The calcium ion carries a charge and contributes to the depolarization during the opening of voltage-sensitive calcium channels. It also functions as a second messenger and triggers transmitter release. Clinically used calcium channel blockers interact with L-type calcium channels, which do not play a significant role in fast synaptic transmission. However, gabapentin, an anticonvulsive drug, binds an accessory calcium channel subunit, leading to a lower expression of calcium channels on the cell surface and, thereby, to a decrease in excitability. This mechanism may be responsible for the reported beneficial effects in patients with neuropathic pain.
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