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Short-Term Plasticity of Cyclic Adenosine 3',5'-Monophosphate Signaling in Anterior Pituitary Corticotrope Cells: The Role of Adenylyl Cyclase Isotypes

Department of Neuroscience, University of Edinburgh, Edinburgh EH8 9JZ, Scotland, United Kingdom

Address all correspondence and requests for reprints to: F. Antoni, Department of Neuroscience, University of Edinburgh, Edinburgh EH8 9JZ, Scotland, United Kingdom. E-mail: ferenc.antoni{at}ed.ac.uk.

Anterior pituitary corticotropes show a wide repertory of responses to hypothalamic neuropeptides and adrenal corticosteroids. The hypothesis that plasticity of the cAMP signaling system underlies this adaptive versatility was investigated. In dispersed rat anterior pituitary cells, depletion of intracellular Ca²⁺ stores with thapsigargin combined with ryanodine or caffeine enhanced the corticotropin releasing-factor (CRF)-evoked cAMP response by 4-fold, whereas reduction of Ca²⁺ entry alone had no effect. CRF-induced cAMP was amplified 15-fold by arginine-vasopressin (AVP) or phorbol-dibutyrate ester. In the presence of inhibitors of cyclic nucleotide phosphodiesterases and phorbol-dibutyrate ester, the depletion of Ca²⁺ stores had no further effect on CRF-induced cAMP accumulation. Adenohypophysial expression of mRNAs for the Ca²⁺-inhibited adenylyl cyclases (ACs) VI and IX, and the protein kinase C-stimulated ACs II and VII was demonstrated. ACIX was detected in corticotropes by immunocytochemistry, whereas ACII and ACVI were not present. The data show negative feedback regulation of CRF-induced cAMP levels by Ca²⁺ derived from ryanodine receptor-operated intracellular stores. Stimulation of protein kinase C by AVP enhances Ca²⁺-independent cAMP synthesis, thus changing the characteristics of intracellular Ca²⁺ feedback. It is proposed that the modulation of intracellular Ca²⁺ feedback in corticotropes by AVP is an important element of physiological control.

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