Lamotrigine is used as a mood stabiliser in bipolar disorder and as an antiepileptic. Its primary mechanism of action is:
- A Enhancement of GABA-mediated chloride conductance via positive allosteric modulation of GABA-A receptors
- B Inhibition of T-type calcium channels in thalamic neurons
- C Selective blockade of NMDA receptors in the hippocampus
- D Blockade of voltage-gated Na+ channels in their inactivated state, reducing glutamate and aspartate release ✓
Explanation
Lamotrigine preferentially binds and stabilises voltage-gated sodium channels in their inactivated (slow-closed) state, reducing the frequency of high-frequency neuronal firing. A secondary consequence is reduced presynaptic release of excitatory amino acids (glutamate, aspartate), contributing to its mood-stabilising and anticonvulsant effects. GABA-A positive allosteric modulation is the mechanism of benzodiazepines and barbiturates. T-type Ca2+ channel blockade characterises ethosuximide. NMDA blockade is the mechanism of memantine and ketamine.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.