The major excitatory neurotransmitter in the cerebral cortex is glutamate.9 When glutamate is released from a presynaptic neuron, it attaches to one of several receptor types on the postsynaptic neuron. The result is opening of membrane channels to allow sodium or calcium to flow into the postsynaptic neuron, thus depolarizing it and transmitting the excitatory signal.10 Many antiepileptic drugs (e.g., phenytoin, car-bamazepine, lamotrigine) work by interfering with this mechanism, either by blocking the release of glutamate or by blocking the sodium or calcium channels, thus preventing excessive excitation.11 These drugs typically do not block normal neuronal signaling, only the excessively rapid firing characteristic of a seizure. For this reason, they do not usually affect normal brain function.

The major inhibitory neurotransmitter in the cerebral cortex is gamma-aminobu-tyric acid (GABA). It attaches to neuronal membranes and opens chloride channels. When chloride flows into the neuron, it becomes hyperpolarized and less excitable. This mechanism is probably critical for shutting off seizure activity by controlling the excessive neuronal firing. Some antiepileptic drugs (AEDs), primarily barbiturates and benzodiazepines, work by enhancing the action of GABA.

Cortical function is modulated by many other neuro-transmitters. However, their role in the pathophysiology of epilepsy and in the action of AEDs is not yet well known.

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