Long term potentiation of paintransmission at the spinal level

1.在新生大鼠脊髓上，研究了刺激下行通路对单突触反射(MSR)产生持久抑制的递质机制。这种下行抑制可被5-羟色胺(5-HT)摄取阻断剂显著增强，并被5-HT拮抗剂阻断，提示5-HT参与了这种抑制。在脊髓-周围神经制备中，研究了皮肤神经诱发抑制MSR的机制。条件性刺激隐神经引起对MSR的抑制。这种抑制作用可被抗胆碱酯酶增强，并几乎完全被阿托品阻断。从M受体激动剂和拮抗剂的作用来看，提示参与MSR抑制作用的受体为M2型。从神经末梢释放的速激肽失活的一个可能机制是酶降解。为了探讨这种可能性，用分离的新生大鼠脊髓-隐神经标本研究了肽酶抑制剂对C-纤维诱发反应的影响。在纳洛酮存在的情况下，应用多肽酶抑制剂的混合物可增强刺激隐神经引起的L3腹根的缓慢去极化。这一结果表明，酶降解在速激肽神经递质作用的终止中起着生理作用。

1. Transmitter mechanisms of a long-lasting inhibition of the monosynaptic reflex (MSR)induced by stimulation of the descending pathway was investigated in the isolated spinal cord of the neonatal rat. The descending inhibition was markedly potentiated by a 5-hydroxytryptamine (5-HT) uptake blocker and was blocked by a 5-HT antagonist, suggesting the involvement of 5-HT in this inhibition.2. The mechanisms of a cutaneous nerve-evoked inhibition of MSR were studied in the spinal cord-peripheral nerve preparation. Conditioning stimulation of the saphenous nerve evoked an inhibition of the MSR. This inhibition was potentiated by an anticholinesterase and almost completely blocked by atropine. From the effects of muscarinic agonists and antagonists, it was suggested that the receptors involved in the inhibition of MSR are of M2 type.3. A possible mechanism of inactivation of tachykinins released from nerve terminals is enzymatic degradation. To investigate this possibility, effect of peptidase inhibitors on C-fiber evoked responses was examined using an isolated spinal cord-saphenous nerve preparation of the newborn rat. A slow depolarization of the L3 ventral root evoked by the saphenous nerve stimulation was enhanced by application of a mixture of peptidase inhibitors in the presence of naloxone. This result suggests that enzymatic degradation plays a physiological role in termination of neurotransmitter action of tachykinins.