PHARMACOLOGY Chapter 24-25

At therapeutic concentrations, phenytoin, carbamazepine, lamotrigine, and zonisamide block voltage-gated sodium channels in neuronal membranes. This action is rate-dependent (ie, dependent on the frequency of neuronal discharge) and results in prolongation of the inactivated state of the Na+ channel and the refractory period of the neuron

In the presence of benzodiazepines, the frequency of chloride ion channel opening is increased; these drugs facilitate the inhibitory effects of GABA

Phenobarbital and other barbiturates also enhance the inhibitory actions of GABA but interact with a different receptor site on chloride ion channels that results in an increased duration of chloride ion channel opening

GABA aminotransaminase (GABA-T) is an important enzyme in the termination of action of GABA
Tiagabine inhibits a GABA transporter (GAT-1) in neurons and glia prolonging the action of the neurotransmitter

Gabapentin is a structural analog of GABA, but it does not activate GABA receptors directly.

Ethosuximide inhibits low-threshold (T type) Ca2+ currents, especially in thalamic neurons that act as pacemakers to generate rhythmic cortical discharge.

In addition to its action on calcium channels, valproic acid causes neuronal membrane hyperpolarization, possibly by enhancing K+ channel permeability

Felbamate blocks glutamate NMDA receptors

Topiramate blocks sodium channels and potentiates the actions of GABA and may also block glutamate receptors.

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