ArticleBrain research bulletin2009
Endothelin-1 raises excitability and reduces potassium currents in sensory neurons.
Article in Brain research bulletin, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Sympathetic Nerve Activity and Blood Pressure Response to Exercise in Peripheral Artery Disease: From Molecular Mechanisms, Human Studies, to Intervention Strategy Development.International journal of molecular sciences · 2022Review
- The Involvement of Endothelin Pathway in Chronic Psychological Stress-Induced Bladder Hyperalgesia Through Capsaicin-Sensitive C-Fiber Afferents.Journal of inflammation research · 2022Article
- Endothelin-1 enhances acid-sensing ion channel currents in rat primary sensory neurons.Acta pharmacologica Sinica · 2020Article
- Endothelin type A receptors mediate pain in a mouse model of sickle cell disease.Haematologica · 2018Article
- Endothelin-1 Decreases Excitability of the Dorsal Root Ganglion Neurons via ETMolecular neurobiology · 2018Article
- Reduced excitability of gp130-deficient nociceptors is associated with increased voltage-gated potassium currents and Kcna4 channel upregulation.Pflugers Archiv : European journal of physiology · 2014Article
- Endothelin-1 induced desensitization in primary afferent neurons.Neuroscience letters · 2014Article
- Article
- Evidence for the endothelin system as an emerging therapeutic target for the treatment of chronic pain.Journal of pain research · 2014Review
- ET-1 induced Elevation of intracellular calcium in clonal neuronal and embryonic kidney cells involves endogenous endothelin-A receptors linked to phospholipase C through Gα(q/11).Pharmacological research · 2011Article
- New perspectives on the endothelin axis in pain.Pharmacological research · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Exposure to endothelin-1 (ET-1, 50 nM) of sensory neurons, acutely isolated from rat dorsal root ganglia (DRG), results in an increase in the number of action potentials elicited by a linear ramp of stimulating current. The changes are complete in 5 min after ET-1 treatment and do not reverse in 5-10 min after ET-1's removal. Neither the resting potential, nor the threshold potential for the first or second action potentials, nor their rate-of-rise or decay, are changed by ET-1 exposure, but the slow depolarizations which occur before the first and second action potentials during the current ramp are increased by ca. 50% by ET-1. The delayed rectifier type of K(+) currents (I(K)), measured under whole-cell voltage clamp, are depressed by approximately 30% during such exposure to ET-1. The voltage-dependent gating of steady-state I(K) and the current kinetics are unchanged by ET-1, leaving the sole effect as a drop in the number of available channels. I(K) is affected by ET-1 only in Isolectin B(4)-positive cells, suggesting that there may be a selective action in enhancing impulse activity on this class of nociceptive neuron. This decrease in I(K) will potentiate the excitability-inducing actions of the previously reported negative shift in tetrodotoxin-resistant Na(+) channel gating in such neurons.
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Registered trials
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