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海马体中树突状钾离子通道的蛋白激酶调节涉及丝裂原活化蛋白激酶途径。

Protein kinase modulation of dendritic K+ channels in hippocampus involves a mitogen-activated protein kinase pathway.

作者信息

Yuan Li-Lian, Adams J Paige, Swank Michael, Sweatt J David, Johnston Daniel

机构信息

Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

J Neurosci. 2002 Jun 15;22(12):4860-8. doi: 10.1523/JNEUROSCI.22-12-04860.2002.

DOI:10.1523/JNEUROSCI.22-12-04860.2002
PMID:12077183
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6757742/
Abstract

We investigated mitogen-activated protein kinase (MAPK) modulation of dendritic, A-type K+ channels in CA1 pyramidal neurons in the hippocampus. Activation of cAMP-dependent protein kinase A (PKA) and protein kinase C (PKC) leads to an increase in the amplitude of backpropagating action potentials in distal dendrites through downregulation of transient K+ channels in CA1 pyramidal neurons in the hippocampus. We show here that both of these signaling pathways converge on extracellular-regulated kinases (ERK)-specific MAPK in mediating this reduction in dendritic K+ current, which is confirmed, in parallel, by biochemical assays using phosphospecific antibodies against the ppERK and pKv4.2. Furthermore, immunostaining indicates dendritic localization of ppERK and pKv4.2. Taken together, these results demonstrate that dendritic, A-type K+ channels are dually regulated by PKA and PKC through a common downstream pathway involving MAPK, and the modulation of these K+ channels may be accounted for by the phosphorylation of Kv4.2 subunits.

摘要

我们研究了丝裂原活化蛋白激酶（MAPK）对海马体CA1锥体神经元中树突状A 型钾通道的调节作用。环磷酸腺苷依赖性蛋白激酶A（PKA）和蛋白激酶C（PKC）的激活通过下调海马体CA1锥体神经元中的瞬时钾通道，导致远端树突中反向传播动作电位的幅度增加。我们在此表明，这两种信号通路在介导树突状钾电流减少方面均汇聚于细胞外调节激酶（ERK）特异性MAPK，同时，使用针对磷酸化ERK（ppERK）和磷酸化Kv4.2的磷酸特异性抗体进行的生化分析也证实了这一点。此外，免疫染色显示了ppERK和pKv4.2的树突定位。综上所述，这些结果表明，树突状A 型钾通道受PKA和PKC通过涉及MAPK的共同下游途径双重调节，这些钾通道的调节可能是由Kv4.2亚基的磷酸化引起的。

相似文献

[1]
Protein kinase modulation of dendritic K+ channels in hippocampus involves a mitogen-activated protein kinase pathway.

J Neurosci. 2002-6-15

[2]
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[3]
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[7]
Dendritic K+ channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons.

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[8]
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[10]
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本文引用的文献

[1]
Dendritic K+ channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons.

Proc Natl Acad Sci U S A. 2002-6-11

[2]
Mitogen-activated protein kinase regulates early phosphorylation and delayed expression of Ca2+/calmodulin-dependent protein kinase II in long-term potentiation.

J Neurosci. 2001-9-15

[3]
Spaced stimuli stabilize MAPK pathway activation and its effects on dendritic morphology.

Nat Neurosci. 2001-2

[4]
Mitogen-activated protein kinase/extracellular signal-regulated kinase activation in somatodendritic compartments: roles of action potentials, frequency, and mode of calcium entry.

J Neurosci. 2001-1-15

[5]
Experience-dependent changes in extracellular spike amplitude may reflect regulation of dendritic action potential back-propagation in rat hippocampal pyramidal cells.

J Neurosci. 2001-1-1

[6]
The A-type potassium channel Kv4.2 is a substrate for the mitogen-activated protein kinase ERK.

J Neurochem. 2000-12

[7]
Input-specific immunolocalization of differentially phosphorylated Kv4.2 in the mouse brain.

Learn Mem. 2000

[8]
Coactivation of beta-adrenergic and cholinergic receptors enhances the induction of long-term potentiation and synergistically activates mitogen-activated protein kinase in the hippocampal CA1 region.

J Neurosci. 2000-8-15

[9]
The extracellular signal-regulated kinase cascade is required for NMDA receptor-independent LTP in area CA1 but not area CA3 of the hippocampus.

J Neurosci. 2000-5-1

[10]
A novel targeting signal for proximal clustering of the Kv2.1 K+ channel in hippocampal neurons.

Neuron. 2000-2

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