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The importance of long-term synaptic plasticity as a cellular substrate for learning and memory is well established. By contrast, little is known about how learning and memory are regulated by voltage-gated ion channels that integrate synaptic information. We investigated this question using mice with general or forebrain-restricted knockout of the HCN1(More)
In contrast to our increasingly detailed understanding of how synaptic plasticity provides a cellular substrate for learning and memory, it is less clear how a neuron's voltage-gated ion channels interact with plastic changes in synaptic strength to influence behavior. We find, using generalized and regional knockout mice, that deletion of the HCN1 channel(More)
are incorrectly labeled. The symbols for control (HCN1 f/f) and forebrain-restricted HCN1 knockout (HCN1 f/f,cre) are reversed. The closed symbols in these panels correspond to data from HCN1 f/f,cre mice, whereas the open symbols refer to data from HCN1 f/f mice. Note that throughout the rest of the paper, closed symbols refer to data from HCN1 f/f mice(More)
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