Sastry B R, Bhagavatula L S
Department of Pharmacology and Therapeutics, University of British Columbia, Vancouver, Canada.
Neuroscience. 1996 Dec;75(4):987-92. doi: 10.1016/0306-4522(96)00348-x.
Miniature end-plate potentials recorded at the neuromuscular junction are caused by a quantal release of acetylcholine and evoked end-plate potentials can be described as integer multiples of the miniature potentials. A variety of factors including the presence of multiple synapses on postsynaptic cells and dendritic filtering, complicate quantal analyses at central synapses. In the present investigation on rat hippocampal slices, transmitter release was blocked except for a localized area on the apical dendrites of CA1 neurons and quantal analysis was performed on miniature excitatory postsynaptic currents (mEPSCs) and evoked EPSCs of low quantum content. The results indicate that under these conditions, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-mediated mEPSCs exhibit a normal size distribution with S.D. values comparable to those at the neuromuscular junction, and the evoked EPSCs can be described as integer multiples of the miniature currents. The results also support reports in literature that long-term potentiation (LTP) is associated with an increase in mEPSC frequency. Whether the increase is due to (a) the enhancement of quantal release at already functional synapses, or (b) the recruitment of nearby silent synapses where a neglible transmitter release becomes measurable, or clusters of functional receptors are uncovered, cannot yet be distinguished.
在神经肌肉接头处记录到的微小终板电位是由乙酰胆碱的量子释放引起的，而诱发终板电位可被描述为微小电位的整数倍。包括突触后细胞上存在多个突触和树突滤波等多种因素，使中枢突触的量子分析变得复杂。在本次对大鼠海马切片的研究中，除了CA1神经元顶端树突上的一个局部区域外，递质释放被阻断，并对微小兴奋性突触后电流（mEPSC）和低量子含量的诱发EPSC进行了量子分析。结果表明，在这些条件下，α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体介导的mEPSC呈现出正常的大小分布，其标准差与神经肌肉接头处的相当，并且诱发EPSC可被描述为微小电流的整数倍。这些结果也支持了文献中的报道，即长时程增强（LTP）与mEPSC频率增加有关。这种增加是由于（a）已经发挥功能的突触处量子释放的增强，还是（b）附近沉默突触的募集（在这些突触处原本可忽略不计的递质释放变得可测量），或者是功能性受体簇的暴露，目前尚无法区分。
