|1.||Bräuer, Anja U: 2 articles (01/2007 - 06/2006)|
|2.||Zhu, Mengye: 1 article (08/2015)|
|3.||Luo, Shiwen: 1 article (08/2015)|
|4.||Liu, Tao: 1 article (08/2015)|
|5.||Zhang, Daying: 1 article (08/2015)|
|6.||Liu, Nana: 1 article (08/2015)|
|7.||Petrou, Steven: 1 article (04/2014)|
|8.||Vargas, Ernesto: 1 article (04/2014)|
|9.||Kim, Taehwan: 1 article (04/2014)|
|10.||Phillips, A Marie: 1 article (04/2014)|
10/05/2011 - "However, the precise onset and mechanistic basis of HCN1 channel loss post-SE was unclear, particularly whether it preceded the onset of spontaneous recurrent seizures and could contribute to epileptogenesis or development of the epileptic state. "
06/01/2006 - "Therefore, we investigated whether the alterations in seizure activity between rats reared differently might be correlated with changes in Ih and its channel subunits hyperpolarization-activated cation channel HCN1, 2 and 4. Whole-cell recordings from layer 5 pyramidal neurons, in situ hybridization and Western blot of the somatosensory cortex revealed an increase in Ih and HCN1 in neonatal handled and maternal deprived, compared to control rats. "
01/15/2007 - "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 (I(h)) precedes the onset of seizures, suggesting that the loss of HCN1 channel expression is inherited rather than acquired. "
04/01/2014 - "Spike-and-wave discharge mediated reduction in hippocampal HCN1 channel function associates with learning deficits in a genetic mouse model of epilepsy."
08/15/2006 - "This decreased responsiveness of Ih to its major cellular modulator preceded epilepsy onset in GAERS, persisted throughout the chronic state, and was accompanied by an enhanced expression of the cAMP-insensitive HCN1 channel mRNA (> 50%), without changes in the mRNA levels of HCN2 and HCN4. "
08/20/2012 - "To clarify the role of the most populous cells, which express the hyperpolarization-activated cation channel (H-channel), in induction of nausea and/or emesis, we investigated the effects of ZD7288 (an H-channel inhibitor) on apomorphine-induced conditioned taste aversion (CTA) to saccharin and c-Fos expression in the area postrema. "
|5.||Status Epilepticus (Complex Partial Status Epilepticus)
|2.||Messenger RNA (mRNA)