Ono H, Fukuda H
Neuropharmacology. 1982 Aug;21(8):739-44. doi: 10.1016/0028-3908(82)90058-2.
The experiments were performed on spinal rats transected at the C 1 level. Intravenous administrations of TRH and its analog DN-1417 (gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide), which has less endocrine activity, produced a marked increase in the monosynaptic reflex (MSR) and depolarization of the ventral root, without affecting the dorsal root reflex (DRR) and the resting potential of the dorsal root. Excitation of the monosynaptic reflex was not antagonized by chlorpromazine, haloperidol, atropine or cyproheptadine, and was not influenced by pretreatment with reserpine. The depolarization of the ventral root persisted in the presence of baclofen or tetrodotoxin. These findings suggest that depolarization of the ventral root induced by TRH and DN-1417 is due to a direct action on motoneuronal membranes, and that an increase in the monosynaptic reflex is in part due to a depolarization of motoneurones. The effect of DN-1417 were longer lasting than those of TRH.
实验在C1水平横断脊髓的大鼠上进行。静脉注射促甲状腺激素释放激素（TRH）及其内分泌活性较低的类似物DN - 1417（γ - 丁内酯 - γ - 羰基 - L - 组氨酰 - L - 脯氨酰胺），可使单突触反射（MSR）显著增强，腹根去极化，而不影响背根反射（DRR）和背根的静息电位。氯丙嗪、氟哌啶醇、阿托品或赛庚啶不能拮抗单突触反射的兴奋，利血平预处理也不影响其兴奋。在巴氯芬或河豚毒素存在的情况下，腹根的去极化仍然持续。这些发现表明，TRH和DN - 1417诱导的腹根去极化是由于对运动神经元膜的直接作用，单突触反射增强部分是由于运动神经元的去极化。DN - 1417的作用比TRH更持久。
