Key result
Expression of HCN1 induced a decrease in Cav3.2 Ba2+ influx along with altered channel kinetics and a depolarizing shift in activation gating.
HCN1 functionally regulates Cav3.2 T-type channels by forming a signaling complex, which may affect synaptic transmission and cellular excitability.
May modulate excitability via channel complexes; leaves open human disease relevance and therapeutic targeting.
Formation of complexes between ion channels is important for signal processing in the brain. Here we investigate the biochemical and biophysical interactions between HCN1 channels and Cav3.2 T-type channels. We found that HCN1 co-immunoprecipitated with Cav3.2 from lysates of either mouse brain or tsA-201 cells, with the HCN1 N-terminus associating with the Cav3.2 N-terminus. Cav3.2 channel activity appeared to be functionally regulated by HCN1. The expression of HCN1 induced a decrease in Cav3.2 Ba2+ influx (IBa2+) along with altered channel kinetics and a depolarizing shift in activation gating. However, a reciprocal regulation of HCN1 by Cav3.2 was not observed. This study highlights a regulatory role of HCN1 on Cav3.2 voltage-dependent properties, which are expected to affect physiologic functions such as synaptic transmission and cellular excitability.
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Fan et al. (2017) studied this question. HCN1 expression was evaluated on Cav3.2 channel activity and Ba2+ influx. Expression of HCN1 induced a decrease in Cav3.2 Ba2+ influx along with altered channel kinetics and a depolarizing shift in activation gating.
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