ArticleThe Journal of biological chemistry2007
Activity-dependent regulation of h channel distribution in hippocampal CA1 pyramidal neurons.
Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 80 citations in OpenAlex.
- Enhanced HCN-Dependent Regulation of Temporoammonic Integration and Entorhinal-Hippocampal Epileptiform Coupling Following Febrile Seizures.Neurochemical research · 2026Article
- Loose-patch recordings reveal differential Kv7-dependent effects on spontaneous excitatory activity in control and epileptic CA1.Frontiers in neurology · 2026Article
- Review
- Distinct Modulation ofeNeuro · 2024Article
- The Impact of Altered HCN1 Expression on Brain Function and Its Relationship with Epileptogenesis.Current neuropharmacology · 2023Review
- Hippocampal cAMP regulates HCN channel function on two time scales with differential effects on animal behavior.Science translational medicine · 2021Article
- Loss of HCN2 in Dorsal Hippocampus of Young Adult Mice Induces Specific Apoptosis of the CA1 Pyramidal Neuron Layer.International journal of molecular sciences · 2021Article
- Homeostatic plasticity and burst activity are mediated by hyperpolarization-activated cation currents and T-type calcium channels in neuronal cultures.Scientific reports · 2021Article
- The structure and function of TRIP8b, an auxiliary subunit of hyperpolarization-activated cyclic-nucleotide gated channels.Channels (Austin, Tex.) · 2020Review
- PRMT7 deficiency causes dysregulation of the HCN channels in the CA1 pyramidal cells and impairment of social behaviors.Experimental & molecular medicine · 2020Article
- CK2 Inhibition Prior to Status Epilepticus Persistently Enhances KFrontiers in cellular neuroscience · 2020Article
- Phosphorylation of the HCN channel auxiliary subunit TRIP8b is altered in an animal model of temporal lobe epilepsy and modulates channel function.The Journal of biological chemistry · 2019Article
- Intra- and Extracellular Pillars of a Unifying Framework for Homeostatic Plasticity: A Crosstalk Between Metabotropic Receptors and Extracellular Matrix.Frontiers in cellular neuroscience · 2019Review
- Store depletion-induced h-channel plasticity rescues a channelopathy linked to Alzheimer's disease.Neurobiology of learning and memory · 2018Article
- Neuroinflammation Alters Integrative Properties of Rat Hippocampal Pyramidal Cells.Molecular neurobiology · 2018Article
- Plasticity of intrinsic excitability during LTD is mediated by bidirectional changes in h-channel activity.Scientific reports · 2017Article
- Allostery between two binding sites in the ion channel subunit TRIP8b confers binding specificity to HCN channels.The Journal of biological chemistry · 2017Article
- The hyperpolarization-activated cyclic nucleotide-gated (HCN) channels contain multiple S-palmitoylation sites.The journal of physiological sciences : JPS · 2016Article
- Homeostatic regulation of h-conductance controls intrinsic excitability and stabilizes the threshold for synaptic modification in CA1 neurons.The Journal of physiology · 2015Article
- Electrophysiological and Immunohistochemical Evidence for an Increase in GABAergic Inputs and HCN Channels in Purkinje Cells that Survive Developmental Ethanol Exposure.Cerebellum (London, England) · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The hyperpolarization-activated cation current, I(h), plays an important role in regulating intrinsic neuronal excitability in the brain. In hippocampal pyramidal neurons, I(h) is mediated by h channels comprised primarily of the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel subunits, HCN1 and HCN2. Pyramidal neuron h channels within hippocampal area CA1 are remarkably enriched in distal apical dendrites, and this unique distribution pattern is critical for regulating dendritic excitability. We utilized biochemical and immunohistochemical approaches in organotypic slice cultures to explore factors that control h channel localization in dendrites. We found that distal dendritic enrichment of HCN1 is first detectable at postnatal day 13, reaching maximal enrichment by the 3rd postnatal week. Interestingly we found that an intact entorhinal cortex, which projects to distal dendrites of CA1 but not area CA3, is critical for the establishment and maintenance of distal dendritic enrichment of HCN1. Moreover blockade of excitatory neurotransmission using tetrodotoxin, 6-cyano-7-nitroquinoxaline-2,3-dione, or 2-aminophosphonovalerate redistributed HCN1 evenly throughout the dendrite without significant changes in protein expression levels. Inhibition of calcium/calmodulin-dependent protein kinase II activity, but not p38 MAPK, also redistributed HCN1 in CA1 pyramidal neurons. We conclude that activation of ionotropic glutamate receptors by excitatory temporoammonic pathway projections from the entorhinal cortex establishes and maintains the distribution pattern of HCN1 in CA1 pyramidal neuron dendrites by activating calcium/calmodulin-dependent protein kinase II-mediated downstream signals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.