascicular nucleus (PFN) of thalamus, as a supraspinal structure, has an important role in processing of nociceptive information. In addition, μ-opioid receptor contributes to supraspinal modulation of nociception. In the present study, the effects of microinjection of naloxone (a non-specific opioid-receptor antagonist) and naloxonazine (a specific μ-opioid receptor antagonist) were investigated on morphine-induced antinociception in a rat model of acute trigeminal pain. Right and left sides of PFN of thalamus were implanted with two guide cannulas. Acute trigeminal pain was induced by local corneal surface application of hypertonic saline and the number of eye wipes as a pain index was recorded for 30 sec. Microinjection of morphine at doses of 1, 2 and 4 μg per site significantly (<em>p</em> < 0.05) decreased the number of eye wipes. Alone microinjection of naloxone (4 μg per site) and naloxonazine (1 and 2 μg per site) significantly (<em>p</em> < 0.05) increased corneal pain severity. Prior microinjection of naloxone (2 and 4 μg per site) and naloxonazine (1 and 2 μg per site) significantly (<em>p</em> < 0.05) prevented the antinociceptive effect induced by morphine (4 μg per site). All the above-mentioned chemicals did not alter locomotor behavior in an open-field test. The results of the present study showed an antinociceptive effect of morphine at the PFN level of thalamus. Mu-opioid receptor of the PFN of thalamus may be involved in morphine-induced antinociception.