Sodium-magnesium antiport in Retzius neurones of the leech Hirudo medicinalis.
Research article published in The Journal of physiology (1996)
Abstract
1. Intracellular free magnesium ([Mg2+]i) and sodium ([Na+]i) concentrations were measured in Retzius neurones of the leech Hirudo medicinalis using ion-sensitive microelectrodes. 2. The mean steady-state values for [Mg2+]i and [Na+]i were 0.46 mM (pMg, 3.34 +/- 0.23; range, 0.1-1.2 mM; n = 32) and 8.95 mM (pNa, 2.05 +/- 0.15; range, 5.1-15.5 mM, n = 21), respectively, at a mean membrane potential (Em) of -35.6 +/- 6.1 mV (n = 32). Thus, [Mg2+]i is far below the value calculated for a passive distribution (16.9 mM) but close to the equilibrium value calculated for a hypothetical 1 Na(+)-1 Mg2+ antiport (0.41 mM). 3. Simultaneous measurements of [Mg2+]i, [Na+]i and Em in Retzius neurones showed that an increase in the extracellular Mg2+ concentration ([Mg2+]o) resulted in an increase in [Mg2+]i, a parallel decrease in [Na+]i and a membrane depolarization, while a decrease in [Mg2+]o had opposite effects. These results are compatible with calculations based on a 1 Na(+)-1 Mg2+ antiport. 4. Na+ efflux at high [Mg2+]o still occurred when the Na(+)-K+ pump was inhibited by the application of ouabain or in K(+)-free solutions. This efflux was blocked by amiloride. 5. In the absence of extracellular Na+ ([Na+]o), no Mg2+ influx occurred. Mg2+ influx at high [Mg2+]o was even lower than in the presence of [Na+]o. Mg2+ efflux was blocked in the absence of [Na+]o. 6. The rate of Mg2+ extrusion was reduced by lowering [Na+]o, even if the Na+ gradient across the membrane remained almost unchanged. 7. Mg2+ efflux was blocked by amiloride (half-maximal effect at 0.25 mM amiloride; Hill coefficient, 1.3) but not by 5-(N-ethyl-N-isopropyl)-amiloride (EIPA). 8. No changes in intracellular Ca2+ and pH (pHi) could be detected when [Mg2+]o was varied between 1 and 30 mM. 9. Changing pHi by up to 0.4 pH units had no effect on [Mg2+]i. 10. The results suggest the presence of an electrogenic 1 Na(+)-1 Mg2+ antiport in leech Retzius neurones. This antiport can be reversed and is inhibited by low extracellular and/or intracellular Na+ and by amiloride.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Zusammenfassung
1. Intracellular free magnesium ([Mg2+]i) and sodium ([Na+]i) concentrations were measured in Retzius neurones of the leech Hirudo medicinalis using ion-sensitive microelectrodes.
Warum dies für die Hirudotherapie relevant ist
This study used ion-sensitive microelectrodes to characterize intracellular Mg2+ and Na+ concentrations and their regulation in Retzius neurons of Hirudo medicinalis, demonstrating the presence of an electrogenic 1 Na+-1 Mg2+ antiport that was reversible, amiloride-sensitive, and independent of the Na+/K+ pump. While this research uses the medicinal leech as a model organism, it is a basic neuroscience study of neuronal ion transport with no connection to hirudotherapy, the salivary secretome, or any therapeutic application. The relevance to ASH's domain is negligible—this work informs leech neurophysiology but provides no insight relevant to clinical leech therapy or leech-derived bioactive compounds.
Zitation
Sodium-magnesium antiport in Retzius neurones of the leech Hirudo medicinalis.
Günzel et al. · The Journal of physiology, 1996
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