Multiple sclerosis (MS) is a chronic, inflammatory, neurodegenerative disease with an autoimmune component. It was suggested that potassium channels, which are involved in crucial biological functions may have a role in different diseases, including MS and its animal model, experimental autoimmune encephalomyelitis (EAE). It was shown that voltage-gated potassium channels Kv1.5 are responsible for fine-tuning in the immune physiology and influence proliferation and differentiation in microglia and astrocytes. Here, we explored the cellular distribution of the Kv1.5 channel, together with its transcript and protein expression in the male rat spinal cord during different stages of EAE. Our results reveal a decrease of Kv1.5 transcript and protein level at the peak of disease, where massive infiltration of myeloid cells occurs, together with reactive astrogliosis and demyelination. Also, we revealed that the presence of this channel is not found in infiltrating macrophages/microglia during EAE. It is interesting to note that Kv1.5 channel is expressed only in resting microglia in the naïve animals. Predominant expression of Kv1.5 channel was found in the astrocytes in all experimental groups, while some vimentin⁺ cells, resembling macrophages, are devoid of Kv1.5 expression. Our results point to the possible link between Kv1.5 channel and the pathophysiological processes in EAE.

多发性硬化症（MS）是一种具有自身免疫成分的慢性炎症性神经退行性疾病。有人认为，参与重要生物学功能的钾通道可能在多种疾病中起作用，包括MS及其动物模型，实验性自身免疫性脑脊髓炎（EAE）。结果表明，电压门控钾通道Kv1.5负责免疫生理学的微调，并影响小胶质细胞和星形胶质细胞的增殖和分化。在这里，我们探讨了在EAE不同阶段，Kv1.5通道在雄性大鼠脊髓中的细胞分布以及其转录本和蛋白质表达。我们的研究结果表明，在疾病高峰期，髓样细胞大量浸润，Kv1.5转录本和蛋白质水平下降，以及反应性星形胶质增生和脱髓鞘。此外，我们揭示了在EAE期间浸润的巨噬细胞/小胶质细胞中未发现该通道的存在。有趣的是，Kv1.5通道仅在幼稚动物的静止小胶质细胞中表达。在所有实验组的星形胶质细胞中发现Kv1.5通道的主要表达，而一些波形蛋白类似于巨噬细胞的⁺细胞缺乏Kv1.5表达。我们的结果表明，Kv1.5通道与EAE的病理生理过程之间可能存在联系。