Schwartz A D, Whitacre C L, Wilson D F
Center for Neuroscience, Department of Zoology, Miami University, Oxford, OH 45056, USA.
Neurosci Lett. 1999 Oct 29;274(3):163-6. doi: 10.1016/s0304-3940(99)00707-7.
It has been suggested that calcium that is stored in nerve terminals can be released via activation of ryanodine receptors and this source of calcium could serve to modulate evoked transmitter release. Calcium influx via voltage dependent calcium channels could lead to calcium induced calcium release via ryanodine receptors in neuronal tissue. This additional source of calcium could contribute to the total calcium that is available for transmitter release or it could result in having a negative feedback action on calcium influx and transmitter release. We examined the effect of blocking and activating the ryanodine receptors on quantal transmitter release at the rat neuromuscular junction. Intracellular recording techniques were used to monitor end-plate potentials and miniature end-plate potentials. The data supports the view that intracellular calcium released via ryanodine receptors suppresses calcium influx leading to depressed quantal release.
有人提出，储存在神经末梢的钙可通过ryanodine受体的激活而释放，并且这种钙源可用于调节诱发的递质释放。通过电压依赖性钙通道的钙内流可导致神经元组织中通过ryanodine受体的钙诱导钙释放。这种额外的钙源可能有助于递质释放可用的总钙量，或者可能对钙内流和递质释放产生负反馈作用。我们研究了阻断和激活ryanodine受体对大鼠神经肌肉接头处量子化递质释放的影响。采用细胞内记录技术监测终板电位和微小终板电位。数据支持这样一种观点，即通过ryanodine受体释放的细胞内钙会抑制钙内流，导致量子化释放减少。
