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Safinamide, an inhibitor of monoamine oxidase, modulates the magnitude, gating, and hysteresis of sodium ion current
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Safinamide, an inhibitor of monoamine oxidase, modulates the magnitude, gating, and hysteresis of sodium ion current
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Journal Article
Safinamide, an inhibitor of monoamine oxidase, modulates the magnitude, gating, and hysteresis of sodium ion current
2024
Overview
Background
Safinamide (SAF), an α-aminoamide derivative and a selective, reversible monoamine oxidase (MAO)-B inhibitor, has both dopaminergic and nondopaminergic (glutamatergic) properties. Several studies have explored the potential of SAF against various neurological disorders; however, to what extent SAF modulates the magnitude, gating, and voltage-dependent hysteresis [Hys
(V)
] of ionic currents remains unknown.
Methods
With the aid of patch-clamp technology, we investigated the effects of SAF on voltage-gated sodium ion (Na
V
) channels in pituitary GH3 cells.
Results
SAF concentration-dependently stimulated the transient (peak) and late (sustained) components of voltage-gated sodium ion current (
I
Na
) in pituitary GH
3
cells. The conductance–voltage relationship of transient
I
Na
[
I
Na(T)
] was shifted to more negative potentials with the SAF presence; however, the steady-state inactivation curve of
I
Na(T)
was shifted in a rightward direction in its existence. SAF increased the decaying time constant of
I
Na(T)
induced by a train of depolarizing stimuli. Notably, subsequent addition of ranolazine or mirogabalin reversed the SAF-induced increase in the decaying time constant. SAF also increased the magnitude of window
I
Na
induced by an ascending ramp voltage
V
ramp
. Furthermore, SAF enhanced the Hys
(V)
behavior of persistent
I
Na
induced by an upright isosceles-triangular
V
ramp
. Single-channel cell-attached recordings indicated SAF effectively increased the open-state probability of Na
V
channels. Molecular docking revealed SAF interacts with both MAO and Na
V
channels.
Conclusion
SAF may interact directly with Na
V
channels in pituitary neuroendocrine cells, modulating membrane excitability.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V
