期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2010
卷号：107
期号：30
页码：13515-13519
DOI：10.1073/pnas.1001695107
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The amount of neurotransmitter released from a presynaptic terminal is the product of the quantal content (number of vesicles) and the presynaptic quantal size (QSpre, amount of transmitter per vesicle). QSpre varies with synaptic use, but its regulation is poorly understood. The motor nerve terminals at the neuromuscular junction (NMJ) contain TGF-{beta} receptors. We present evidence that TGF-{beta}2 regulates QSpre at the NMJ. Application of TGF-{beta}2 to the rat diaphragm NMJ increased the postsynaptic response to both spontaneous and evoked release of acetylcholine, whereas antibodies to TGF-{beta}2 or its receptor had the converse effect. L-vesamicol and bafilomycin blocked the actions of TGF-{beta}2, indicating that TGF-{beta}2 acts by altering the extent of vesicular filling. Recordings of the postsynaptic currents from the diaphragm were consistent with TGF-{beta}2 having this presynaptic action and a lesser postsynaptic effect on input resistance. TGF-{beta}2 also decreased quantal content by an atropine-sensitive pathway, indicating that this change is secondary to cholinergic feedback on vesicular release. Consequently, the net actions of TGF-{beta}2 at the NMJ were to amplify the postsynaptic effects of spontaneous transmission and to diminish the number of vesicles used per evoked stimulus, without diminishing the amount of acetylcholine released.
