Leibowitz D H
CNS Research Foundation, Inc., New York, New York 10025-0038.
Proc Biol Sci. 1992 Dec 22;250(1329):287-95. doi: 10.1098/rspb.1992.0161.
The propagation mechanism of spreading depression (SD), which has been implicated in the pathophysiology of the neurological auras of migraine, remains enigmatic but is widely believed to depend primarily upon the behaviour of assemblies of neurons. It is proposed here, based upon a program of theoretical research, that the most essential constituent of SD is a slowly propagating, regenerative event in the neuroglial compartment. By altering the neuronal microenvironment, this glial spike helps trigger and coordinate the neuronal depolarization of SD; the glial spike is in turn facilitated by neuronally released agents acting at the neuroglial plasma membrane. The conduction velocity-determining propagation mechanism of SD is further proposed to be a wave of intracellular Ca(2+)-induced Ca2+ release (cytocal wave) that travels through the glial compartment of nervous tissue. Some implications for the improved understanding and clinical management of migraine are suggested. Excitability of glial cells of vertebrates has until now been demonstrated only in vitro, and its physiological significance has remained unknown. This work identifies a macroscopic reaction of neuronal tissue, known from the in vivo vertebrate brain for over 45 years, as a manifestation of neuroglial excitability.
扩散性抑制（SD）的传播机制一直与偏头痛的神经学先兆的病理生理学有关，至今仍不明朗，但人们普遍认为它主要取决于神经元集合的行为。基于一项理论研究计划，本文提出，SD最基本的组成部分是神经胶质区室中一种缓慢传播的再生事件。通过改变神经元微环境，这种胶质尖峰有助于触发和协调SD的神经元去极化；而胶质尖峰又受到作用于神经胶质质膜的神经元释放因子的促进。本文还进一步提出，SD的传导速度决定传播机制是一种细胞内Ca(2+)诱导Ca2+释放波（细胞钙波），它穿过神经组织的胶质区室。文中还提出了一些对改善偏头痛的理解和临床治疗的启示。到目前为止，脊椎动物胶质细胞的兴奋性仅在体外得到证实，其生理意义仍然未知。这项研究确定了一种在体内脊椎动物大脑中已被知晓超过45年的神经元组织的宏观反应，是神经胶质兴奋性的一种表现。
