An Analysis of Disuse Effects on Central Synapses

中枢突触废用效应分析

• 批准号: 61480107
• 负责人: KUNO Motoi
• 金额: $ 3.84万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1986
• 资助国家: 日本
• 起止时间: 1986 至 1987
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-61480107/
• 关键词: Spinal cord; Motoneurons; Synapses; Plasticity; Disuse; テトロドトキシン; 脊髄; ラット; 筋紡錘; EPSP

In the mammal, spinal motoneurons receive direct excitatory synaptic inputs from Group Ia sensory fibers arising from muscle spindles. The efficiency of this synapse can be quantified in terms of the mean amplitude of monosynaptic excitatory postsynaptic potentials (EPSPs) recoeded from motoneurons with intracellular electrodes in response to stimulation of a muscle nerve. When a muscle nerve is sectioned in the rat, monosynaptic EPSPs evoked by stimulation of the muscle nerve show a transient enhancement for a few days but are significantly depressed in a few weeks. The mechanisms underlying these two phenomena which occur with different latencies have been investigated. When the conduction of a peripheral nerve was blocked with the local application of tetrodotoxin for a few days, the monosynaptic EPSPs elicited by stimulation of the peripheral nerve were significantly enhanced. This plastic change at Ia synapses on motoneurons was maximally expressed by a conduction block of the per … More ipheral nerve for 2 days. Thus, the early enhancement of Ia synaptic transmission in motoneurons observed for a few days after periphral nerve section can be attributed to plastic changes of the synapses induced by the deprivation of sensory impulse activity.Depression of Ia synaptic transmission observed with a long latency following section of the peripheral nerve proceeded slowly as long as reinnervation by the cut nerve had been prevented. This depression could be restored to normal levels when the cut nerve had been allowed to rein- nervate the muscle. Therefore, this synaptic depression appears to be induced by interruption of the peripheral axonal continuity of sensory fibers. The normal function of sensory neurons is known to be maintained by nerve growth factor (NGF) supplied from the target tissue. There- fore, NGF was daily applied to neonatal rats after crushing the peripheral nerve on the day after birth. This treatment significantly prevented depression of Ia synaptic transmission expected to occur after the peripheral nerve injury. Thus, it is concluded that depression of Ia synaptic transmission produced by peripheral nerve section is due to interruption of NGF or an analogous trophic supply from the target tissue to the sensory neurons. Less

在哺乳动物中，脊髓运动神经元接收来自肌梭产生的 Ia 组感觉纤维的直接兴奋性突触输入。该突触的效率可以根据单突触兴奋性突触后电位（EPSP）的平均振幅来量化，该平均振幅是响应于肌肉神经的刺激而用细胞内电极从运动神经元重新编码的。当对大鼠进行肌肉神经切片时，刺激肌肉神经引起的单突触 EPSP 在几天内短暂增强，但在几周内显着降低。已经研究了以不同延迟发生的这两种现象背后的机制。当局部使用河豚毒素阻断周围神经的传导几天后，刺激周围神经引起的单突触 EPSP 显着增强。运动神经元 Ia 突触的这种塑性变化通过每周神经的传导阻滞 2 天来最大程度地表达。因此，在周围神经切断几天后观察到的运动神经元中 Ia 突触传递的早期增强可归因于感觉冲动活动的剥夺引起的突触的可塑性变化。只要阻止了被切断的神经的重新神经支配，在外周神经切断后观察到的长潜伏期的 Ia 突触传递的抑制就会缓慢进行。当被切断的神经被允许重新支配肌肉时，这种抑制可以恢复到正常水平。因此，这种突触抑制似乎是由感觉纤维的外周轴突连续性中断引起的。已知感觉神经元的正常功能是由靶组织提供的神经生长因子（NGF）维持的。因此，在出生后第二天压碎周围神经后，每天将 NGF 应用于新生大鼠。这种治疗显着防止了周围神经损伤后预期发生的 Ia 突触传递抑制。因此，可以得出结论，周围神经部分产生的 Ia 突触传递抑制是由于 NGF 或从靶组织到感觉神经元的类似营养供应的中断所致。较少的

项目成果

S. Sekiya: J. Neurosci.6. 2019-2025 (1986)

S. Sekiya：J. Neurosci.6。

MANABE, T. et al.: "Early enhancement of monosynaptic transmission in rat spinal motoneurons by conduction block of the peripheral nerve." Neuroscience research. 5. (1988)

MANABE, T. 等人：“通过周围神经传导阻滞早期增强大鼠脊髓运动神经元的单突触传递。”

MANABE, T. et al.: "Effects of disuse on Ia synapses in rat spinal motoneurons." Journal of Physiological Society of Japan. 50. (1988)

MANABE, T. 等人：“废弃对大鼠脊髓运动神经元 Ia 突触的影响。”

Y. Miyata: J. Neurosci.6. 2012-2018 (1986)

Y.宫田：J. Neurosci.6。

T. Manade: Neurosci. Res.6. (1988)

T. Manade：神经科学。