ArticleThe Journal of physiology1996
ATP-sensitive K+ channels are functional in expiratory neurones of normoxic cats.
Article in The Journal of physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 39 citations in OpenAlex.
- Caloric Restriction and Ketogenic Diet Therapy for Epilepsy: A Molecular Approach InvolvingFrontiers in neurology · 2020Review
- Functional characterization of ABCC9 variants identified in sudden unexpected natural death.Forensic science international · 2019Article
- The role of KActa pharmacologica Sinica · 2018Review
- Modulation of Excitability of Stellate Neurons in the Ventral Cochlear Nucleus of Mice by ATP-Sensitive Potassium Channels.The Journal of membrane biology · 2018Article
- BAD and KeLife · 2018Article
- Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia.Acta pharmacologica Sinica · 2013Review
- Single K ATP channel opening in response to action potential firing in mouse dentate granule neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Stimulation of neuronal KATP channels by cGMP-dependent protein kinase: involvement of ROS and 5-hydroxydecanoate-sensitive factors in signal transduction.American journal of physiology. Cell physiology · 2010Article
- Outward Currents Contributing to Inspiratory Burst Termination in preBötzinger Complex Neurons of Neonatal Mice Studied in Vitro.Frontiers in neural circuits · 2010Article
- 4-Aminopyridine-sensitive outward currents in preBötzinger complex neurons influence respiratory rhythm generation in neonatal mice.The Journal of physiology · 2008Article
- The effects induced by the sulphonylurea glibenclamide on the neonatal rat spinal cord indicate a novel mechanism to control neuronal excitability and inhibitory neurotransmission.British journal of pharmacology · 2007Article
- Activation of ATP-sensitive K+ (K(ATP)) channels by H2O2 underlies glutamate-dependent inhibition of striatal dopamine release.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Sensory afferent selective role of P2 receptors in the nucleus tractus solitarii for mediating the cardiac component of the peripheral chemoreceptor reflex in rats.The Journal of physiology · 2002Article
- Dynamic activation of K(ATP) channels in rhythmically active neurons.The Journal of physiology · 2001Article
- Potentiation of quantal catecholamine secretion by glibenclamide: evidence for a novel role of sulphonylurea receptors in regulating the Ca(2+) sensitivity of exocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Neurotransmitters and neuromodulators controlling the hypoxic respiratory response in anaesthetized cats.The Journal of physiology · 1999Article
- Hypoxia activates ATP-dependent potassium channels in inspiratory neurones of neonatal mice.The Journal of physiology · 1998Article
- Hypoxic response of hypoglossal motoneurones in the in vivo cat.The Journal of physiology · 1997Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We analysed spontaneously active expiratory neurones (n = 48) of anaesthetized cats for the presence of ATP-sensitive K+ (KATP) channels. 2. Intracellular injection of ATP reversibly depolarized neurones during all phases of the respiratory cycle. During expiration, membrane potential depolarized by an average of 1.5 +/- 0.1 mV leading to a 25% increase of discharge frequency. During inspiration, ATP induced a 1.8 +/- 0.2 mV depolarization, which was accompanied by a maximum of 20% increase of input resistance (Rn). 3. Extracellular application of diazoxide, an agonist of KATP channels, resulted in reversible membrane hyperpolarization in 68% of neurones (n = 19). This hyperpolarization (2.5 mV during expiration and 3.1 mV during inspiration) was accompanied by a 22% decrease in Rn. 4. Extracellular application of tolbutamide and glibenclamide, two antagonists of KATP channels, evoked reversible depolarizations in 76% of neurones (n = 21). The depolarization was relatively constant throughout the respiratory cycle (1.4 mV during expiration and 2.3 mV during inspiration). Rn increased by 22%. 5. The same sulphonylureas also changed the steepness of membrane depolarization when neurones escaped spontaneous synaptic inhibition during postinspiration. Extracellularly applied tolbutamide and glibenclamide increased the steepness of depolarization by 21%, while diazoxide reduced it by 20%. 6. Antagonism of drugs was verified by simultaneous extra- and intracellular application of diazoxide and glibenclamide, respectively. 7. During voltage clamp at holding potential at -60 to -67 mV, intracellular or extracellular application of tolbutamide and glibenclamide blocked a persistent outward current. 8. We conclude that KATP channels are functional in expiratory neurones of adult cats and contribute to the control of excitability even during normoxia.
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.