Gabapentin MOA as described in the material.

Gabapentin MOA as described in the material.

• A. Exact mechanism unknown; thought to bind to voltage-gated Ca channels and NMDA receptors
• B. Direct GABA receptor agonist
• C. Inhibits COX enzymes
• D. Blocks sodium channels exclusively

Answer: (A)

Gabapentin’s exact mechanism isn’t fully understood, which is the point this question tests. It behaves like a GABA analog but does not activate GABA receptors. The best-supported idea is that gabapentin interacts with the alpha-2-delta subunit of voltage-gated calcium channels in the central nervous system. This binding reduces calcium influx when neurons fire, which in turn decreases the release of excitatory neurotransmitters such as glutamate. That dampens neuronal excitability and helps alleviate neuropathic pain and has antiseizure effects. Some data have suggested involvement with NMDA receptor activity, but there is no direct action on GABA receptors, nor does gabapentin inhibit COX enzymes or exclusively block sodium channels. So describing the mechanism as unknown with a plausible link to voltage-gated calcium channels (and any NMDA-related ideas as a less central or speculative note) best fits current understanding.

Gabapentin’s exact mechanism isn’t fully understood, which is the point this question tests. It behaves like a GABA analog but does not activate GABA receptors. The best-supported idea is that gabapentin interacts with the alpha-2-delta subunit of voltage-gated calcium channels in the central nervous system. This binding reduces calcium influx when neurons fire, which in turn decreases the release of excitatory neurotransmitters such as glutamate. That dampens neuronal excitability and helps alleviate neuropathic pain and has antiseizure effects.

Some data have suggested involvement with NMDA receptor activity, but there is no direct action on GABA receptors, nor does gabapentin inhibit COX enzymes or exclusively block sodium channels. So describing the mechanism as unknown with a plausible link to voltage-gated calcium channels (and any NMDA-related ideas as a less central or speculative note) best fits current understanding.