1) Those acting on voltage gated channels
2) Drugs that inhibit excitation
3) Drugs that enhance inhibition
History of anti-epileptic drugs( AED) discovery was discussed. Mechanisms of action of AED on sodium channel (transient and persistent currents, action on inactivation cycle of sodium channel) were discussed. Experimental evidence from electrophysiology was also touched upon. Neuropharmacology of AED was also discussed in detail (Ureide ring binding to the S6 segment and peculiarity of action of ethosuximide).
Retigabine is the only marketed AED that acts on potassium channels. High voltage and low voltage calcium channel mechanisms were covered. Peculiarity of action of ethosuximide on low voltage activated calcium channels and its role in treating absence seizures and role of high voltage activated calcium channel blockers like pregabalin and gabapentin and their role in some diabetic neuropathies and pain related disorders deliberated. A short slide from the work of Hanada T (2014) which discussed the role of AMPA receptors in epileptognesis and refractory epilepsy was very informative. AMPA receptors lacking GluA2 subunits are permeable to calcium ions in developmental phases and in epilepsy was a surprising one!
References for a recap: