ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Inward-rectifying potassium (Kir) channels regulate pacemaker activity in spinal nociceptive circuits during early life.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Activation of mu-opioid receptors slows pacemaking in hypothalamic A11 dopamine neurons.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Preclinical Insights into the Role of Kir4.1 in Chronic Pain and Depression: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- An electrophysiologist's guide to dorsal horn excitability and pain.Frontiers in cellular neuroscience · 2025Review
- Noise or signal? Spontaneous activity of dorsal horn neurons: patterns and function in health and disease.Pflugers Archiv : European journal of physiology · 2024Review
- Intrinsic burst-firing in lamina I spinoparabrachial neurons during adolescence.Neuroscience letters · 2021Article
- The development of pain circuits and unique effects of neonatal injury.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Article
- Kir2.1 Channel Regulation of Glycinergic Transmission Selectively Contributes to Dynamic Mechanical Allodynia in a Mouse Model of Spared Nerve Injury.Neuroscience bulletin · 2019Article
- AThe Journal of general physiology · 2018Article
- Article
- Origin and classification of spontaneous discharges in mouse superficial dorsal horn neurons.Scientific reports · 2018Article
- Potassium channel dysfunction underlies Purkinje neuron spiking abnormalities in spinocerebellar ataxia type 2.Human molecular genetics · 2017Article
- Inward-rectifying KNeuroscience · 2016Article
- Neuronal Atrophy Early in Degenerative Ataxia Is a Compensatory Mechanism to Regulate Membrane Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Connectivity of pacemaker neurons in the neonatal rat superficial dorsal horn.The Journal of comparative neurology · 2015Article
- Strain differences in pH-sensitive K+ channel-expressing cells in chemosensory and nonchemosensory brain stem nuclei.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Age-dependent sensitization of cutaneous nociceptors during developmental inflammation.Molecular pain · 2014Article
- Pacemaker Neurons and the Development of Nociception.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2014Review
- Neonatal tissue injury reduces the intrinsic excitability of adult mouse superficial dorsal horn neurons.Neuroscience · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pacemaker neurons in neonatal spinal nociceptive circuits generate intrinsic burst firing and are distinguished by a lower "leak" membrane conductance compared with adjacent nonbursting neurons. However, little is known about which subtypes of leak channels regulate the level of pacemaker activity within the developing rat superficial dorsal horn (SDH). Here we demonstrate that a hallmark feature of lamina I pacemaker neurons is a reduced conductance through inward-rectifying potassium (K(ir)) channels at physiological membrane potentials. Differences in the strength of inward rectification between pacemakers and nonpacemakers indicate the presence of functionally distinct K(ir) currents in these two populations at room temperature. However, K(ir) currents in both groups showed high sensitivity to block by extracellular Ba²⁺ (IC₅₀ ~ 10 μm), which suggests the presence of "classical" K(ir) (K(ir)2.x) channels in the neonatal SDH. The reduced K(ir) conductance within pacemakers is unlikely to be explained by an absence of particular K(ir)2.x isoforms, as immunohistochemical analysis revealed the expression of K(ir)2.1, K(ir)2.2, and K(ir)2.3 within spontaneously bursting neurons. Importantly, Ba²⁺ application unmasked rhythmic burst firing in ∼42% of nonbursting lamina I neurons, suggesting that pacemaker activity is a latent property of a sizeable population of SDH cells during early life. In addition, the prevalence of spontaneous burst firing within lamina I was enhanced in the presence of high internal concentrations of free Mg²⁺, consistent with its documented ability to block K(ir) channels from the intracellular side. Collectively, the results indicate that K(ir) channels are key modulators of pacemaker activity in newborn central pain networks.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.