An Analysis of Disuse Effects on Central Synapses

在哺乳动物中，脊髓运动神经元接受来自肌纺锤体产生的Ia组感觉纤维的直接兴奋性突触输入。这种突触的效率可以用细胞内电极从运动神经元接收到的对肌肉神经刺激的单突触兴奋性突触后电位（EPSPs）的平均振幅来量化。对大鼠的肌神经进行切片观察，肌神经刺激引起的单突触epsp在几天内表现出短暂的增强，但在几周内明显下降。这两种不同潜伏期现象背后的机制已被研究。局部应用河豚毒素阻断周围神经传导数日后，刺激周围神经引起的单突触epsp明显增强。这种可塑性变化在运动神经元上的突触上最大程度地表现为2天的外周神经传导阻滞。因此，在周围神经切断后的几天内观察到的运动神经元中Ia突触传递的早期增强可归因于剥夺感觉冲动活动引起的突触的可塑性变化。只要切断神经的再神经支配被阻止，周围神经切片后的Ia突触传递抑制就会缓慢进行，并伴有长潜伏期。当切断的神经控制肌肉时，这种凹陷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。感觉神经元的正常功能是由靶组织提供的神经生长因子维持的。因此，在新生大鼠出生后第1天粉碎周围神经后，每天应用神经生长因子。这种治疗可以显著防止周围神经损伤后发生的Ia突触传递抑制。因此，我们得出结论，周围神经切断产生的Ia突触传递的抑制是由于NGF或类似的从目标组织到感觉神经元的营养供应的中断。少

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