ArticleBrain research2007
ATP-sensitive potassium currents reduce the PGE2-mediated enhancement of excitability in adult rat sensory neurons.
Article in Brain research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Meningeal K ATP channels contribute to behavioral responses in preclinical migraine models.Pain · 2025Article
- Nitrergic modulation of ion channel function in regulating neuronal excitability.Channels (Austin, Tex.) · 2021Article
- Loss of SUR1 subtype KBehavioural brain research · 2021Article
- Molecular biochemical aspects of salt (sodium chloride) in inflammation and immune response with reference to hypertension and type 2 diabetes mellitus.Lipids in health and disease · 2021Review
- Modulation of SUR1 KInternational journal of molecular sciences · 2019Article
- Morphine Efficacy, Tolerance, and Hypersensitivity Are Altered After Modulation of SUR1 Subtype KFrontiers in neuroscience · 2019Article
- Dissociation between CSD-Evoked Metabolic Perturbations and Meningeal Afferent Activation and Sensitization: Implications for Mechanisms of Migraine Headache Onset.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Profound alteration in cutaneous primary afferent activity produced by inflammatory mediators.eLife · 2016Article
- Antinociceptive effects of hydroalcoholic extract from Euterpe oleracea Mart. (Açaí) in a rodent model of acute and neuropathic pain.BMC complementary and alternative medicine · 2015Article
- Blockade of ATP-sensitive potassium channels prevents the attenuation of the exercise pressor reflex by tempol in rats with ligated femoral arteries.American journal of physiology. Heart and circulatory physiology · 2012Article
- Stimulation of peripheral kappa opioid receptors inhibits inflammatory hyperalgesia via activation of the PI3Kγ/AKT/nNOS/NO signaling pathway.Molecular pain · 2012Article
- Activation of ATP-sensitive potassium channels antagonize nociceptive behavior and hyperexcitability of DRG neurons from rats.Molecular pain · 2011Article
- Sex differences in the contribution of ATP-sensitive K+ channels in trigeminal ganglia under an acute muscle pain condition.Neuroscience · 2011Article
- Morphine peripheral analgesia depends on activation of the PI3Kgamma/AKT/nNOS/NO/KATP signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Regulation of N-type voltage-gated calcium channels (Cav2.2) and transmitter release by collapsin response mediator protein-2 (CRMP-2) in sensory neurons.Journal of cell science · 2009Article
- Nitric oxide activates ATP-sensitive potassium channels in mammalian sensory neurons: action by direct S-nitrosylation.Molecular pain · 2009Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Behavioral studies have shown that the hyperalgesia arising from inflammatory agents, such as prostaglandin E(2) (PGE(2)), can be antagonized by activators of the ATP-sensitive potassium current (K(ATP)). This observation raises questions as to whether this suppression results from a direct action on sensory neurons and what are the cellular mechanisms giving rise to this inhibition. We found that small to medium diameter sensory neurons isolated from the L4-6 DRGs expressed the mRNAs for Kir6.1, Kir6.2, and SUR1. In perforated-patch clamp recordings from acutely dissociated sensory neurons from the young adult rat, exposure to 300 microM diazoxide, a K(ATP) channel agonist, significantly hyperpolarized the resting membrane potential, reduced the number of action potentials evoked by a ramp of depolarizing current, and increased the amplitude of inward K(ATP) currents evoked by the voltage ramp. Similar results were obtained with the protonophore FCCP, which is known to reduce the levels of intracellular ATP and lead to the activation of K(ATP). Only a subpopulation of sensory neurons was sensitive to diazoxide whereas other neurons were unaffected. Treatment with 1 microM PGE(2) significantly enhanced the excitability of these small to medium diameter capsaicin-sensitive sensory neurons; this enhancement was reversed by subsequent exposure to diazoxide in a subpopulation of neurons. Similar to diazoxide, exposure to 8-Br-cyclic GMP antagonized the PGE(2)-induced increase in excitability. The effects of 8-Br-cyclic GMP could be reversed by exposure to glibenclamide, an antagonist of K(ATP) channels. As with diazoxide, only a subpopulation of sensory neurons were affected by 8-Br-cyclic GMP. These results demonstrate that activation of K(ATP) can reverse the sensitization produced by PGE(2) and may be an important means to modulate the enhanced excitability that results from inflammatory or injury conditions.
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