ArticleThe Journal of physiology2003
PKA-mediated inhibition of a novel K+ channel underlies the slow after-hyperpolarization in enteric AH neurons.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 43 citations in OpenAlex.
- Endoplasmic Reticulum and Mitochondrial Calcium Handling Dynamically Shape Slow Afterhyperpolarizations in Vasopressin Magnocellular Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Asprosin promotes feeding through SK channel-dependent activation of AgRP neurons.Science advances · 2023Article
- PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice.Communications biology · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Histamine, histamine receptors, and neuropathic pain relief.British journal of pharmacology · 2020Review
- Cholera Toxin Induces Sustained Hyperexcitability in Myenteric, but Not Submucosal, AH Neurons in Guinea Pig Jejunum.Frontiers in physiology · 2017Article
- Assessing the role of IKCa channels in generating the sAHP of CA1 hippocampal pyramidal cells.Channels (Austin, Tex.) · 2016Article
- Depressed perivascular sensory innervation of mouse mesenteric arteries with advanced age.The Journal of physiology · 2016Article
- PKA reduces the rat and human KCa3.1 current, CaM binding, and Ca2+ signaling, which requires Ser332/334 in the CaM-binding C terminus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- β₁-Adrenoceptor stimulation suppresses endothelial IK(Ca)-channel hyperpolarization and associated dilatation in resistance arteries.British journal of pharmacology · 2013Article
- Lactobacillus reuteri enhances excitability of colonic AH neurons by inhibiting calcium-dependent potassium channel opening.Journal of cellular and molecular medicine · 2009Article
- Modulation of endothelial cell KCa3.1 channels during endothelium-derived hyperpolarizing factor signaling in mesenteric resistance arteries.Circulation research · 2008Article
- cAMP response element-binding protein-mediated gene expression increases the intrinsic excitability of CA1 pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postspike after-hyperpolarizations (AHPs) control the excitability of neurons and are important in shaping firing patterns. The duration of some of these events extends to tens of seconds and they can render neurons inexcitable for much of their time course. While consensus is strong that the medium duration (< 1 s AHPs are mediated by the opening of small conductance Ca2+-activated K+ channels, the K+ channels mediating slow AHPs (> 5 s in a subset of enteric (AH) neurons) have an intermediate unit conductance (IKCa). Using whole-cell and excised-patch recording, we have demonstrated that the cAMP-protein kinase A (PKA) pathway regulates the activity of these channels. In whole-cell mode, forskolin (0.003-1 microM) inhibited the current underlying the slow AHP (IsAHP) by 90 %, and this was partially sensitive to inhibition of PKA with internal Rp-cAMPS (500 microM). Rp-cAMPS alone increased the current following break-in and caused a 20 mV hyperpolarization, suggesting that PKA maintains slow AHP channels in the closed state. Internal perfusion of the inhibitory peptide PKI5-24 slightly increased the IsAHP and opposed the inhibitory action of forskolin. Internal perfusion of the catalytic subunit of PKA (PKAcat) suppressed the IsAHP by 50 % without affecting membrane potential or action potential configuration. In inside-out patches containing IKCa-like channels, PKAcat decreased the open probability of IKCa-like channels while alkaline phosphatase activated them. These results suggest that the IKCa-like channels that underlie the slow AHP in myenteric AH neurons are subject to inhibition by PKA-dependent phosphorylation and that PKA plays an integral role in their gating.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.