IndraLab

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"For example, HCN1 subunits form channels with fast voltage dependent gating and reduced cAMP sensitivity, whereas HCN2 and HCN4 channels respond more efficiently to cAMP and have slower kinetics (Santoro et al. 1998; Seifert et al. 1999; Ishii et al. 1999; Ludwig et al. 1999; this work)."

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"The GOF property of WAG-HCN1 (animal model of absence seizures) is caused by N-terminal deletion, change in N-terminal wild-type sequence (GNSVCF) motif, increased current, enhanced HCN1 expression, reduced cAMP sensitivity, and suppressed HCN2 and HCN4 currents according to the functional analysis performed on Xenopus oocytes and thalamus of WAG/Rij rat strain (Wemhöner et al., 2015)."

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"2) Developmental dysregulation of cortical and/or thalamic HCN channel expression may contribute to epileptogenesis in genetic models of absence epilepsy : In two models, the Wistar Albino Glaxo and Rijswijk (WAG and Rij) and the Genetic Absence Epileptic Rats of Strasbourg (GAERS), the relative contribution of HCN1 channels to the channel pool and thalamic I h was increased in thalamocortical relay (TC) neurons, resulting in reduced cAMP responsiveness of I h."