@article {4047,
	title = {HCN1 channels constrain synaptically evoked Ca2+ spikes in distal dendrites of CA1 pyramidal neurons.},
	journal = {Neuron},
	volume = {56},
	year = {2007},
	month = {2007 Dec 20},
	pages = {1076-89},
	abstract = {<p>HCN1 hyperpolarization-activated cation channels act as an inhibitory constraint of both spatial learning and synaptic integration and long-term plasticity in the distal dendrites of hippocampal CA1 pyramidal neurons. However, as HCN1 channels provide an excitatory current, the mechanism of their inhibitory action remains unclear. Here we report that HCN1 channels also constrain CA1 distal dendritic Ca2+ spikes, which have been implicated in the induction of LTP at distal excitatory synapses. Our experimental and computational results indicate that HCN1 channels provide both an active shunt conductance that decreases the temporal integration of distal EPSPs and a tonic depolarizing current that increases resting inactivation of T-type and N-type voltage-gated Ca2+ channels, which contribute to the Ca2+ spikes. This dual mechanism may provide a general means by which HCN channels regulate dendritic excitability.</p>
},
	keywords = {Animals, Calcium, Calcium Channel Blockers, Computer Simulation, Cyclic Nucleotide-Gated Cation Channels, Dendrites, Dose-Response Relationship, Electric Stimulation, Excitatory Amino Acid Antagonists, Excitatory Postsynaptic Potentials, Hippocampus, Knockout, Mice, Newborn, Patch-Clamp Techniques, Potassium Channels, Pyramidal Cells, Pyrimidines, Radiation, Reaction Time, Synapses},
	issn = {0896-6273},
	doi = {10.1016/j.neuron.2007.11.015},
	author = {Tsay, David and Dudman, Joshua T and Siegelbaum, Steven A}
}
@article {4048,
	title = {A role for synaptic inputs at distal dendrites: instructive signals for hippocampal long-term plasticity.},
	journal = {Neuron},
	volume = {56},
	year = {2007},
	month = {2007 Dec 6},
	pages = {866-79},
	abstract = {<p>Synaptic potentials originating at distal dendritic locations are severely attenuated when they reach the soma and, thus, are poor at driving somatic spikes. Nonetheless, distal inputs convey essential information, suggesting that such inputs may be important for compartmentalized dendritic signaling. Here we report a new plasticity rule in which stimulation of distal perforant path inputs to hippocampal CA1 pyramidal neurons induces long-term potentiation at the CA1 proximal Schaffer collateral synapses when the two inputs are paired at a precise interval. This subthreshold form of heterosynaptic plasticity occurs in the absence of somatic spiking but requires activation of both NMDA receptors and IP(3) receptor-dependent release of Ca(2+) from internal stores. Our results suggest that direct sensory information arriving at distal CA1 synapses through the perforant path provide compartmentalized, instructive signals that assess the saliency of mnemonic information propagated through the hippocampal circuit to proximal synapses.</p>
},
	keywords = {4, 5-Trisphosphate Receptors, Absorptiometry, AMPA, Animals, Calcium, Computer Simulation, Dendrites, Dendritic Spines, Electrophysiology, Excitatory Postsynaptic Potentials, Hippocampus, Inositol 1, Memory, Mice, Models, N-Methyl-D-Aspartate, Neurological, Neuronal Plasticity, Neurophysiological, Patch-Clamp Techniques, Photon, Pyramidal Cells, Receptors, Recruitment, Signal Transduction, Synapses, Synaptic Transmission},
	issn = {0896-6273},
	doi = {10.1016/j.neuron.2007.10.020},
	author = {Dudman, Joshua T and Tsay, David and Siegelbaum, Steven A}
}
