CALCIUM RELEASED BY PHOTOLYSIS OF DM-NITROPHEN STIMULATES TRANSMITTER RELEASE AT SQUID GIANT SYNAPSE
CALCIUM RELEASED BY PHOTOLYSIS OF DM-NITROPHEN STIMULATES TRANSMITTER RELEASE AT SQUID GIANT SYNAPSE
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DOI：
10.1113/jphysiol.1990.sp018150
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发表时间：
1990-07-01
影响因子：
5.5
通讯作者：
ZUCKER, RS
中科院分区：
文献类型：
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作者：
DELANEY, KR;ZUCKER, RS
1.鱿鱼巨大突触的递质释放是由插入突触前末梢的“笼状"Ca 2+化合物DM-硝基酚（Kaplan和Ellis-Davies，1988）的Ca 2+光解释放刺激的。2.竞争结合反应导致由DM-硝基菲林光解释放的Ca 2+的量依赖于DM-硝基菲林、总Ca 2+、Mg+、ATP和天然细胞质Ca 2+缓冲液的浓度。通过共注射荧光指示剂染料Fura-2测量突触前[Ca 2 +]的变化表明，DM-硝基菲的光解导致Ca 2+的瞬时上升，然后在约150 ms内衰减到增加的稳态水平。3.快速光解的Ca 2 +-加载nitrophen内突触前终端随后在不到一毫秒的突触后膜的去极化。与动作电位诱发的兴奋性突触后电位（EPSP）一样，光诱发的反应被1-3 mM红藻氨酸部分可逆地阻断，红藻氨酸使突触后谷氨酸受体脱敏。4.释放的幅度和速率与正常动作电位介导的EPSP相似。5.从盐水中去除Ca ~（2+）或加入河豚毒素不影响DM-nitrophen光解释放递质。在不加Ca ~（2+）的情况下，将DM-Nitrophen注入突触前末梢，光解既不刺激递质的释放，也不干扰正常的动作电位介导的释放。6.刺激突触前动作电位在无钙生理盐水中的光诱发反应过程中没有引起增加释放的递质，如果神经节沐浴在无钙生理盐水中，即在没有Ca 2+流入。增加光照强度或刺激突触前动作电位可增加递质的释放。因此，突触前电压的变化，以增加发射器的释放所造成的释放笼中的Ca 2+的失败是不是由于饱和或光释放的Ca 2+的释放机制的抑制。7.降低温度的准备增加延迟的光诱发反应的发病，并降低其幅度和上升率的程度类似于观察到的动作电位诱发EPSP。
1. Transmitter release at the squid giant synapse was stimulated by photolytic release of Ca2+ from the ''caged'' Ca2+ compound DM-nitrophen (Kaplan and Ellis-Davies, 1988) inserted into presynaptic terminals. 2. Competing binding reactions cause the amount of Ca2+ released by DM-nitrophen photolysis to depend on the concentrations of DM-nitrophen, total Ca2+, Mg+, ATP and native cytoplasmic Ca2+ buffer. Measurements of presynaptic [Ca2+] changes by co-injection of the fluorescent indicator dye Fura-2 show that DM-nitrophen photolysis causes a transient rise in Ca2+ followed by decay within about 150 ms to an increased steady-state level. 3. Rapid photolysis of Ca2+-loaded nitrophen within the presynaptic terminal was followed in less than a millisecond by depolarization of the postsynaptic membrane. As with action potential-evoked excitatory postsynaptic potentials (EPSPs), the light-evoked response was partially and reversibly blocked by 1-3 mM-kainic acid which desensitizes postsynaptic glutamate receptors. 4. Release was similar in magnitude and rate to normal action potential-mediated EPSPs. 5. The release of transmitter by photolysis of Ca2+-loaded DM-nitrophen was not affected by removal of Ca2+ from the saline or addition of tetrodotoxin. Photolysis of DM-Nitrophen injected into presynaptic terminal without added Ca2+ did not stimulate release of transmitter nor did it interfere with normal action potential-mediated release. 6. Stimulation of presynaptic action potentials in Ca2+-free saline during the light-evoked response did not elicit increased release of transmitter if the ganglion was bathed in Ca2+-free saline, i.e. in the absence of Ca2+ influx. Increasing the intensity of the light or stimulating presynaptic action potentials in Ca2+-containing saline increased the release of transmitter. Therefore the failure of presynaptic voltage change to increase transmitter release resulting from release of caged Ca2+ was not due to saturation or inhibition of the release mechanism by light-released Ca2+. 7. Decreasing the temperature of the preparation increased the delay to onset of the light-evoked response and reduced its amplitude and rate of rise to an extent similar to that observed for action potential-evoked EPSPs.