ArticleThe Journal of physiology1997
Growth hormone-releasing hormone triggers pacemaker activity and persistent Ca2+ oscillations in rat somatotrophs.
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 13 papers.
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Who cites it
13 citing papers in PubMed, 36 citations in OpenAlex.
- Distribution and calcium signaling function of somatostatin receptor subtypes in rat pituitary.Cell calcium · 2024Article
- Review
- Dependence of the excitability of pituitary cells on cyclic nucleotides.Journal of neuroendocrinology · 2012Review
- Ion channels and signaling in the pituitary gland.Endocrine reviews · 2010Review
- Motivations and methods for analyzing pulsatile hormone secretion.Endocrine reviews · 2008Review
- Ghrelin reduces voltage-gated potassium currents in GH3 cells via cyclic GMP pathways.Endocrine · 2005Article
- Sustained stimulation of exocytosis triggers continuous membrane retrieval in rat pituitary somatotrophs.The Journal of physiology · 2001Article
- Growth hormone secretagogues and hypothalamic networks.Endocrine · 2001Review
- Somatostatin-induced control of cytosolic free calcium in pituitary tumour cells.British journal of pharmacology · 2000Article
- Human GHRH reduces voltage-gated K+ currents via a non-cAMP-dependent but PKC-mediated pathway in human GH adenoma cells.The Journal of physiology · 1999Article
- Expression of Ca(2+)-mobilizing endothelin(A) receptors and their role in the control of Ca(2+) influx and growth hormone secretion in pituitary somatotrophs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Endogenous pacemaker activity of rat tumour somatotrophs.The Journal of physiology · 1998Article
- Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of brief applications of growth hormone-releasing hormone (GHRH) to male rat somatotrophs in culture were analysed with the perforated patch clamp technique to record changes in potential or with fura-2 imaging techniques to measure variations of cytosolic Ca2+ concentration ([Ca2+]i). 2. Silent somatotrophs (n = 61) had a mean resting potential of -37 +/- 1 mV and a mean basal [Ca2+]i of 30 +/- 4 nM. Brief GHRH applications (30 nM, 40 s) triggered rhythmic action potentials (23.6 +/- 0.9 mV, 613 +/- 82 ms, 0.21 +/- 0.02 Hz) and [Ca2+]i increase (to 352 +/- 30 nM) followed by rhythmic [Ca2+]i transients (to 138 +/- 6 nM) that persisted up to 90 min after the last GHRH application. Both action potentials and [Ca2+]i transients were totally and reversibly blocked by removing external Ca2+ or Na+ or by adding inorganic Ca2+ channel blockers or nifedipine (3 microM). 3. Somatostatin (1-300 nM), carbamylcholine (0.1-1 microM) and muscarine (0.1-1 microM) each had a dose-dependent inhibitory effect, from a decrease of Ca2+ spike duration and frequency to a complete block of the GHRH-evoked action potentials. 4. The present results show that somatotrophs in culture have intrinsic membrane properties that allow them to sustain a pacemaker activity and subsequent long-lasting sequences of [Ca2+]i oscillations triggered by short pulses of GHRH and inhibited by somatostatin and muscarinic agonists.
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