ArticleBritish journal of pharmacology2002
Pharmacological characterization of a non-inactivating outward current observed in mouse cerebellar Purkinje neurones.
Article in British journal of pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A review of the neural mechanisms of action and clinical efficiency of riluzole in treating amyotrophic lateral sclerosis: what have we learned in the last decade?CNS neuroscience & therapeutics · 2011Pooled it
- Purkinje cell models: past, present and future.Frontiers in computational neuroscience · 2024Review
- Regulation of the two-pore domain potassium channel, THIK-1 and THIK-2, by G protein coupled receptors.PloS one · 2023Article
- Contribution of K2P Potassium Channels to Cardiac Physiology and Pathophysiology.International journal of molecular sciences · 2021Review
- Ion channel dysfunction in cerebellar ataxia.Neuroscience letters · 2019Review
- Adenosine AThe Journal of physiology · 2018Article
- Activation of TREK currents by riluzole in three subgroups of cultured mouse nodose ganglion neurons.PloS one · 2018Article
- Potassium channel dysfunction underlies Purkinje neuron spiking abnormalities in spinocerebellar ataxia type 2.Human molecular genetics · 2017Article
- 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
- Much more than a leak: structure and function of K₂p-channels.Pflugers Archiv : European journal of physiology · 2015Review
- The role of two-pore-domain background K⁺ (K₂p) channels in the thalamus.Pflugers Archiv : European journal of physiology · 2015Review
- THIK-1 (K2P13.1) is a small-conductance background K(+) channel in rat trigeminal ganglion neurons.Pflugers Archiv : European journal of physiology · 2014Article
- Activation of TREK currents by the neuroprotective agent riluzole in mouse sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Anesthetic activation of central respiratory chemoreceptor neurons involves inhibition of a THIK-1-like background K(+) current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Advances in imaging of new targets for pharmacological intervention in stroke: real-time tracking of T-cells in the ischaemic brain.British journal of pharmacology · 2010Article
- Article
- Maturation of rat cerebellar Purkinje cells reveals an atypical Ca2+ channel current that is inhibited by omega-agatoxin IVA and the dihydropyridine (-)-(S)-Bay K8644.The Journal of physiology · 2007Article
- Neuronal two-pore-domain potassium channels and their regulation by G protein-coupled receptors.The Journal of physiology · 2007Review
- GABA mediates autoreceptor feedback inhibition in the rat carotid body via presynaptic GABAB receptors and TASK-1.The Journal of physiology · 2003Article
- Hipnic modulation of cerebellar information processing: implications for the cerebro-cerebellar dialogue.Cerebellum (London, England) · 2003Review
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Abstract
Whole-cell patch clamp recordings were used to investigate the properties of a non-inactivating outward current observed in mouse cerebellar Purkinje neurones at a holding potential of -20 mV. Increasing the external potassium (K(+)) concentration from 3 mM to 20 mM produced a rightward shift in the observed reversal potential of approximately 30 mV or approximately 40 mV for a K(+)-or a caesium (Cs(+))-based intracellular solution respectively, indicating the outward current was a K(+) current. The outward current was partially inhibited by the K(+) channel blocker, tetraethylammonium (TEA; IC(50)=0.15 mM). Subsequently, the background or TEA-insensitive current was measured in the presence of 1 mM TEA. The background current was reversibly inhibited by barium (Ba(2+); 300 microM, 50%) and potentiated by the application of arachidonic acid (AA; 1 mM, 62%). The volatile anaesthetic, halothane (1 mM), and the neuroprotectant, riluzole (500 microM), both reversibly inhibited the background current by 54% and 36% respectively. The background current was insensitive to changes in both intracellular and extracellular acidification. The GABA(B) and mu-opioid receptor agonists, baclofen and [D-Ala(2), N-MePhe(4)-Gly-ol(5)] enkephalin (DAMGO) both reversibly potentiated the outward current by 42% and 26% respectively. In contrast, the metabotropic glutamate receptor and acetylcholine receptor agonists, (S)-3,5-dihydroxyphenylglycine (DHPG) and muscarine both reversibly inhibited the outward current by 48% and 42% respectively. These data suggest that cerebellar Purkinje neurones possess a background current which shares several properties with recently cloned two-pore K(+) channels, particularly THIK-1.
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