Long term potentiation of paintransmission at the spinal level

1.在离体新生大鼠脊髓中研究了刺激下行通路引起的单突触反射（MSR）持久抑制的递质机制。5-羟色胺（5-HT）摄取阻断剂可明显增强这种抑制作用，而5-HT拮抗剂可阻断这种抑制作用，提示5-HT参与了这种抑制作用.在脊髓-周围神经制备中研究了MSR的皮神经诱发抑制的机制。隐神经的条件性刺激引起MSR的抑制。抗胆碱酯酶剂可增强这种抑制作用，阿托品几乎可完全阻断这种抑制作用。从毒蕈碱受体激动剂和拮抗剂的作用来看，参与抑制MSR的受体为M2型.从神经末梢释放的速激肽失活的可能机制是酶降解。为了研究这种可能性，肽酶抑制剂对C-纤维诱发反应的影响进行了检查，使用一个孤立的脊髓隐神经制备的新生大鼠。在纳洛酮存在下，通过应用肽酶抑制剂的混合物增强隐神经刺激诱发的L3腹根的缓慢去极化。这一结果表明，酶降解在终止速激肽的神经递质作用中起生理作用。

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.