Matsuto T, Yanagisawa M, Otsuka M, Kanazawa I, Munekata E
Neurosci Res. 1984 Dec;2(1-2):105-10. doi: 10.1016/0168-0102(84)90008-7.
The actions of two new mammalian tachykinins, neurokinin alpha and neurokinin beta, were examined using the isolated spinal cords of newborn rats. Depolarizing responses of spinal motoneurons were recorded extracellularly from the lumbar ventral root during application of neurokinin alpha or neurokinin beta at concentrations ranging from 3 X 10(-8) M to 10(-6) M. The potencies of various tachykinins in depolarizing the motoneurons showed the following order: physalaemin greater than neurokinin beta divided by kassinin divided by substance P greater than neurokinin alpha. When the synaptic transmission in the spinal cord was blocked by tetrodotoxin, the depolarizing action of neurokinin alpha and neurokinin beta was markedly reduced but not completely abolished. The depolarizing action of neurokinin alpha and neurokinin beta was depressed by a substance P antagonist, [D-Arg1, D-Pro2, D-Trp7,9, Leu11]SP. The possibility that neurokinin alpha and neurokinin beta act as neurotransmitters in the mammalian spinal cord is discussed.
利用新生大鼠的离体脊髓,研究了两种新的哺乳动物速激肽——神经激肽α和神经激肽β的作用。在应用浓度范围为3×10⁻⁸ M至10⁻⁶ M的神经激肽α或神经激肽β期间,从腰段腹根细胞外记录脊髓运动神经元的去极化反应。各种速激肽使运动神经元去极化的效力呈现以下顺序:蛙皮素>神经激肽β>卡斯inin>P物质>神经激肽α。当脊髓中的突触传递被河豚毒素阻断时,神经激肽α和神经激肽β的去极化作用明显减弱,但并未完全消除。神经激肽α和神经激肽β的去极化作用被P物质拮抗剂[D-Arg1, D-Pro2, D-Trp7,9, Leu11]SP抑制。讨论了神经激肽α和神经激肽β在哺乳动物脊髓中作为神经递质发挥作用的可能性。