Frequency-dependent release of peptide cotransmitters from identified cholinergic motor neurons in Aplysia.
Frequency-dependent release of peptide cotransmitters from identified cholinergic motor neurons in Aplysia.
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DOI：
10.1073/pnas.86.22.9034
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发表时间：
1989-11
影响因子：
11.1
通讯作者：
M. Whim;P. E. Lloyd
中科院分区：
文献类型：
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作者：
M. Whim;P. E. Lloyd
我们研究了两种肽共递质的释放从终端的胆碱能运动神经元在澳大利亚。已鉴定的运动神经元B15除了合成乙酰胆碱外，还合成两种小心脏活性肽（SCP） A和B。对称的一对B15神经元支配对称的颊肌，称为I5，它参与产生咬动作。SCPs增强了I5的收缩幅度。与未受刺激的对照肌肉相比，细胞内刺激一个B15会产生受刺激肌肉中scp的消耗。显著耗竭需要高频刺激或较低频率的长时间脉冲。第二个胆碱能运动神经元B16也支配I5，但不合成scp。B16的刺激不会导致SCPs的消耗。外源性SCPs能有效地增加肌肉中的cAMP水平。如果消耗是释放的反映，应该有可能证明B15刺激对肌肉cAMP水平的影响。事实上，B15的刺激确实提高了I5的cAMP水平。B16刺激对cAMP水平无影响。只有当B15以一种显著促进乙酰胆碱释放的方式刺激时，才观察到cAMP的增加。这种促进作用可以通过增加刺激频率、延长脉冲持续时间或缩短脉冲间隔来实现。然而，B15能够产生胆碱能介导的收缩，其刺激参数不会引起scp的释放。因此，B15在缓慢放电时表现为纯胆碱能运动神经元，而在快速放电时表现为胆碱能/肽能神经元。
We have investigated the release of two peptide cotransmitters from the terminals of a cholinergic motor neuron in Aplysia. Identified motor neuron B15 synthesizes the two small cardioactive peptides (SCP) A and B in addition to acetylcholine. A symmetrical pair of B15 neurons innervate symmetrical buccal muscles, termed I5, which are involved in generating biting movements. The amplitude of I5 contractions is enhanced by the SCPs. Intracellular stimulation of one B15 produces depletion of the SCPs from the stimulated muscle as compared to the unstimulated control muscle. Significant depletion requires either high-frequency stimulation or prolonged bursts at lower frequencies. A second cholinergic motor neuron, B16, also innervates I5 but does not synthesize the SCPs. Stimulation of B16 produced no depletion of the SCPs. Exogenous SCPs potently increase cAMP levels in the muscle. If depletion is a reflection of release, it should be possible to demonstrate an effect of B15 stimulation on muscle cAMP levels. Indeed, stimulation of B15 did elevate cAMP levels in I5. Stimulation of B16 had no effect on cAMP levels. Increases in cAMP were observed only when B15 was stimulated in a manner that would produce significantly facilitated acetylcholine release. This facilitation could be produced by increased stimulation frequency, longer burst durations, or shorter interburst intervals. However, B15 is capable of producing cholinergically mediated contractions with stimulation parameters that would not cause release of the SCPs. Thus, B15 appears to function as a purely cholinergic motor neuron when firing slowly, and as a cholinergic/peptidergic neuron when firing rapidly.