29-30 January, 2020 - Szeged, Hungary


Abstract details



Krisztián Pajer1, Tamás Bellák1, Bernát Nógrádi3, Tímea Grósz2, Miklós Erdélyi2, Antal Nógrádi1

1 Department of Anatomy, Histology and Embryology, Faculty of Medicine, University of Szeged, Szeged, Hungary, 2Department of Optics and Quantum Electronics, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary, 3Foundation for the Future of Biomedical Sciences in Szeged, Szeged, Hungary

Down regulation of KCC2 is associated with developing spasticity and increased excitatory transmission in the acute spinal cord injury. In this study we examined the alterations of membrane-bound KCC2 expression of injured motoneurons with or without riluzole treatment.The left lumbar 4 (L4) ventral root of the spinal cord was avulsed. Animals were treated with riluzole (4 mg/kg) for 2 weeks. Riluzole treatment started immediately on the day of surgery daily for 1 week and every second day for the next 1 week. In control animals the L4 ventral root was avulsed without riluzole treatment. Expression of KCC2 in the injured motoneurons and in the affected side of the L4 spinal segment were detected 5, 10, 16, 21 and 63 days after the injury with immunohistochemistry followed by confocal microscopy and dSTORM imaging.The KCC2 labelling in the lateral and ventrolateral part of the L4 ventral horn was weaker compared to the medial gray matter of L4 ventral horn in both groups. The quantitative analysis of mean fluorescence signal revealed that KCC2 staining remained stable in the injured motoneurons of both groups 5 and 10 days after the injury. At later time points KCC2 expression was sporadic or could not be located in the plasma membrane in both groups. Restored KCC2 expression could be observed at day 63. Taking together, the present results indicate that pharmacological blockade of voltage activated Na+ and Ca2+ channels do not influence the membrane expression of KCC2 during the examined period of time.