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Anticonvulsant drug. Neurontin in the structure is similar to GABA, but its mechanism of action differs from that of some other drugs that interact with GABA-receptors, including valproate, barbiturates, benzodiazepines, GABA-transaminase inhibitors, inhibitors of the capture of GABA, GABA agonists and prodrugs of GABA: GABA does not have -ergic properties and does not affect the capture and metabolism of GABA. Preliminary studies suggest that Neurontin binds to the ?2-?-subunit of voltage-dependent calcium channels and inhibits the flow of calcium ions, which plays an important role in the development of neuropathic pain. Other mechanisms involved in the action of Neurontin for neuropathic pain are: reduction of glutamate-dependent neuronal death, increased synthesis of GABA, inhibition of monoamine neurotransmitter release group. Neurontin in clinically relevant concentrations does not bind to receptors of other common drugs, or neurotransmitters, receptors, including GABAA, GABAB, benzodiazepine, glutamate, glycine, or N-methyl-d-aspartate (NMDA). In contrast to phenytoin and carbamazepine Neurontin does not interact with sodium channels in vitro. Neurontin partially attenuated the effects of glutamate NMDA receptor agonist in some tests in vitro, but only at concentrations greater than 100 micromoles, which is not achieved in vivo. Neurontin reduces the release of several monoamine neytrotransmitterov in vitro.

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