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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Inhibition of the rat brain sodium channel Nav1.2 after prolonged exposure to gabapentin.

Prolonged exposure of neurons to gabapentin inhibits repetitive firing of Na(+)-dependent action potentials. Here, we studied the effect of such prolonged exposure to gabapentin on a rat sodium channel, Nav1. 2. After 3 days of continuous incubation with gabapentin (10-1000 microM), Nav1.2 current density was decreased dose-dependently relative to untreated cells. The reduction was 57% at 30 microM gabapentin, while higher concentrations (100-1000 microM) did not result in greater effects. Prolonged treatment with gabapentin also caused the channel to inactivate at more hyperpolarized potentials. These effects provide a mechanistic basis for the inhibition of Na(+)-dependent repetitive firing upon prolonged exposure to gabapentin and may contribute to its anticonvulsant activity.[1]

References

  1. Inhibition of the rat brain sodium channel Nav1.2 after prolonged exposure to gabapentin. Liu, Y., Qin, N., Reitz, T., Wang, Y., Flores, C.M. Epilepsy Res. (2006) [Pubmed]
 
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