ISSN:
1432-1017
Keywords:
Sodium channel
;
Patch clamp
;
Cerebellar
;
granule cells
;
Intracellular magnesium
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Physics
Notes:
Abstract The aim of this study was to determine from macroscopic current analysis how intracellular magnesium ions, Mg i 2+ , interfere with sodium channels of mammalian neurones. It is reported here that permeation across the sodium channel is voltage- and concentration-dependently reduced by Mg i 2+ . This results in a general reduction of sodium membrane conductance and an outward sodium peak current at large positive potentials. 30 mM Mg i 2+ leads to a negative shift of voltage dependence of sodium channel gating parameters, probably due to the surface potential change of the membrane. This shift alone is, however, insufficient to explain the reduction of outward sodium currents. The blockage by Mg i 2+ is decreased upon increasing intracellular or extracellular Na+ concentration, which suggests that Mg?' interferes with sodium permeation by competitively occupying sodium channels. Using a kinetic model to describe the sodium permeation, the dissociation constant (at zero membrane potential) of Mg i 2+ for the sodium channel has been calculated to be 8.65 ± 1.51 mM, with its binding site located at 0.26 ± 0.05 electrical distance from the inner membrane. This dissociation constant is smaller than that of Na i +, which is 83.76 ± 7.60 mM with its binding site located at 0.75 ± 0.23. The low dissociation constant of Mg i 2+ reflects its high affinity for the sodium channel.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00185451
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