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Reduction of thalamic and cortical Ih by deletion of TRIP8b produces a mouse model of human absence epilepsy
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文摘

TRIP8b is an auxiliary subunit of HCN channels that regulates neuronal excitability.

We noted spontaneous absence seizures during EEG recordings of TRIP8b knockout mice.

We found reduced HCN channel function (Ih) in neurons of the cortex and thalamus.

Normal Ih in the reticular thalamic nucleus may limit seizure severity in these mice.

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