Ferré J P, Ruckebusch Y, Soldani G
Department of Physiology, National Veterinary School, Toulouse, France.
Pharmacology. 1992;44(4):196-205. doi: 10.1159/000138919.
The effects of intraperitoneal, intrathecal and intracerebroventricular injections of the peptide galanin (GAL) on duodenojejunal and colonic motility were studied in conscious fed rats. At 0.3-3.0 nmol/rat, intraperitoneal GAL restored the 'fasted pattern' of duodenojejunal activity, i.e. the migrating myo-electric complex (MMC) was restored for a short period of time, and the MMC frequency was not significantly different from that observed before feeding. In addition, the activity of the proximal but not of the distal colon was significantly increased by GAL administration. The intracerebroventricular administration of GAL (0.03-0.3 nmol/rat) induced an MMC fasted pattern on the duodenojejunum after a latency period of about 1 h. In these experiments proximal colonic motor activity was significantly increased for 120-180 min. GAL given intrathecally (0.03-0.3 nmol/rat) induced a long-lasting fasted pattern of the intestinal activity within 10-20 min which was not dose dependent in duration, while the motility index of the proximal colon was significantly increased. Pretreatment with naloxone prevented the specific effects of GAL, given intracerebroventricularly or intrathecally, on the duodenojejunum and colon and the colonic response, but not the restoration of the MMC pattern on the duodenojejunum, induced by GAL given intraperitoneally. Ketoprofen pretreatment was completely ineffective. These observations indicate a plurality of sites of action of GAL on digestive tract motility including local duodenal receptors and suggest the importance of a spinal component in the control of motility by GAL when given intrathecally. Moreover the present results indicate the involvement of opioid receptors in the fasted pattern induced by GAL given intracerebroventricularly or intrathecally and in the colonic effects regardless of the route of administration.
在清醒的进食大鼠中，研究了腹腔内、鞘内和脑室内注射肽类物质甘丙肽（GAL）对十二指肠空肠和结肠运动的影响。腹腔注射GAL，剂量为0.3 - 3.0 nmol/大鼠时，可恢复十二指肠空肠活动的“禁食模式”，即移行性肌电复合波（MMC）在短时间内恢复，且MMC频率与进食前观察到的频率无显著差异。此外，给予GAL可显著增加近端结肠而非远端结肠的活动。脑室内注射GAL（0.03 - 0.3 nmol/大鼠），约1小时的潜伏期后，十二指肠空肠出现MMC禁食模式。在这些实验中，近端结肠运动活动在120 - 180分钟内显著增加。鞘内注射GAL（0.03 - 0.3 nmol/大鼠）在10 - 20分钟内诱导出肠道活动的持久禁食模式，其持续时间不依赖于剂量，同时近端结肠的运动指数显著增加。用纳洛酮预处理可阻止脑室内或鞘内注射GAL对十二指肠空肠和结肠以及结肠反应的特定作用，但不能阻止腹腔注射GAL诱导的十二指肠空肠MMC模式的恢复。酮洛芬预处理完全无效。这些观察结果表明GAL对消化道运动的作用位点具有多样性，包括局部十二指肠受体，并提示鞘内注射GAL时脊髓成分在运动控制中的重要性。此外，目前的结果表明阿片受体参与了脑室内或鞘内注射GAL诱导的禁食模式以及结肠效应，而与给药途径无关。
