摘要
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.
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.
作者
Jie Feng1,Ning Jia1,Jun-yang Wang2,Xin-ai Song1,Xiao-ying Li1,Jing-shi Tang11. Department of Physiology and Pathophysiology,Key Laboratory of Environment and Genes Related to Diseases,Ministry of Education,Medical School of Xi’an Jiaotong University,Xi’an 710061
2. Department of Immunology and Pathogenic Biology,Medical School of Xi’an Jiaotong University,Xi’an 710061,China.
基金
supported by the National Natural Science Foundation of China (No.30270453
30570592)
