ArticleThe Journal of physiology1993
Sulphonylureas reduce the slowly inactivating D-type outward current in rat hippocampal neurons.
Article in The Journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 36 citations in OpenAlex.
- Hydrogen peroxide inhibits neurons in the paraventricular nucleus of the hypothalamus via potassium channel activation.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
- KATP channels modulate intrinsic firing activity of immature entorhinal cortex layer III neurons.Frontiers in cellular neuroscience · 2014Article
- Pinacidil induces vascular dilation and hyperemia in vivo and does not impact biophysical properties of neurons and astrocytes in vitro.Cleveland Clinic journal of medicine · 2009Article
- Partial mitochondrial inhibition causes striatal dopamine release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Endogenous hydrogen peroxide regulates the excitability of midbrain dopamine neurons via ATP-sensitive potassium channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Changes in [Ca2+]i and membrane currents during impaired mitochondrial metabolism in dissociated rat hippocampal neurons.The Journal of physiology · 1998Article
- ATP-sensitive K+ channels are functional in expiratory neurones of normoxic cats.The Journal of physiology · 1996Article
- KATP channel mediation of anoxia-induced outward current in rat dorsal vagal neurons in vitro.The Journal of physiology · 1995Article
- Ionic currents and inhibitory effects of glibenclamide in seminal vesicle smooth muscle cells.British journal of pharmacology · 1995Article
- Metabolic inhibition and low internal ATP activate K-ATP channels in rat dopaminergic substantia nigra neurones.Pflugers Archiv : European journal of physiology · 1995Article
- Subgroups among mu-opioid receptor agonists distinguished by ATP-sensitive K+ channel-acting drugs.British journal of pharmacology · 1995Article
- Calcium-dependent, slowly inactivating potassium currents in cultured neurons of rat neocortex.Experimental brain research · 1995Article
- Effect of cromakalim and glibenclamide on spontaneous and evoked motility of the guinea-pig isolated renal pelvis and ureter.British journal of pharmacology · 1994Article
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. Using intracellular recording in hippocampal slices, we have examined, in CA3 pyramidal neurons, the effects of sulphonylureas (blockers of ATP-sensitive K+ channels) on the slowly inactivating D-type K+ current (ID). 2. In the presence of TTX (1 microM) to block Na+ currents, ID had the following characteristics: activation by large depolarizing pulses from membrane potentials negative to -75 mV, slow inactivation kinetics, high sensitivity to 4-aminopyridine (4-AP, 3-40 microM), insensitivity to tetraethylammonium (TEA, 10 mM), Cs+ (3 mM) and carbachol (50 microM). 3. Applications of glibenclamide (10 microM) did not modify the input conductance of the cell, but reduced the amplitude of ID by 31.2 +/- 5.6% (n = 16), without altering its voltage dependence and inactivation kinetics. The effects were usually reversible. 4. Glibenclamide also reduced ID in the presence of TEA (10 mM), Cs+ (3 mM) and carbachol (50 microM), to block several K+ currents (IK, IC, IQ, IM), as well as kynurenate (1 mM) and bicuculline (10 microM) to block on-going synaptic currents mediated by activation of non-NMDA (N-methyl-D-aspartate) and GABA (gamma-aminobutyrate)-A receptors, respectively. 5. Comparable depressions of ID were produced by two other sulphonylureas: gliquidone (10 microM), 42.6 +/- 7.9% (n = 13) and tolbutamide (500 microM), 39.1 +/- 12.8 (n = 8). 6. It is concluded that, in the central nervous system, sulphonylureas can modulate K+ currents which are not generated by ATP-sensitive K+ channels.
Indexed as
Identifiers
8410699PMC1175465W2149462569What 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.