The Hyperpolarization-Activated HCN4 Channel is Important for Proper Maintenance of Oscillatory Activity in the Thalamocortical System.
Ih
HCN4 channels
HCN4 knock out mice
thalamocortical dysrhythmia
thalamocortical oscillations
Journal
Cerebral cortex (New York, N.Y. : 1991)
ISSN: 1460-2199
Titre abrégé: Cereb Cortex
Pays: United States
ID NLM: 9110718
Informations de publication
Date de publication:
01 05 2019
01 05 2019
Historique:
received:
26
12
2018
revised:
15
02
2019
accepted:
21
02
2019
pubmed:
17
3
2019
medline:
17
7
2020
entrez:
17
3
2019
Statut:
ppublish
Résumé
Hyperpolarization-activated cation channels are involved, among other functions, in learning and memory, control of synaptic transmission and epileptogenesis. The importance of the HCN1 and HCN2 isoforms for brain function has been demonstrated, while the role of HCN4, the third major neuronal HCN subunit, is not known. Here we show that HCN4 is essential for oscillatory activity in the thalamocortical (TC) network. HCN4 is selectively expressed in various thalamic nuclei, excluding the thalamic reticular nucleus. HCN4-deficient TC neurons revealed a massive reduction of Ih and strongly reduced intrinsic burst firing, whereas the current was normal in cortical pyramidal neurons. In addition, evoked bursting in a thalamic slice preparation was strongly reduced in the mutant mice probes. HCN4-deficiency also significantly slowed down thalamic and cortical oscillations during active wakefulness. Taken together, these results establish that thalamic HCN4 channels are essential for the production of rhythmic intrathalamic oscillations and determine regular TC oscillatory activity during alert states.
Identifiants
pubmed: 30877792
pii: 5382209
doi: 10.1093/cercor/bhz047
pmc: PMC6458902
doi:
Substances chimiques
Hcn4 protein, mouse
0
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2291-2304Informations de copyright
© The Author(s) 2019. Published by Oxford University Press.
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