Inherited cortical HCN1 loss amplifies dendritic calcium electrogenesis and burst firing in an rat absence epilepsy model
While idiopathic generalized epilepsies are thought to evolve from temporal highly synchronized oscillations between thalamic and cortical networks, their cellular basis remains poorly understood. Here we show in a genetic rat model of absence epilepsy (WAG/Rij) that a rapid decline in expression of hyperpolarization-activated cyclic-nucleotide gated (HCN1) channels (Ih) precedes the onset of seizures, suggesting that the loss of HCN1 channel expression is inherited rather than acquired. Loss...[Show more]
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|Source:||Journal of Physiology|
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