| Abstrakt: |
Magnesium (Mg²⁺) plays a central role in neurons, influencing several biochemical processes. Imbalances in Mg²⁺ levels, such as hypomagnesemia or hypermagnesemia, have been implicated in the pathophysiology of many diseases and can directly affect intracellular calcium (Ca²⁺) homeostasis. Low magnesium levels disrupt the regulation of Ca²⁺ channels, including inositol 1,4,5-trisphosphate receptors and ryanodine receptors, leading to excessive intracellular Ca²⁺ accumulation, particularly in neurons and muscle cells. Conversely, hypermagnesemia suppresses Ca²⁺ influx by stabilizing the plasma membrane and reducing cell excitability, potentially resulting in muscle weakness, hypotension, and impaired neuronal signaling. In cultured hippocampal neurons, elevated extracellular magnesium concentration (5.0 mM MgCl₂) resulted in a 6% reduction in basal intracellular Ca²⁺ levels compared to control conditions (2 mM MgCl₂). In addition, the amplitude of calcium responses to depolarization (50 mM KCl, 5 seconds) was reduced by 8%. Conversely, decreasing the extracellular magnesium concentration to 0.5 mM resulted in a 12% increase in basal intracellular Ca²⁺ levels relative to control, along with a 13% increase in the amplitude of calcium responses to depolarization. These results demonstrate that extracellular magnesium exerts a regulatory effect on intracellular calcium dynamics. The present study underscores that alterations in extracellular magnesium significantly influence intracellular calcium concentration, potentially affecting neuronal function not only under normal conditions but also in neurodegenerative diseases associated with chronic Mg²⁺ imbalance. Such imbalances exacerbate Ca²⁺ signaling dysfunction, potentially leading to cellular pathology. [ABSTRACT FROM AUTHOR] |
