ArticleThe Journal of physiology1997
Mechanism underlying corticotropin-releasing hormone (CRH) triggered cytosolic Ca2+ rise in identified rat corticotrophs.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 65 citations in OpenAlex.
- Expression and Role of Thyrotropin Receptors in Proopiomelanocortin-Producing Pituitary Cells.Thyroid : official journal of the American Thyroid Association · 2021Article
- The Mechanisms Underlying Autonomous Adrenocorticotropic Hormone Secretion in Cushing's Disease.International journal of molecular sciences · 2020Review
- Neurotransmitter receptors as signaling platforms in anterior pituitary cells.Molecular and cellular endocrinology · 2018Review
- Modeling the diversity of spontaneous and agonist-induced electrical activity in anterior pituitary corticotrophs.Journal of neurophysiology · 2017Article
- Heterogeneity of Calcium Responses to Secretagogues in Corticotrophs From Male Rats.Endocrinology · 2017Article
- Review
- Spontaneous and CRH-Induced Excitability and Calcium Signaling in Mice Corticotrophs Involves Sodium, Calcium, and Cation-Conducting Channels.Endocrinology · 2016Article
- Large conductance Ca²⁺-activated K⁺ (BK) channels promote secretagogue-induced transition from spiking to bursting in murine anterior pituitary corticotrophs.The Journal of physiology · 2015Article
- Sex-specific cell signaling: the corticotropin-releasing factor receptor model.Trends in pharmacological sciences · 2013Review
- B-Raf and CRHR1 internalization mediate biphasic ERK1/2 activation by CRH in hippocampal HT22 Cells.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Activation of CRH receptor type 1 expressed on glutamatergic neurons increases excitability of CA1 pyramidal neurons by the modulation of voltage-gated ion channels.Frontiers in cellular neuroscience · 2013Article
- Dependence of the excitability of pituitary cells on cyclic nucleotides.Journal of neuroendocrinology · 2012Review
- The expression and role of hyperpolarization-activated and cyclic nucleotide-gated channels in endocrine anterior pituitary cells.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Control of hypothalamic-pituitary-adrenal stress axis activity by the intermediate conductance calcium-activated potassium channel, SK4.The Journal of physiology · 2011Article
- Role of nonselective cation channels in spontaneous and protein kinase A-stimulated calcium signaling in pituitary cells.American journal of physiology. Endocrinology and metabolism · 2011Article
- Reciprocal regulation of TREK-1 channels by arachidonic acid and CRH in mouse corticotropes.Endocrinology · 2011Article
- Ion channels and signaling in the pituitary gland.Endocrine reviews · 2010Review
- CRF facilitates calcium release from intracellular stores in midbrain dopamine neurons.Neuron · 2008Article
- Patterning of endocytic vesicles and its control by voltage-gated Na+ channel activity in rat prostate cancer cells: fractal analyses.European biophysics journal : EBJ · 2004Article
- Endocytosis in identified rat corticotrophs.The Journal of physiology · 2001Article
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. The patch-clamp technique was used in conjunction with the fluorescent Ca2+ indicator indo-1 to measure simultaneously cytosolic Ca2+ concentration ([Ca2+]i) and membrane potential in single rat corticotrophs identified with the reverse haemolytic plaque assay. 2. Application of the adrenocorticotropin (ACTH) secretagogue, corticotropin-releasing hormone (CRH), triggered a sustained [Ca2+]i elevation and membrane depolarization. 3. The CRH action was mediated via the cAMP-dependent protein kinase cascade. Both the CRH-induced depolarization and [Ca2+]i elevation could be mimicked by extracellular application of the adenylate cyclase activator forskolin or the membrane-permeable cAMP analogue, 8-(4-chlorophenylthio)-adenosine-3',5'-cyclic monophosphate (8-CPT-cAMP). Intracellular adenosine cyclic 3',5'-(Rp)-phosphothioate (Rp-cAMPS), a protein kinase A inhibitor, abolished the CRH effects. 4. Voltage-clamp studies suggest that the CRH-triggered depolarization was due to the reduction of background K+ conductances. The CRH-sensitive current was Ca2+ independent and was insensitive to the K+ channel blockers tetraethylammonium (TEA) or 4-aminopyridine (4-AP), but could be partially inhibited by Ba2+. 5. The CRH-triggered steady-state depolarization stimulated extracellular Ca2+ entry via voltage-gated Ca2+ channels and raised [Ca2+]i. CRH failed to stimulate [Ca2+]i rise in cells that were voltage clamped at their resting potential. Removal of extracellular Ca2+ or inhibition of Ca2+ channels by Ni2+ abolished the [Ca2+]i rise. 6. Voltage-clamp studies of voltage-gated Ca2+ channels using Ba2+ as charge carrier show that approximately 90% of the channels were available for activation at the resting potential. CRH did not enhance the voltage-gated Ca2+ channels.
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