Dibenzodiazepine antipsychotics have strong blocking effects on 5-hydroxytryptamine (5-HT2A) receptors and dopamine (DA1) receptors in the brain, have blocking effects on dopamine (DA4) receptors, and weaker blocking effects on dopamine (DA2) receptors. They have anticholinergic (M1), antihistamine (H1) and anti-α-adrenaline receptor effects, rarely cause extrapyramidal reactions, do not cause increased prolactin in the blood, can directly inhibit the ascending activation system of the brainstem reticular formation, and have a powerful sedative and hypnotic effect.

The mechanism of gabapentin's anticonvulsant effect is still unclear, but animal studies suggest that, similar to other marketed anticonvulsant drugs, gabapentin can inhibit epileptic seizures. It is structurally related to the neurotransmitter GABA, but does not interact with GABA receptors, and is neither metabolized into GABA or GABA agonists nor an inhibitor of GABA uptake or degradation. Its high-affinity binding protein has been confirmed to be an auxiliary subunit of voltage-activated calcium channels, and its related functions have not yet been elucidated.

The mechanism of gabapentin's anticonvulsant effect is still unclear, but animal experiments suggest that gabapentin can inhibit epileptic seizures, similar to other marketed anticonvulsant drugs. Results from the maximum electric shock test in mice and rats, the benzotetrazole epilepsy seizure test, and other animal experiments (such as genetic epilepsy models) suggest that gabapentin has antiepileptic effects, but the relevance of these epilepsy models to humans is unclear. Gabapentin is structurally related to the neurotransmitter GABA, but does not interact with GABA receptors. It can neither be metabolized into GABA or GABA agonists, nor is it an inhibitor of GABA uptake or degradation. Radioligand binding assays have found that gabapentin has no affinity for many common receptor sites when the concentration reaches 100 μM, including benzodiazepine receptors, glutamate receptors, NMDA receptors, quisqualate receptors, kainate receptors, strychnine-insensitive or -sensitive aminoacetic acid receptors, α1, α2 or β receptors, adenosine A1 or A2 receptors, M or N receptors, dopamine D1 or D2 receptors, H1 receptors, 5-hydroxytryptamine S1 or S2 receptors, opioid μ, δ or k receptors, voltage-sensitive calcium channel sites labeled with nitrendipine or diltiazem, and voltage-sensitive sodium channel sites labeled with batrachotoxin A20-α-benzoate. Since the results obtained in several commonly used tests for evaluating the effects of drugs on NMDA receptors are opposite, there is currently no unified understanding of the effects of gabapentin on NMDA receptors. In vitro studies have shown that the binding sites of gabapentin in the rat brain are distributed in the neocortex and hippocampus, and its high-affinity binding protein has been confirmed to be an auxiliary subunit of the voltage-activated calcium channel, but its related functions have not yet been elucidated.

The mechanism of gabapentin's anticonvulsant effect is still unclear, but animal studies suggest that gabapentin can inhibit epileptic seizures, similar to other marketed anticonvulsant drugs. Its high-affinity binding protein has been confirmed to be an auxiliary subunit of voltage-activated calcium channels, and its related functions have not yet been elucidated.

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