Manipulating Kv4.2 identifies a specific component of hippocampal pyramidal neuron A‐current that depends upon Kv4.2 expression

Lauver, Aaron; Li, Yuan; Jeromin, Andreas; Nadin, Brian M.; Rodrı́guez, José J.; Davies, Heather A.; Stewart, Michael G.; Wu, Gang; Pfaffinger, Paul J.

doi:10.1111/j.1471-4159.2006.04185.x

Cited by 19 publications

(19 citation statements)

References 44 publications

(124 reference statements)

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“…Only by the creation of ternary complexes between Kv4s, KChIPs and DPLs can other characteristic I SA functional properties such as rapid activation and rapid inactivation be reconstituted (Nadal et al, 2003;Jerng et al, 2005). The physiological significance of these observations are supported by gene knock-out, dominant negative, RNA interference, and coimmunoprecipitation studies that suggest that these three proteins are all part of the native channel complex responsible for producing I SA (Malin and Nerbonne, 2000;Nadal et al, 2003;Jerng et al, 2005;Hu et al, 2006;Lauver et al, 2006).…”

Section: Introductionsupporting

confidence: 52%

DPP10 splice variants are localized in distinct neuronal populations and act to differentially regulate the inactivation properties of Kv4-based ion channels

Jerng

Lauver

Pfaffinger

2007

Molecular and Cellular Neuroscience

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Dipeptidyl peptidase-like proteins (DPLs) and Kv-channel interacting proteins (KChIPs) join Kv4 pore-forming subunits to form multi-protein complexes that underlie subthreshold A-type currents (I SA ) in neuronal somatodendritic compartments. Here, we characterize the functional effects and brain distributions of N-terminal variants belonging to the DPL dipeptidyl peptidase 10 (DPP10). In the Kv4.2+KChIP3+DPP10 channel complex, all DPP10 variants accelerate channel gating kinetics; however, the splice variant DPP10a produces uniquely fast inactivation kinetics that accelerates with increasing depolarization. This DPP10a-specific inactivation dominates in coexpression studies with KChIP4a and other DPP10 isoforms. Real-time qRT-PCR and in situ hybridization analyses reveal differential expression of DPP10 variants in rat brain. DPP10a transcripts are prominently expressed in the cortex, whereas DPP10c and DPP10d mRNAs exhibit more diffuse distributions. Our results suggest that DPP10a underlies rapid inactivation of cortical I SA , and the regulation of isoform expression may contribute to the variable inactivation properties of I SA across different brain regions.

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Section: Introductionsupporting

confidence: 52%

DPP10 splice variants are localized in distinct neuronal populations and act to differentially regulate the inactivation properties of Kv4-based ion channels

Jerng

Lauver

Pfaffinger

2007

Molecular and Cellular Neuroscience

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“…Somatodendritic IA current performs a pivotal function in synaptic integration and synaptic plasticity, by modulating membrane excitability or by inhibiting the back-propagation of dendritic APs (3-7). Kv4.2, a pore-forming α-subunit of voltage-gated A-type potassium channels, is expressed abundantly within the soma and dendrites of hippocampal neurons (8)(9)(10)(11), and is responsible for most of the somatodendritic IA current (7,(11)(12)(13) -dependent down-regulation of Kv4.2 channels in the membrane surfaces of hippocampal neurons (14,15).…”

Section: Introductionmentioning

confidence: 99%

Dendritic localization and a cis-acting dendritic targeting element of Kv4.2 mRNA

Nam²,

Oh³

et al. 2010

BMB Reports

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Kv4.2, a pore-forming α-subunit of voltage-gated A-type potassium channels, is expressed abundantly in the soma and dendrites of hippocampal neurons, and is responsible for somatodendritic IA current. Recent studies have suggested that changes in the surface levels of Kv4.2 potassium channels might be relevant to synaptic plasticity. Although the function and expression of Kv4.2 protein have been extensively studied, the dendritic localization of Kv4.2 mRNA is not well described. In this study, Kv4.2 mRNAs were shown to be localized in the dendrites near postsynaptic regions. The dendritic transport of Kv4.2 mRNAs were mediated by microtubule-based movement. The 500 nucleotides of specific regions within the 3'-untranslated region of Kv4.2 mRNA were found to be necessary and sufficient for its dendritic localization. Collectively, these results suggest that the dendritic localization of Kv4.2 mRNAs might regulate the dendritic surface level of Kv4.2 channels and synaptic plasticity. [BMB reports 2010; 43(10): 677-682]

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“…Neuromodulators strongly regulate these channels through phosphorylation, association with auxiliary subunits, and expression-level control. A-type potassium channels modulate the action potential broadening, b-AP (backpropagation of action potentials), spike generation, and integration of synaptic inputs (Ramakers and Storm 2002;Watanabe et al 2002;Yuan et al 2002;Birnbaum et al 2004;Lauver et al 2006;Hammond et al 2008;Kim and Hoffman 2008). Among the A-type potassium channels, the Kv4 channels adjust dendritic function by limiting spike-timing-dependent plasticity.…”

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confidence: 99%

Kv4 potassium channels modulate hippocampal EPSP-spike potentiation and spatial memory in rats

Truchet¹,

Manrique²,

Sréng³

et al. 2012

Learn. Mem.

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Kv4 channels regulate the backpropagation of action potentials (b-AP) and have been implicated in the modulation of longterm potentiation (LTP). Here we showed that blockade of Kv4 channels by the scorpion toxin AmmTX3 impaired reference memory in a radial maze task. In vivo, AmmTX3 intracerebroventricular (i.c.v.) infusion increased and stabilized the EPSP-spike (E-S) component of LTP in the dentate gyrus (DG), with no effect on basal transmission or short-term plasticity. This increase in E-S potentiation duration could result from the combination of an increase in excitability of DG granular cells with a reduction of GABAergic inhibition, leading to a strong reduction of input specificity. Radioactive in situ hybridization (ISH) was used to evaluate the amounts of Kv4.2 and Kv4.3 mRNA in brain structures at different stages of a spatial learning task in naive, pseudoconditioned, and conditioned rats. Significant differences in Kv4.2 and Kv4.3 mRNA levels were observed between conditioned and pseudoconditioned rats. Kv4.2 and Kv4.3 mRNA levels were transiently up-regulated in the striatum, nucleus accumbens, retrosplenial, and cingulate cortices during early stages of learning, suggesting an involvement in the switch from egocentric to allocentric strategies. Spatial learning performance was positively correlated with the levels of Kv4.2 and Kv4.3 mRNAs in several of these brain structures. Altogether our findings suggest that Kv4 channels could increase the signal-to-noise ratio during information acquisition, thereby allowing a better encoding of the memory trace.

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Manipulating Kv4.2 identifies a specific component of hippocampal pyramidal neuron A‐current that depends upon Kv4.2 expression

Cited by 19 publications

References 44 publications

DPP10 splice variants are localized in distinct neuronal populations and act to differentially regulate the inactivation properties of Kv4-based ion channels

DPP10 splice variants are localized in distinct neuronal populations and act to differentially regulate the inactivation properties of Kv4-based ion channels

Dendritic localization and a cis-acting dendritic targeting element of Kv4.2 mRNA

Kv4 potassium channels modulate hippocampal EPSP-spike potentiation and spatial memory in rats

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