pharmachologic effect

Gabapentin is structurally similar to the GABA neurotransmitter, however its mechanism of action differs from that of some other drugs interacting with GABA receptors, including valproic acid, barbiturates, benzodiazepines, GABA transaminase inhibitors, GABA capture inhibitors, GABA agonists and prodrugs of GABA: it is not has GABA-ergic properties and does not affect the capture and metabolism of GABA.

Preliminary studies indicate that gabapentin binds to the α2-δ subunit of potential-dependent calcium channels and suppresses the flow of calcium ions, which plays an important role in the occurrence of neuropathic pain. Other mechanisms involved in the action of gabapentin in neuropathic pain are: reduction of glutamate-dependent neuronal death, an increase in GABA synthesis, inhibition of the release of neurotransmitters of the monoamine group. Gabapentin does not bind to other receptors at clinically significant concentrations, including the GABAA, GABAB, benzodiazepine, glutamate, glycine, or N-methyl-d-acanthate receptors. Unlike phenytoin and carbamazepine, gabapentin does not interact with sodium channels in vitro. Gabapentin partially attenuated the effects of the glutamate receptor agonist N-methyl-d-aspartate in some tests in vitro, but only at a concentration of more than 100 μmol / L, which is not achieved in vivo. Gabapentin somewhat reduces the release of monoamine neurotransmitters in vitro.

Indications

- epilepsy: in adults and children older than 12 years - as a monotherapy or as part of a combination therapy for the treatment of partial epileptic seizures, incl. proceeding with secondary generalization;

- for the treatment of neuropathic pain in adults.