TWIK-1 contributes to the intrinsic excitability of dentate granule cells in mouse hippocampus

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Title
TWIK-1 contributes to the intrinsic excitability of dentate granule cells in mouse hippocampus
Author(s)
O Yarishkin; Da Yong Lee; E Kim; C H Cho; J H Choi; C J Lee; E M Hwang; J Y Park
Bibliographic Citation
Molecular Brain, vol. 7, pp. 80-80
Publication Year
2014
Abstract
BackgroundTwo-pore domain K+ (K2P) channels have been shown to modulate neuronal excitability. However, physiological function of TWIK-1, the first identified member of the mammalian K2P channel family, in neuronal cells is largely unknown.ResultsWe found that TWIK-1 proteins were expressed and localized mainly in the soma and proximal dendrites of dentate gyrus granule cells (DGGCs) rather than in distal dendrites or mossy fibers. Gene silencing demonstrates that the outwardly rectifying K+ current density was reduced in TWIK-1-deficient granule cells. TWIK-1 deficiency caused a depolarizing shift in the resting membrane potential (RMP) of DGGCs and enhanced their firing rate in response to depolarizing current injections. Through perforant path stimulation, TWIK-1 deficient granule cells showed altered signal input-output properties with larger EPSP amplitude values and increased spiking compared to control DGGCs. In addition, supra-maximal perforant path stimulation evoked a graded burst discharge in 44% of TWIK-1-deficient cells, which implies impairment of EPSP-spike coupling.ConclusionsThese results showed that TWIK-1 is functionally expressed in DGGCs and contributes to the intrinsic excitability of these cells. The TWIK-1 channel is involved in establishing the RMP of DGGCs; it attenuates sub-threshold depolarization of the cells during neuronal activity, and contributes to EPSP-spike coupling in perforant path-to-granule cell synaptic transmission.
Keyword
K2P channelTWIK-1Intrinsic excitabilityDentate gyrus granule cell
ISSN
1756-6606
Publisher
Springer-BMC
DOI
http://dx.doi.org/10.1186/s13041-014-0080-z
Type
Article
Appears in Collections:
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
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