Schools of Physiology and Pharmacology and Clinical Sciences, University of Bristol, Bristol, BS8 1TD, United Kingdom.
Mol Pain. 2012 Dec 5;8:87. doi: 10.1186/1744-8069-8-87.
Galanin is a key modulator of nociception, and it is also required for the developmental survival of a subset of C-fibre sensory neurons which are critical to the mediation of neuropathic and inflammatory pain. However, the potential modulatory roles played by galanin, or the galanin-dependent neurons, in pruritoceptive mechanisms underlying the sensation of itch have not been investigated.
Here we report that mice carrying a loss-of-function mutation in the galanin gene (Gal-KO) show no differences in spontaneous behavioural itch responses compared to wild-type (WT) controls. Similarly, the responses to a range of pruritogens are not significantly different between the two genotypes.
These results suggest that neither galanin expression, nor the galanin-dependent subpopulation of sensory neurons is required for itch-related behaviours.
甘丙肽是痛觉的关键调节因子，它对于一组 C 纤维感觉神经元的发育存活也是必需的，而这些神经元对于神经性和炎性疼痛的介导至关重要。然而，甘丙肽或甘丙肽依赖的神经元在瘙痒感觉的瘙痒感受机制中可能发挥的调节作用尚未得到研究。
在这里，我们报告说，携带甘丙肽基因功能丧失突变的小鼠（Gal-KO）与野生型（WT）对照相比，在自发性行为瘙痒反应中没有差异。同样，两种基因型对一系列瘙痒原的反应也没有显著差异。
这些结果表明，瘙痒相关行为既不需要甘丙肽表达，也不需要甘丙肽依赖的感觉神经元亚群。
