Lamotrigine exerts its primary antiepileptic mechanism by:
- A Enhancing GABA-A receptor chloride conductance
- B Blocking T-type calcium channels in thalamic relay neurons
- C Use-dependent blockade of voltage-gated sodium channels stabilising the inactive state ✓
- D Selective agonism at GABA-B presynaptic autoreceptors
Explanation
Lamotrigine preferentially binds to the inactivated state of voltage-gated sodium channels, prolonging their inactivation and reducing high-frequency neuronal firing. This use-dependent (activity-dependent) mechanism also applies to phenytoin and carbamazepine. T-type calcium channel blockade is the mechanism of ethosuximide (absence seizures), and GABA-A enhancement is the mechanism of benzodiazepines.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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