Cropper E C, Miller M W, Tenenbaum R, Kolks M A, Kupfermann I, Weiss K R
Center for Neurobiology and Behavior, New York State Psychiatric Institute, NY 10032.
Proc Natl Acad Sci U S A. 1988 Aug;85(16):6177-81. doi: 10.1073/pnas.85.16.6177.
A model system that consists of a muscle utilized in biting, the accessory radula closer (ARC), and the two cholinergic motor neurons innervating this muscle, neurons B15 and B16, has been used to study the expression of food-induced arousal in the marine mollusk Aplysia. The ARC muscle receives modulatory input from an extrinsic source, the serotonergic metacerebral cells, which partially accounts for the progressive increase in the strength of biting seen in aroused animals. Another source of modulation may arise from the ARC motor neurons themselves, which synthesize neuropeptides that can potentiate ARC contractions. Neuron B15 synthesizes the two homologous peptides, small cardioactive peptides A and B, whereas neuron B16 synthesizes the structurally unrelated peptide myomodulin. Here we report the purification and sequencing of a neuropeptide termed buccalin and show that it is colocalized with the small cardioactive peptides to neuron B15. Buccalin is also bioactive at the ARC neuromuscular junction but, in contrast to the small cardioactive peptides, when exogenously applied, it decreases rather than increases the size of muscle contractions elicited by firing of the motor neurons. Also unlike the small cardioactive peptides, which exert postsynaptic actions, buccalin seems to act only presynaptically. It has no effect on muscle relaxation rate and decreases motor neuron-elicited excitatory junction potentials in the ARC without affecting contractions produced by direct application of acetylcholine to the muscle. Neuron B15, therefore, appears to contain three modulatory neurotransmitters, two of which may act postsynaptically on the muscle to potentiate the action of the primary neurotransmitter acetylcholine and one of which may act presynaptically on nerve terminals to inhibit acetylcholine release.
一个由用于咬合的肌肉、副齿舌闭合肌（ARC）以及支配该肌肉的两个胆碱能运动神经元（神经元B15和B16）组成的模型系统，已被用于研究海洋软体动物海兔中食物诱导的觉醒表达。ARC肌肉从外部来源——血清素能的大脑后叶细胞接收调节性输入，这部分解释了在觉醒动物中观察到的咬合力逐渐增强的现象。另一个调节来源可能来自ARC运动神经元本身，它们合成的神经肽可以增强ARC的收缩。神经元B15合成两种同源肽，即小的心脏活性肽A和B，而神经元B16合成结构不相关的肽肌调节素。在这里，我们报告了一种名为口铃肽的神经肽的纯化和测序，并表明它与小的心脏活性肽共定位于神经元B15。口铃肽在ARC神经肌肉接头处也具有生物活性，但与小的心脏活性肽不同，当外源性应用时，它会减小而不是增加运动神经元放电引起的肌肉收缩大小。与发挥突触后作用的小的心脏活性肽也不同，口铃肽似乎仅在突触前起作用。它对肌肉松弛速率没有影响，并且在不影响直接向肌肉施加乙酰胆碱所产生的收缩的情况下，降低ARC中运动神经元引发的兴奋性接头电位。因此，神经元B15似乎包含三种调节性神经递质，其中两种可能在突触后作用于肌肉以增强主要神经递质乙酰胆碱的作用，而其中一种可能在突触前作用于神经末梢以抑制乙酰胆碱的释放。
