ArticleBritish journal of pharmacology2002
Rapid neuromodulation by cortisol in the rat paraventricular nucleus: an in vitro study.
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 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 53 citations in OpenAlex.
- Glucocorticoids Selectively Inhibit Hippocampal CA1 Pyramidal Neurons Activity Through HCN Channels.International journal of molecular sciences · 2024Article
- Glucocorticoids Rapidly Modulate CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Mechanistic insights regarding neuropsychiatric and neuropathologic impacts of air pollution.Critical reviews in toxicology · 2024Review
- Glucocorticoids modulate neural activity via a rapid non-genomic effect on Kv2.2 channels in the central nervous system.Neurobiology of stress · 2024Article
- Ion Channels in the Paraventricular Hypothalamic Nucleus (PVN); Emerging Diversity and Functional Roles.Frontiers in physiology · 2018Review
- Cellular Mechanisms of Cortisol-Induced Changes in Mauthner-Cell Excitability in the Startle Circuit of Goldfish.Frontiers in neural circuits · 2017Article
- TRPV4 and K(Ca) ion channels functionally couple as osmosensors in the paraventricular nucleus.British journal of pharmacology · 2015Article
- GABAA receptor-acting neurosteroids: a role in the development and regulation of the stress response.Frontiers in neuroendocrinology · 2015Review
- The depressor response to intracerebroventricular hypotonic saline is sensitive to TRPV4 antagonist RN1734.Frontiers in pharmacology · 2015Article
- Dysfunctional astrocytic and synaptic regulation of hypothalamic glutamatergic transmission in a mouse model of early-life adversity: relevance to neurosteroids and programming of the stress response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Function and pharmacology of spinally-projecting sympathetic pre-autonomic neurones in the paraventricular nucleus of the hypothalamus.Current neuropharmacology · 2011Article
- Two emerging concepts for elite athletes: the short-term effects of testosterone and cortisol on the neuromuscular system and the dose-response training role of these endogenous hormones.Sports medicine (Auckland, N.Z.) · 2011Review
- Assessing the neuroendocrine stress response in the functional neuroimaging context.NeuroImage · 2009Review
- Minireview: rapid glucocorticoid signaling via membrane-associated receptors.Endocrinology · 2006Review
- Inhibition by alpha-tetrahydrodeoxycorticosterone (THDOC) of pre-sympathetic parvocellular neurones in the paraventricular nucleus of rat hypothalamus.British journal of pharmacology · 2006Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We have used a range of in vitro electrophysiological techniques to investigate the mechanism of rapid cortisol neuromodulation of parvocellular neurones in the rat paraventricular nucleus. 2. In our study, we found that cortisol (10 microM) increased spontaneous action-current firing frequency to 193%. This effect was insensitive to the glucocorticoid intracellular-receptor antagonist mifepristone. 3. Cortisol (0.1-10 microM) had no detectable effects on whole-cell GABA current amplitudes, or GABA(A) single-channel kinetics. 4. Cortisol (10 microM) inhibited whole-cell potassium currents in parvocellular neurones by shifting the steady-state activation curve by 14 mV to the right. 5. Additionally, in a cell line expressing both the glucocorticoid intracellular receptor and recombinant, fast inactivating potassium channels (hKv1.3), cortisol (1 and 10 microM) inhibited potassium currents by shifting their steady-state activation curves to the right by 12 mV (10 microM cortisol). This effect was also insensitive to the cortisol antagonist, mifepristone. 6. These data suggest that inhibition of voltage-gated potassium channels may contribute to the rapid neuromodulatory effects of cortisol, possibly by direct interaction with the ion channel itself.
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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.