ABSTRACT
Objective To examine whether microinjectlon of morphine into the rat thaiamle nucleus submedlus (Sin) could depress the bee venom (BV)-induced nociceptive behaviours. Methods In inflammatory pain model induced by BV subcutaneous injection into rat unilateral hind paw, the inhibitory effects of morphine microinjection into thalamic nucleus suhmedius (Sin) on the spontaneous nociecptlve behavior, heat hyperalgesia and tactile ailodynia, and the influence of naioxone on the morphine effects were observed in the rat. Results A single dose of morphine (5.0 μg, 0. 5μL) applied into the Sm ipsilaterni to the BV injected paw significantly depressed the spontaneous paw flinching response. Morphine also significantly increased the heat paw withdrawal iateneies in the bilateral hind paw and the tactile paw withdrawal threshold in the ipsilnteral hind paw 2 hours after BV injection. All these depressive effects could be effectively antagonized by pre-treatment with the opiuld receptor antagonist naloxone (1.0μg, 0. 5μL) in the Sm 5rain prior to morphine administration. Naloxone alone injected to the Sm had no effect on the BV-induecd nociceptive behavior. Conclusion These results suggest that Sm is involved in opioid receptor-mediated antt-nociception in the rat with the BV-induced inflammatory pain. Together with results from previous studies, it is likely that this effect is produced by activation of the Sm-ventrolateral orbital cortex-periaqueductal gray pathway, leading to activation of the brainstem descending inhibitory system and depression of the nodceptive inputs at the spinal cord level.
ABSTRACT
Objective: To examine whether microinjection of morphine into the rat thalamic nucleus submedius (Sm) could depress the bee venom (BV)-induced nociceptive behaviours. Methods: In inflammatory pain model induced by BV subcutaneous injection into rat unilateral hind paw, the inhibitory effects of morphine microinjection into thalamic nucleus submedius (Sm) on the spontaneous nociceptive behavior, heat hyperalgesia and tactile allodynia, and the influence of naloxone on the morphine effects were observed in the rat. Results: A single dose of morphine (5. 0 μg, 0.5 μL) applied into the Sm ipsilateral to the BV injected paw significantly depressed the spontaneous paw flinching response. Morphine also significantly increased the heat paw withdrawal latencies in the bilateral hind paw and the tactile paw withdrawal threshold in the ipsilateral hind paw 2 hours after BV injection. All these depressive effects could be effectively antagonized by pre-treatment with the opioid receptor antagonist naloxone (1.0 μg, 0.5 μL) in the Sm 5min prior to morphine administration. Naloxone alone injected to the Sm had no effect on the BV-induced nociceptive behavior. Conclusion: These results suggest that Sm is involved in opioid receptor-mediated anti-nociception in the rat with the BV-induced inflammatory pain. Together with results, from previous studies, it is likely that this effect is produced by activation of the Sm-ventrolateral orbital cortex-periaqueductal gray pathway, leading to activation of the brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.
ABSTRACT
Objective To investigate whether the μ- and δ-opioid receptors were involved in mediating the a ntinociceptive effect of opioid injection into the nucleus submedius (Sm). Methods Nociceptive behavior produced by subcutaneous injection of formalin (65 mmol/L, 50 μL) into the hind paw of the rat was assessed quantitatively using an automated movement detection system. The effects of morphine and selectiveμ- and δ-opioid receptor antagonists microinjected unilaterally into the Sm were determined in the awake rats. Results Morphine (31 mmol/L, 0. 5 μL) depressed the nociceptive behavior elicited by formalin, and this effect was antagonized completely by the selective μ-receptor antagonist β-funaltrexamine (β-FNA, 0. 4 mmol/L, 0. 5 μL) and naloxonazine (0.8 mmol/L, 0.5 μL), and partly by the δ-receptor antagonist naltrindole (0.4 mmol/L, 0.5μL).Administration of morphine into thalamic regions more than 0. 5 mm dorsal to the Sm had no effect on the nociceptive behavior. Conclusion Antinociceptive effects produced by opioid acting on Sm neurons are mediated mainly by μ-opioid receptors, and partly by δ-receptors.