Stebbing M J, Balasubramanyan S, Smith P A
School of Medical Sciences and Health Innovations Research Institute, RMIT University, Bundoora 3083, Victoria, Australia.
Department of Pharmacology, University of Alberta, Edmonton, T6G 2H7 Alberta, Canada.
Neuroscience. 2016 Jun 2;324:330-43. doi: 10.1016/j.neuroscience.2016.03.016. Epub 2016 Mar 11.
The neuropathic pain that results from peripheral nerve injury is associated with alterations in the properties of neurons in the superficial spinal laminae. Chronic constriction injury (CCI) of the rat sciatic nerve increases excitatory synaptic drive to excitatory neurons in the substantia gelatinosa while limiting that to inhibitory neurons. Since the calcium-binding protein calbindin D-28K has been associated with excitatory neurons, we examined whether CCI altered the properties of neurons expressing calbindin-like immunoreactivity (Cal+). These account for 30% of the neurons in lamina I and II. Calbindin did not co-localize with any particular electrophysiological phenotype of neuron; in substantia gelatinosa, it was found in some tonic, delay, irregular, phasic and transient firing neurons and in some cells that displayed central, radial or vertical morphology. When neuronal phenotype was defined more precisely in terms of both morphology and electrophysiological properties, no strong correlation with calbindin expression was found. The frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSC) in calbindin negative (Cal-) neurons was greater than that in Cal+ neurons. CCI did not alter the proportion of Cal+ neurons in the dorsal horn. Although CCI promoted a fourfold increase in sEPSC frequency in Cal+ neurons, sEPSC amplitude was reduced by 22% and charge transfer per second was unchanged. Since synaptic drive to Cal+ neurons is weak and there is no firm correlation between neuronal phenotype and calbindin expression, it is doubtful whether these neurons play a major role in the generation of central sensitization.
周围神经损伤所致的神经性疼痛与脊髓浅层板层神经元特性的改变有关。大鼠坐骨神经慢性压迫损伤（CCI）增加了对胶状质中兴奋性神经元的兴奋性突触驱动，同时限制了对抑制性神经元的驱动。由于钙结合蛋白钙结合蛋白D-28K与兴奋性神经元有关，我们研究了CCI是否改变了表达钙结合蛋白样免疫反应性（Cal+）的神经元的特性。这些神经元占I层和II层神经元的30%。钙结合蛋白并不与任何特定的神经元电生理表型共定位；在胶状质中，它存在于一些紧张性、延迟性、不规则性、相位性和瞬态放电的神经元中，以及一些呈现中央、放射状或垂直形态的细胞中。当根据形态学和电生理特性更精确地定义神经元表型时，未发现与钙结合蛋白表达有强相关性。钙结合蛋白阴性（Cal-）神经元中自发兴奋性突触后电流（sEPSC）的频率和幅度大于Cal+神经元。CCI并未改变背角中Cal+神经元的比例。尽管CCI使Cal+神经元的sEPSC频率增加了四倍，但sEPSC幅度降低了22%，每秒的电荷转移不变。由于对Cal+神经元的突触驱动较弱，且神经元表型与钙结合蛋白表达之间没有确定的相关性，因此这些神经元是否在中枢敏化的产生中起主要作用值得怀疑。
