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PMID:22880098
| Citation |
Ying, SW, Kanda, VA, Hu, Z, Purtell, K, King, EC, Abbott, GW and Goldstein, PA (2012) Targeted deletion of Kcne2 impairs HCN channel function in mouse thalamocortical circuits. PLoS ONE 7:e42756 |
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| Abstract |
Hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels generate the pacemaking current, I(h), which regulates neuronal excitability, burst firing activity, rhythmogenesis, and synaptic integration. The physiological consequence of HCN activation depends on regulation of channel gating by endogenous modulators and stabilization of the channel complex formed by principal and ancillary subunits. KCNE2 is a voltage-gated potassium channel ancillary subunit that also regulates heterologously expressed HCN channels; whether KCNE2 regulates neuronal HCN channel function is unknown. |
| Links |
PubMed PMC3411840 Online version:10.1371/journal.pone.0042756 |
| Keywords |
4-Aminopyridine/pharmacology; Animals; Cerebral Cortex/drug effects; Cerebral Cortex/physiology; Cyclic Nucleotide-Gated Cation Channels/metabolism; Down-Regulation/drug effects; Female; Gene Deletion; Gene Targeting; Glutamates/secretion; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; Ion Channel Gating/drug effects; Ion Channels/metabolism; Male; Mice; Mice, Inbred C57BL; Nerve Net/drug effects; Nerve Net/physiology; Neurons/drug effects; Neurons/metabolism; Potassium Channels/metabolism; Potassium Channels, Voltage-Gated/genetics; Pyramidal Cells/drug effects; Pyramidal Cells/metabolism; Pyrimidines/pharmacology; Somatosensory Cortex/drug effects; Somatosensory Cortex/metabolism; Thalamus/drug effects; Thalamus/physiology |
| edit table |
Significance
Annotations
| Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
|---|---|---|---|---|---|---|---|---|
| GO:0006811: ion transport |
ECO:0000247: |
UniProtKB: |
P |
Figure 4: Activation time constants for Ih in pyramidal cells were fast in both genotypes compared to those in VB neurons, Kcne2 deletion again increased time constants in pyramidal neurons Figure 6: he frequency of spontaneous EPSPs in layer 6 pyramidal neurons in the absence of 4-AP was increased by Kcne2 deletion, suggesting a possible alteration in glutamate release machinery. |
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Notes
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