期刊
JOURNAL OF NEUROSCIENCE
卷 26, 期 47, 页码 12143-12151出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2667-06.2006
关键词
k(+) channels; long-term potentiation; hippocampus; dendrites; backpropagating action potential; knock-out mouse
资金
- NIMH NIH HHS [R01 MH057014, MH57014, MH48432, R03 MH070857, MH70857, MH44754, R37 MH044754, R01 MH048432] Funding Source: Medline
- NINDS NIH HHS [P01 NS037444, NS37444] Funding Source: Medline
Dendritic, backpropagating action potentials (bAPs) facilitate the induction of Hebbian long-term potentiation (LTP). Although bAPs in distal dendrites of hippocampal CA1 pyramidal neurons are attenuated when propagating from the soma, their amplitude can be increased greatly via downregulation of dendritic A-type K+ currents. The channels that underlie these currents thus may represent a key regulatory component of the signaling pathways that lead to synaptic plasticity. We directly tested this hypothesis by using Kv4.2 knock-out mice. Deletion of the Kv4.2 gene and a loss of Kv4.2 protein resulted in a specific and near-complete elimination of A-type K+ currents from the apical dendrites of CA1 pyramidal neurons. The absence of dendritic Kv4.2-encoded A-type K+ currents led to an increase of bAP amplitude and an increase of concurrent Ca2+ influx. Furthermore, CA1 pyramidal neurons lacking dendritic A-type K+ currents from Kv4.2 knock-out mice exhibited a lower threshold than those of wild-type littermates for LTP induction with the use of a theta burst pairing protocol. LTP triggered with the use of a saturating protocol, on the other hand, remained indistinguishable between Kv4.2 knock-out and wild-type neurons. Our results support the hypothesis that dendritic A-type K+ channels, composed of Kv4.2 subunits, regulate action potential backpropagation and the induction of specific forms of synaptic plasticity.
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