Abstract
Trigeminal neuralgia (TN) is a unique pain disorder in which affected individuals experience intense paroxysmal pain in the territory of the trigeminal nerve. Although most cases of TN are sporadic, occurrence of familial TN suggests a genetic contribution to this disorder. Here we used Ca2+ and Na+ imaging and whole-cell patch clamp to assess a variant in the TRPM7 channel kinase, p.Ala931Thr, found in a man suffering from unilateral TN. We found that A931T generated a 20-fold higher inward currents than TRPM7 WT and unchanged outward currents. The inward current recorded in A931T had the following properties: i) it was carried by Na+ ions under physiological conditions; ii) it was insensitive to the pore blocker Gd3+; iii) it was observed when Na+ was replaced by Guanidinium, but it was completely suppressed by application of NMDG+.
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