Name two major mechanisms of action of common antiseizure drugs.

• A. Sodium channel blockade and enhancement of GABAergic inhibition
• B. Voltage-gated calcium channel activation and NMDA receptor activation
• C. Acetylcholine receptor antagonism and dopamine receptor blockade
• D. Glycine receptor activation and serotonin reuptake inhibition

Answer: (A)

The effect you’re looking for centers on reducing neuronal excitability through two main pathways. First, blocking voltage-gated sodium channels prevents neurons from firing rapidly, stabilizing them in a less excitable state and dampening the high-frequency discharges that fuel seizures. Second, enhancing GABAergic inhibition increases the activity of the main inhibitory system in the brain. By boosting GABA at its receptors, chloride channels open more easily, hyperpolarizing neurons and raising the threshold needed to trigger seizures. Together, these actions curb the synchronous, excessive firing that characterizes seizures.

Why the other options don’t fit: activating calcium channels or NMDA receptors would raise excitability rather than calm it, which is opposite of an antiseizure goal. Acetylcholine or dopamine receptor blockade is not how these drugs typically control seizures; and glycine receptor activation or serotonin reuptake inhibition aren’t the primary mechanisms used for common antiseizure meds.