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运动单位由运动神经元及其支配的肌纤维组成。神经肌肉接头(neuromuscular junction,NMJ)传递受到严密的调节,因而能和运动单位的活动协调一致。在NMJ,神经调制物质的释放与运动单位的活动有关,并能决定突触传递的效能。脑源性神经营养因子(brain-derived ncurotrophic factor,BDNF)和神经营养因子4(neurotrophin-4,NT-4)由运动神经末梢和肌纤维产生。肌肉释放营养因子受肌肉活动调节。在NMJ,BDNF和NT-4通过激活酪氨酸激酶B受体(tyrosine kinase receptor BrkB),能加强自发性和诱导性的突触活动。突触前Ca2+量的迅速增加或突触胞吐过程的易化,都能增加突触囊泡的释放,从而改善NMJ的突触传递。事实上,BDNF能促进突触前细胞内Ca2+的释放,TrkB的激活也能通过有丝分裂活化蛋白激酶,引起突触素I(synapsin I)的磷酸化,进而增加可释放的突触囊泡的数量。在NMJ,神经营养因子还能通过影响神经调节素(neuregulin)或其他神经源性调制物质的局部释放,对接头传递进行调节。本文对近年来在NMJ突触传递的调节,运动单位的NMJ特性以及神经营养因子对突触传递效能的影响等方面的研究进展做一综述。
The motor unit consists of motor neurons and their dominant muscle fibers. Transmission of the neuromuscular junction (NMJ) is tightly regulated and therefore coordinated with the activity of the motor unit. At NMJ, the release of neuromodulatory substances is related to the activity of motor units and determines the potency of synaptic transmission. Brain-derived nurotrophic factor (BDNF) and neurotrophin-4 (NT-4) are produced by motor nerve endings and muscle fibers. Muscle-releasing nutrients is regulated by muscle activity. In NMJ, both BDNF and NT-4 potentiate spontaneous and induced synaptic activity by activating the tyrosine kinase receptor BrkB. The rapid increase of presynaptic Ca2 + or the facilitation of synaptic exocytosis can increase the release of synaptic vesicles and thus improve the synaptic transmission of NMJ. In fact, BDNF promotes the release of intracellular Ca2 + from presynaptic cells. Activation of TrkB also leads to the phosphorylation of synapsin I by mitogen-activated protein kinase, which in turn increases the number of synaptic vesicles that can be released . At NMJ, neurotrophins can also modulate adapter delivery by affecting the local release of neuregulin or other neurotransmitters. This review summarizes recent advances in the regulation of NMJ synaptic transmission, the NMJ characteristics of motor units, and the effects of neurotrophic factors on synaptic transmission.