Caffeine stores and dopamine differentially require Ca(2+) channels in goldfish somatotropes

The regulation of growth hormone (GH) secretion by intracellular Ca(2+) stores was studied in dissociated goldfish somatotropes. We characterized a caffeine-activated intracellular store that had been shown to mediate GH release in response to gonadotropin-releasing hormone. The peak response of caf...

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Bibliographic Details
Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2001-02, Vol.280 (2), p.R494-R503
Main Authors: Wong, C J, Johnson, J D, Yunker, W K, Chang, J P
Format: Article
Language:English
Subjects:
Animals
Cadmium - pharmacology
Caffeine - pharmacology
Calcium - physiology
Calcium Channels - drug effects
Calcium Channels - physiology
Cells, Cultured
Chelating Agents - pharmacology
Cyclic AMP-Dependent Protein Kinases - metabolism
Dopamine - pharmacology
Egtazic Acid - analogs & derivatives
Egtazic Acid - pharmacology
Enzyme Inhibitors - pharmacology
Female
Goldfish
Growth Hormone - secretion
Isoquinolines - pharmacology
Kinetics
Male
Pituitary Gland, Anterior - cytology
Pituitary Gland, Anterior - drug effects
Pituitary Gland, Anterior - physiology
Receptors, Dopamine D1 - physiology
Ryanodine - pharmacology
Sulfonamides
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Summary:The regulation of growth hormone (GH) secretion by intracellular Ca(2+) stores was studied in dissociated goldfish somatotropes. We characterized a caffeine-activated intracellular store that had been shown to mediate GH release in response to gonadotropin-releasing hormone. The peak response of caffeine stimulation was reduced by approximately 28% by 100 microM ryanodine in a use-dependent manner suggesting that the first 10 min of GH release is partially mediated by a caffeine-activated ryanodine receptor. The temporal sensitivities of caffeine- and dopamine-evoked GH release to blockade of Cd(2+)-sensitive Ca(2+) channels were compared. We demonstrated that the initial phase of dopamine-evoked release was dependent on Ca(2+) channels, whereas the initial phase of caffeine-evoked release was sensitive only to pretreatment blockade. This would suggest that the maintenance of one class of caffeine-activated intracellular stores requires entry of Ca(2+) through Cd(2+)-sensitive Ca(2+) channels. This differential temporal requirement for Ca(2+) channels in Ca(2+) signaling may be a mechanism to segregate intracellular signaling pathways of multiple neuroendocrine regulators in the teleost pituitary.
ISSN:0363-6119
DOI:10.1152/ajpregu.2001.280.2.r494