Long term potentiation of paintransmission at the spinal level

脊髓水平疼痛传递的长期增强

• 批准号: 03670096
• 负责人: YOSHIOKA Koichi
• 金额: $ 0.96万
• 依托单位: Tokyo Medical and Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1991
• 资助国家: 日本
• 起止时间: 1991 至 1992
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-03670096/
• 关键词: substance P; tachykinins; spinal cord; pain; serotonin; アセチルコリン; 鎮痛; ムスカリン性受容体

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.

1. 在新生大鼠离体脊髓中研究了刺激下行通路诱导的单突触反射（MSR）长期抑制的递质机制。 5-羟色胺(5-HT)摄取阻滞剂显着增强了下行抑制作用，并被5-HT拮抗剂阻断，表明5-HT参与了这种抑制作用。2．在脊髓周围神经制剂中研究了皮神经诱发的 MSR 抑制机制。对隐神经的调节刺激会引起 MSR 的抑制。这种抑制作用被抗胆碱酯酶增强，并且几乎被阿托品完全阻断。从毒蕈碱激动剂和拮抗剂的作用提示，参与抑制MSR的受体为M2型。 3．神经末梢释放的速激肽失活的可能机制是酶促降解。为了研究这种可能性，使用新生大鼠的分离脊髓-隐神经标本检查了肽酶抑制剂对 C 纤维诱发反应的影响。在纳洛酮存在下应用肽酶抑制剂混合物可增强隐神经刺激引起的 L3 腹侧根的缓慢去极化。该结果表明酶促降解在终止速激肽的神经递质作用中发挥生理作用。

项目成果

Suzuki H.et al.: "Potentiating effect of peptidase inhibitors on a C fiber-evoked response in the isolated spinal cord preparation of the neonatal rat." Regul.Pept.Suppl.1. S152- (1992)

Suzuki H.等人：“肽酶抑制剂对新生大鼠离体脊髓标本中 C 纤维诱发反应的增强作用。”

MAEHARA T.et al.: "Substance P-eboked release of aminoacid transmitters from the newborn rat spinal cord." Regul.Pept.Suppl.1. S102 (1992)

MAEHARA T.et al.：“P 物质引起新生大鼠脊髓氨基酸递质的释放。”

Kobayashi N.: "Substance P-evoked release of acetylcholine from isolated spinal cord of the newborn rat." Neuroscience. 45. 330-337 (1991)

Kobayashi N.：“P 物质诱发新生大鼠离体脊髓释放乙酰胆碱。”

SUZUKI H.et al.: "Potentiating effect of peptidase inhibitors on a C fiber-evoked response in the isolated spinal cord preparation of the neonatal rat." Regul.Pept.Suppl.1. S152 (1992)

SUZUKI H.等人：“肽酶抑制剂对新生大鼠离体脊髓标本中 C 纤维诱发反应的增强作用。”

Suzuki H.et al.: "Peptidase inhibitors potentiate a cutaneous nerve-evoked slow depolarization in the isolated spinal cord of the neonatal rat." Neurosci.Res.Suppl.17. S118- (1992)

Suzuki H.等人：“肽酶抑制剂可增强新生大鼠离体脊髓中皮神经诱发的缓慢去极化。”