29. 10. 2024
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A new study by neuroscientists from the IEM CAS, published in Frontiers in Cellular Neuroscience journal (open in a new window) (IF 4.2), shows impaired potassium uptake by astrocytes in the spinal cord in amyotrophic lateral sclerosis (ALS). In addition to scientists from the Department of Cellular Neurophysiology, colleagues from the IOCB CAS also participated in the study.
Astrocytes are cells in the brain and spinal cord that play a key role in the support and proper functioning of the nervous system. They maintain ions and neurotransmitter homeostasis, provide nutrients to neurons and remove neural metabolites. Astrocytes also help regulate blood flow in the brain and are involved in protecting tissue during injury. They are important for cell communication and help protect the nervous system from harmful influences. In the case of disorders such as ALS, their function can be impaired, negatively affecting the health of neurons.
Within the study, researchers monitored changes in the volume of astrocytes in the brain and spinal cord in an animal model of ALS to determine the extent of their damage. The researchers measured the volume of astrocytes during and after exposure to high levels of potassium and compared the results with other markers such as astrocyte morphology, the amount of the potassium channel Kir4.1 and the level of potassium in the cerebrospinal fluid. They found that astrocytes in the spinal cord had a reactive morphology and were less responsive to high potassium concentrations, suggesting functional impairment. In addition, they also found reduced expression of the Kir4.1 channel in the spinal cord, contributing to impaired regulation of astrocyte volume. In contrast, no changes in astrocyte volume or Kir4.1 levels were observed in the cerebral cortex. Spinal fluid potassium levels remained normal. The results of the study indicate that in this model of ALS, the ability of spinal astrocytes to uptake potassium at high concentrations is impaired, which can be put in the context of reduced Kir4.1 channel levels. This problem was not observed in the cerebral cortex and thus appears to be independent of changes in astrocyte morphology.