Morin-Surun M P, Boudinot E, Fournie-Zaluski M C, Champagnat J, Roques B P, Denavit-Saubie M
Laboratoire de Physiologie Nerveuse, C.N.R.S., Gif-sur-Yvette, France.
Neurochem Int. 1992 Jan;20(1):103-7. doi: 10.1016/0197-0186(92)90132-b.
Experiments have been performed in order to evaluate the respiratory consequences of a suppression or accumulation of endogenous opioid peptides, in the neuronal network which generates the motor respiratory activity. Iontophoretic application of naloxone onto respiratory neurons increases their firing activity and increases their respiratory modulation. On the other hand the local injection of kelatorphan (an enkephalinase inhibitor) decreases the firing of respiratory neurons and thus reduces the respiratory modulation. This effect of kelatorphan mimics the effect on respiratory neuron of an iontophoretic application of met-enkephalin. Furthermore the local injection of kelatorphan reduces the frequency of the respiratory output recorded from the phrenic nerve. This effect is reversed by systemic administration of naloxone. The results demonstrate the involvement of endogenous opioid peptides in the control of breathing suggesting that in Sudden Infant Death Syndrome a possible dysregulation in opioidergic system could occur.
为了评估内源性阿片肽的抑制或积累在产生呼吸运动活动的神经网络中对呼吸的影响，已经进行了实验。将纳洛酮离子导入呼吸神经元可增加其放电活动并增强其呼吸调节作用。另一方面，局部注射凯托芬（一种脑啡肽酶抑制剂）可降低呼吸神经元的放电，从而减少呼吸调节。凯托芬的这种作用模拟了甲硫脑啡肽离子导入对呼吸神经元的作用。此外，局部注射凯托芬可降低从膈神经记录到的呼吸输出频率。这种作用可被纳洛酮全身给药所逆转。结果表明内源性阿片肽参与呼吸控制，提示在婴儿猝死综合征中可能发生阿片能系统的调节异常。
