- 作者：Jun Zhaoa ; b ; 1 ; Baozhu Gaoa ; b ; gaobaozhumed@163.com" class="auth_mail ; Yu Zhangc ; 1 ; Baosen Zhengd ; He Liue ; Jun-Li Caoe
- 关键词：Motilin ; Hippocampus ; Motilin receptor ; Gastrointestinal motility ; Naloxone ; Incisional pain
- 刊名：Life Sciences
- 出版年：17 May 2014
- 年：2014
- 卷：103
- 期：2
- 页码：88-94
- 全文大小：814 K
Main methods
An intrathecal catheter was implanted, and saline, opioids (morphine and fentanyl) and naloxone were intrathecally administered 7 days later. An incisional pain model was established to induce pain behaviors in rats by unilateral plantar incision. Thermal hyperalgesia and mechanical allodynia were measured by using a radiant heat and electronic Von Frey filament, respectively. The expression of motilin in the hippocampus, stomach, duodenum, and plasma was determined by ELISA; and the expression of motilin receptor in the hippocampus was detected by Western blot assay.
Key findings
Motilin and its receptor were detected in the hippocampus. Acute incisional pain increased the motilin expression in the hippocampus and duodenum, while decreasing its expression in the gastric body and plasma. Postoperative analgesia with morphine + fentanyl upregulated the expression of motilin in the hippocampus; however, motilin was downregulated in peripheral sites. Naloxone at 1 ng/kg restored motilin to baseline levels. Acute pain, morphine + fentanyl, and naloxone all induced the expression of motilin receptor in the hippocampus.
Significance
Acute pain, postoperative analgesia with opioids, and naloxone significantly impacted the expression of hippocampal and peripheral motilin. Variation trends in all sites were not identical. Intrathecal injection of low-dose naloxone upregulated paw withdrawal thermal latency and enhanced the analgesic effects of opioids. The findings presented here provide a new basis for central and peripheral regulations in GI motility, clinical postoperative analgesia, and management of analgesic complications.