RAPID AMPLIFICATION AND FACILITATION OF MECHANOSENSORY DISCHARGE IN APLYSIA BY NOXIOUS-STIMULATION
RAPID AMPLIFICATION AND FACILITATION OF MECHANOSENSORY DISCHARGE IN APLYSIA BY NOXIOUS-STIMULATION
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DOI：
10.1152/jn.1993.70.3.1181
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发表时间：
1993-09-01
影响因子：
2.5
通讯作者：
WALTERS, ET
中科院分区：
文献类型：
--
作者：
CLATWORTHY, AL;WALTERS, ET
1. 在防御反应过程中，机械感觉神经元的动作电位放电调控机制尚不清楚。本研究考察了有害刺激（发生在0.5-10秒内）对传递到尾部的测试刺激所引起的动作电位数量的快速影响。在胸膜神经节中监测机械感觉器的反应。需要验证的一个主要假设是，先前描述的感觉神经元体膜电导改变的一个重要功能是，在细胞的感受野受到严重有害刺激时，产生一种放大感觉信号的后放电。对尾部感觉神经元接受野的一部分进行适度的轻击所引起的尖刺放电，在10秒前对另一部分进行强电击时得到增强。这种增强的部分原因似乎是由于感觉神经元中央区域传导阻滞的减少。每隔5秒重复施加无害的中等强度尾震会导致放电逐渐增加（“发条”），而重复施加弱尾震对放电没有显著影响。在某些情况下，动作电位数的增加与后放电的积累有关。一次强烈的尾夹有时会引起持续时间小于或等于2秒的后放电。在孤立的神经系统中，强烈的电刺激包含感觉神经元主轴突的神经也能诱发放电后。一些观察结果表明，后放电需要测试通路中相对大量的共激活纤维的协同作用。与掐刺激（刺激尾巴的更大部分）相比，强烈的、点状的冯弗雷毛刺激不能产生后放电。较弱的尾刺激或神经刺激不能产生后放电，即使在感觉神经元中诱发了短潜伏期、高频放电。后放电的协同效应可能不同于突触前便利的活动依赖性增强，因为单个被测感觉神经元的高频激活与缺乏被测感觉神经元轴突的外周神经的强刺激同时配对，不足以产生后放电。后放电的协同效应可能对损伤的严重程度和空间广泛性信息进行编码。通过刺激神经或尾部引起放电后，躯体的人工超极化常可逆地减少或消除。因此，后放电常在感觉神经元体内或附近产生。通过将CNS浸泡在阻断Ca2+电导和突触传递的溶液中，可以消除体细胞后放电和相关的去极化后电位（DAP）。这一结果进一步暗示了后放电的中心位点，并支持了后放电和DAP依赖于中枢神经系统内神经调节剂释放的假设。有害刺激可以通过在胞体或胞体附近以及可能在神经元的其他部分触发后放电来放大宽动态范围伤害感受器的反应。因为后放电和短潜伏期放电的增加都增加了到达感觉神经元突触末端的尖峰的数量，这两种效应都可能有助于伤口周围的部位特异性致敏（类似于原发性痛觉过敏的现象）。
1. Little is known about modulation of action potential discharge in Aplysia mechanosensory neurons during defensive responses. The present studies examined rapid effects of noxious stimulation (occurring within 0.5-10 s) on the number of action potentials evoked by test stimuli delivered to the tail. Responses were monitored in the somata of mechanonociceptors in the pleural ganglion. A major hypothesis to be tested was that an important function of previously described alterations of membrane conductances in the sensory neuron soma is to generate an afterdischarge that amplifies sensory signals during severe noxious stimulation of the cell's receptive field.2. Discharge of spikes evoked by a moderate tap to one part of a sensory neuron's receptive field on the tail was enhanced by strong shock delivered 10 s earlier to another part of the field. Part of this enhancement appears to be due to a decrease in conduction block in central regions of the sensory neuron.3. Repeated delivery of innocuous, moderately intense tail shock at 5-s intervals caused a progressive increase (''windup'') of discharge, whereas repeated delivery of weak tail shock had no significant effect on discharge. In some cases the increase in action potential number involved a buildup of afterdischarge.4. A single strong tail pinch sometimes induced an afterdischarge lasting less-than-or-equal-to 2 s. After discharge could also be induced in the isolated nervous system by intense electrical stimulation of the nerve containing the sensory neuron's main axon.5. Several observations suggest that afterdischarge requires cooperative effects of a relatively large number of coactivated fibers in the test pathway. In contrast to pinching stimuli (which stimulated a larger part of the tail), intense, punctate stimulation with von Frey hairs failed to produce afterdischarge. Weaker tail or nerve stimulation failed to produce afterdischarge, even when short-latency, high-frequency discharge was evoked in the sensory neuron.6. Cooperative effects on afterdischarge may differ from those involved in activity-dependent enhancement of presynaptic faciiitation because simultaneous pairing of high-frequency activation of a single test sensory neuron with strong stimulation of a peripheral nerve lacking an axon of the tested sensory neuron was not sufficient to produce afterdischarge. The cooperative effects on afterdischarge may function to encode information about both the severity and spatial extensiveness of an injury.7. Artificial hyperpolarization of the soma often reversibly reduced or abolished afterdischarge evoked by stimulating the nerve or tail. Thus the afterdischarge is often generated in or near the sensory neuron soma.8. Soma afterdischarge and an associated depolarizing afterpotential (DAP) were eliminated by bathing the CNS in solutions that block Ca2+ conductances and synaptic transmission. This result further implicated a central locus of afterdischarge and supported the hypothesis that afterdischarge and the DAP depend on release of neuromodulators within the CNS.9. Noxious stimuli can amplify the responses of wide-dynamic range nociceptors in Aplysia by triggering afterdischarge in or near the soma and possibly in other parts of the neuron. Because both afterdischarge and the increase in short-latency discharge increase the number of spikes that reach the sensory neuron's synaptic terminals, both effects are likely to contribute to site-specific sensitization around a wound (a phenomenon resembling primary hyperalgesia).