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Take a cortical slice from a transgenic mouse brain that expresses light-activated cation channels in excitatory pyramidal neurons of the cortex.
Secure the slice in a recording chamber and perfuse it with artificial cerebrospinal fluid to maintain tissue viability.
Insert a recording electrode into the superficial cortical layer and record baseline neuronal activity.
Introduce a seizure-inducing drug that blocks voltage-gated potassium channels, preventing potassium outflow and maintaining the neurons in a hyperexcitable state.
The hyperexcitable neurons spontaneously generate bursts of action potentials, termed ictal events, for a prolonged duration.
To generate ictal events on-demand, apply a brief light pulse to activate the cation channels on the excitatory pyramidal neurons.
The resulting cation influx generates action potentials, triggering the release of excitatory neurotransmitters.
These neurotransmitters bind to receptors on postsynaptic neurons, causing an influx of cations.
The influx results in bursts of action potential, generating ictal events for a short duration.
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