Katayama Yoshifumi, Homma Tomoo, Honda Kazuki, Hirai Keiji
Department of Autonomic Physiology, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kandasurugadai, Chiyoda-ku, Tokyo 101-0062, Japan.
Neuroreport. 2003 Aug 6;14(11):1515-8. doi: 10.1097/00001756-200308060-00023.
Orexins and orexin-receptors are localized by displaying their immunoreactivity in the enteric nervous system. Intracellular recordings were made from isolated myenteric neurons to investigate actions of orexin-A in the myenteric plexus of the guinea-pig ileum. Superfusion of orexin-A caused membrane depolarizations in a subset of S and AH neurons. Orexin-A responses were preserved in Ca2+ free/high Mg2+ solution and associated with an increase in input membrane resistance; their reversal potential was about -90 mV. Orexin-A augmented nicotinic fast EPSPs, whereas it did not affect the postsynaptic sensitivity to acetylcholine; this indicates that orexin-A increased the presynaptic release of acetylcholine. In conclusion, orexin-A contributes in the regulation of gut motility via its pre- and postsynaptic actions in the myenteric plexus.
食欲肽和食欲肽受体通过在肠神经系统中显示其免疫反应性来定位。从分离的肌间神经元进行细胞内记录，以研究食欲肽A在豚鼠回肠肌间神经丛中的作用。食欲肽A的灌流引起了一部分S神经元和AH神经元的膜去极化。在无钙/高镁溶液中，食欲肽A的反应得以保留，并与输入膜电阻的增加有关；其反转电位约为-90 mV。食欲肽A增强了烟碱型快速兴奋性突触后电位，而不影响突触后对乙酰胆碱的敏感性；这表明食欲肽A增加了乙酰胆碱的突触前释放。总之，食欲肽A通过其在肌间神经丛中的突触前和突触后作用，参与肠道运动的调节。
