Yanagisawa M, Yoshioka K, Kurihara T, Saito K, Seno N, Suzuki H, Hosoki R, Otsuka M
Department of Pharmacology, Faculty of Medicine, Tokyo Medical and Dental University, Japan.
Neurosci Res. 1992 Dec;15(4):289-92. doi: 10.1016/0168-0102(92)90050-m.
A mixture of peptidase inhibitors increased the magnitude of the saphenous nerve-evoked slow depolarization of a lumbar ventral root and prolonged the similarly evoked inhibition of monosynaptic reflex (MSR) in the isolated spinal cord of the newborn rat in the presence of naloxone. The saphenous nerve-evoked MSR inhibition was curtailed by a tachykinin antagonist, GR71251, and after the treatment with GR71251, the peptidase inhibitor mixture no more prolonged the MSR inhibition. The present results suggest that enzymatic degradation plays a role in the termination of action of tachykinins released from primary afferents in the newborn rat spinal cord. The results provide a further support for the notion that tachykinins serve as neurotransmitters in the spinal cord of the newborn rat.
在纳洛酮存在的情况下,肽酶抑制剂混合物增强了新生大鼠离体脊髓中隐神经诱发的腰腹根慢去极化幅度,并延长了类似诱发的单突触反射(MSR)抑制。速激肽拮抗剂GR71251可减弱隐神经诱发的MSR抑制,在用GR71251处理后,肽酶抑制剂混合物不再延长MSR抑制。目前的结果表明,酶促降解在新生大鼠脊髓中初级传入神经释放的速激肽作用终止中起作用。这些结果进一步支持了速激肽在新生大鼠脊髓中作为神经递质的观点。