Jänig W, Koltzenburg M
Physiologisches Institut, Christian-Albrechts-Universität, Kiel, F.R.G.
J Auton Nerv Syst. 1990 Jul;30 Suppl:S89-96. doi: 10.1016/0165-1838(90)90108-u.
The neurophysiological basis of visceral sensations in general and pain in particular have been mainly studied with short-lasting stimuli that simulate the acute events of visceral organ function. Pelvic viscera are supplied by spinal afferents which are involved in the coordinated reflex regulation of continence and evacuation of bowel and bladder and are capable of signalling impending or frank tissue damage. Typically, each afferent neuron innervates one viscus only. The organ-specific subtypes are functionally homogenous and encode by their discharge frequency the information for organ regulation, non-painful and painful sensations. Thus, pain elicited from these organs under physiological conditions is probably not elicited by a specific set of nociceptive visceral afferents. While the use of brief stimuli has yielded invaluable neurophysiological information for normal, healthy viscera, it has fallen somewhat short of providing information about the neuronal basis of chronic visceral pain states. Using pathological models such as experimental inflammation of the urinary bladder and ischaemia of the colon we have shown that the receptor properties of most afferents change dramatically. Of particular interest is the discovery of a novel type of visceral receptor which is not excited by extreme noxious mechanical stimuli applied to the healthy tissue but which is vigorously activated at the onset of an inflammation. This means that the number of functionally active primary afferents is not immutable, but critically depends on the state of the tissue. This new principle of plasticity in the peripheral nervous system bears some considerable importance for the understanding of the genesis of chronic visceral pain states.(ABSTRACT TRUNCATED AT 250 WORDS)
一般内脏感觉尤其是疼痛的神经生理基础,主要是通过模拟内脏器官功能急性事件的短暂刺激来研究的。盆腔脏器由脊髓传入神经支配,这些神经参与肠道和膀胱控尿与排空的协调反射调节,并且能够发出即将发生或明显组织损伤的信号。通常,每个传入神经元仅支配一个脏器。器官特异性亚型在功能上是同质的,并通过其放电频率编码器官调节、非疼痛和疼痛感觉的信息。因此,在生理条件下从这些器官引发的疼痛可能不是由特定的伤害性内脏传入神经引发的。虽然使用短暂刺激已经为正常、健康的内脏提供了宝贵的神经生理信息,但在提供有关慢性内脏疼痛状态的神经元基础的信息方面,它有点不足。使用诸如膀胱实验性炎症和结肠缺血等病理模型,我们已经表明大多数传入神经的受体特性发生了巨大变化。特别令人感兴趣的是发现了一种新型内脏受体,它不会被施加于健康组织的极端有害机械刺激所激发,但在炎症开始时会被强烈激活。这意味着功能活跃的初级传入神经的数量不是一成不变的,而是严重依赖于组织的状态。外周神经系统可塑性的这一新原理对于理解慢性内脏疼痛状态的发生具有相当重要的意义。(摘要截取自250词)