Lamotrigine is particularly useful in bipolar depression. Its primary mechanism of action in seizure control is:
- A Blockade of voltage-gated sodium channels in a use-dependent manner, reducing repetitive neuronal firing ✓
- B Potentiation of GABA-A receptor chloride currents at the barbiturate-binding site
- C Inhibition of T-type calcium channels in thalamic relay neurons
- D Antagonism of NMDA-type glutamate receptors
Explanation
Lamotrigine stabilises neuronal membranes by blocking voltage-sensitive sodium channels in a use-dependent (state-dependent) fashion — preferentially binding to channels in the inactivated state, thereby reducing high-frequency neuronal firing. It also inhibits presynaptic voltage-gated calcium channels and reduces glutamate release. T-type calcium channel blockade is the mechanism of ethosuximide. Its sodium-channel mechanism explains efficacy in both focal and generalised seizures.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.