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Growth hormone‐releasing hormone triggers pacemaker activity and persistent Ca2+ oscillations in rat somatotrophs.
Author(s) -
Kwiecien R,
Tseeb V,
Kurchikov A,
Kordon C,
Hammond C
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1997.sp021954
Subject(s) - somatotropic cell , somatostatin , endocrinology , medicine , growth hormone–releasing hormone , chemistry , muscarine , nifedipine , muscarinic acetylcholine receptor , inhibitory postsynaptic potential , hormone , biology , calcium , receptor , pituitary gland , growth hormone
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.