Susceptibility gene that codes a calcium channel in the thalamus can get switched on, according to paper in the Journal of Neuroscience.

Scientists report that an epilepsy susceptibility gene can get switched on in mice that have not inherited the active form of the gene, which subsequently increases the tendency to have seizures. This finding helps explain how some people without a genetic predisposition to epilepsy can develop the disorder, according to the team from Wake Forest University School of Medicine.

The gene codes a calcium channel in the brain that underlies seizures, according to the study called “An Acquired Channelopathy Involving Thalamic T-Type Ca^2+ Channels after Status Epilepticus” appearing this month in the Journal of Neuroscience.

Some epilepsies are linked to inherited traits, but many appear to arise through acquired alterations in neuronal excitability. Status epilepticus (SE) is associated with numerous changes that promote spontaneous recurrent seizures (SRS). Studies have suggested that hippocampal T-type Ca^2+ channels underlie increased bursts of activity integral to the generation of these seizures.

The thalamus also contributes to epileptogenesis, but no studies have directly assessed channel alterations in the thalamus during SE or subsequent periods of SRS, according to the Wake Forest group. They thus decided to investigate longitudinal changes in thalamic T-type channels in a mouse model of epilepsy. They measured changes at different time intervals as the mice developed epilepsy.

The researchers found that after an initial seizure, a particular type of calcium channel begins to be expressed where it wasn’t before. They observed that the particular gene that codes for the misplaced channel was upregulated during the SRS period. They verified the functional involvement of this gene by using inhibitors, which reduced the activity of the calcium channels in the thalamus.

“Certain kinds of channels are normal and expected in the thalamus, but after an initial seizure, more copies of a channel that aren’t normally found in this brain region begin to appear,” explains graduate student John Graef, the first author on the study. “The brain activity then becomes dominated by the new copies of this channel. It helps explain how seizures can develop and spread.”

The scientists thus conclude that SE produces an acquired calcium channel network by inducing long-term alterations in thalamic T-type channels. This contributes to characteristic changes in excitability observed during SRS.

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