Inhibitory effect of adenosine on electrical activity of frog melanotrophs mediated through A1 purinergic receptors.

Mei, Yan‐Ai; Vaudry, Hubert; Cazin, L.

doi:10.1113/jphysiol.1994.sp020444

Cited by 17 publications

(10 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Extracellular purines are now recognised as important signalling molecules in a variety of cells/tissues including melanotrophs expressing POMC (18–21). With respect to the corticotroph cells in the pituitary gland, Anand‐Srivastava et al .…”

Section: Discussionmentioning

confidence: 99%

Purinergic Receptor Ligands Stimulate Pro‐Opiomelanocortin Gene Expression in AtT‐20 Pituitary Corticotroph Cells

Zhao

Iwasaki

Osuga

et al. 2006

J Neuroendocrinology

View full text Add to dashboard Cite

Although recent studies have suggested that purinergic receptors are expressed in the anterior pituitary gland, their involvement in the regulation of pituitary hormone gene expression is not completely understood. In the present study, we examined the expression of purinergic receptors and the effects of purinergic receptor ligands on pro-opiomelanocortin (POMC) gene expression, in AtT20 mouse corticotroph cells. We identified the expression of most of the purinergic receptor subtypes (A1, A2, P2X1, 3-7, P2Y1, 2, 4) mRNAs, analysed by the reverse transcriptase-polymerase chain reaction. We also found that adenosine and ATP, two representative and endogenous agonists of A1-3 and P2X/P2Y receptors, respectively, stimulated the 5'-promoter activity of the POMC gene in a dose- and time-related manner. When these ligands were simultaneously used with corticotrophin-releasing hormone (CRH), effects that were more than additive were observed, suggesting an enhancing role of these compounds in CRH-mediated adrenocorticotrophic hormone (ACTH) synthesis. These ligands also stimulated the expression of transcription factors involved in the regulation of the POMC gene, but did not enhance ACTH secretion. Finally, the positive effect of adenosine as well as CRH was completely inhibited by the protein kinase A inhibitor H89, whereas that of ATP was not influenced, indicating that different intracellular signalling pathways mediate these effects. Altogether, our results suggest a stimulatory role for these purinergic receptor ligands in the regulation of POMC gene expression in corticotroph cells. Because adenosine and ATP are known to be produced within the pituitary gland, it is possible they may be acting in an autocrine/paracrine fashion.

show abstract

Section: Discussionmentioning

confidence: 99%

Purinergic Receptor Ligands Stimulate Pro‐Opiomelanocortin Gene Expression in AtT‐20 Pituitary Corticotroph Cells

Zhao

Iwasaki

Osuga

et al. 2006

J Neuroendocrinology

View full text Add to dashboard Cite

show abstract

“…Electrophysiological experiments revealed that adenosine inhibits electrical activity-driven Ca 2ϩ transients in GH cell lines (645). In frog melanotrophs, adenosine also inhibits spontaneous electrical activity (646), presumably reflecting the inhibitory action on Ca v channels (647), facilitation of A-type K v channels (151), and/or potentiation of delayed rectifier K ϩ channels (150).…”

Section: Other Pituitary Receptors Linked To the G I/o Signaling Pathwaymentioning

confidence: 99%

Ion Channels and Signaling in the Pituitary Gland

2010

View full text Add to dashboard Cite

Endocrine pituitary cells are neuronlike; they express numerous voltage-gated sodium, calcium, potassium, and chloride channels and fire action potentials spontaneously, accompanied by a rise in intracellular calcium. In some cells, spontaneous electrical activity is sufficient to drive the intracellular calcium concentration above the threshold for stimulus-secretion and stimulus-transcription coupling. In others, the function of these action potentials is to maintain the cells in a responsive state with cytosolic calcium near, but below, the threshold level. Some pituitary cells also express gap junction channels, which could be used for intercellular Ca(2+) signaling in these cells. Endocrine cells also express extracellular ligand-gated ion channels, and their activation by hypothalamic and intrapituitary hormones leads to amplification of the pacemaking activity and facilitation of calcium influx and hormone release. These cells also express numerous G protein-coupled receptors, which can stimulate or silence electrical activity and action potential-dependent calcium influx and hormone release. Other members of this receptor family can activate calcium channels in the endoplasmic reticulum, leading to a cell type-specific modulation of electrical activity. This review summarizes recent findings in this field and our current understanding of the complex relationship between voltage-gated ion channels, ligand-gated ion channels, gap junction channels, and G protein-coupled receptors in pituitary cells.

show abstract

“…Until recently, however, little was known about the effects of adenosine on the transient outward A-current (Pan, Osmanovic & Shefner, 1994). In a previous electrophysiological study, we have shown that adenosine and the A, receptor agonist R-PIA inhibit spontaneous action potentials in cultured frog melanotrophs (Mei, Vaudry & Cazin, 1994), suggesting that modulation of potassium conductances could be involved in the mechanism of action of adenosine. In the present report, we explored the possibility that an A-type current exists in frog melanotrophs and that adenosine could activate this current.…”

mentioning

confidence: 99%

A‐type potassium current modulated by A1 adenosine receptor in frog melanotrophs.

Mei

Louiset

Vaudry

et al. 1995

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

1. Transient outward current was recorded in cultured frog melanotrophs with the whole‐cell configuration of the patch‐clamp technique. The ionic dependence, kinetics and pharmacological properties of the current were studied. The effects of the A1 adenosine receptor agonist R‐N6‐phenylisopropyl‐adenosine (R‐PIA) on this current were also investigated. 2. In tetrodotoxin‐ and cobalt‐containing solution, depolarization from ‐120 mV elicited both transient and delayed outward currents. Pulses from ‐60 mV activated only a sustained late current. 3. 4‐Aminopyridine (4 mM) reduced the transient outward current much more than the delayed outward current. In contrast, tetraethylammonium (10‐20 mM) selectively reduced the delayed current. 4. Tail current measurements showed a positive shift in the reversal potential when external K+ concentration was increased, indicating that K+ was the predominant charge carrier. 5. Steady‐state inactivation was complete at potentials positive to ‐10 mV and removed by hyperpolarization. 6. Inactivation of the transient current was slowed and accelerated in oxidizing and reducing conditions, respectively, confirming the involvement of an inactivating ‘ball and chain’ peptide. 7. R‐PIA increased the transient current. The steady‐state inactivation curve was shifted towards more positive potentials without changing the activation kinetics. Pretreatment with pertussis toxin (1 microgram ml‐1) blocked the response to R‐PIA. 8. It is concluded that frog melanotrophs possess an A‐type current that is likely to play an important role in excitability. This current, which is directly modulated by A1 adenosine receptors through a Gi/G(o) protein, appears to be responsible for the inhibitory effects of adenosine on electrical activity.

show abstract

Inhibitory effect of adenosine on electrical activity of frog melanotrophs mediated through A1 purinergic receptors.

Cited by 17 publications

References 31 publications

Purinergic Receptor Ligands Stimulate Pro‐Opiomelanocortin Gene Expression in AtT‐20 Pituitary Corticotroph Cells

Purinergic Receptor Ligands Stimulate Pro‐Opiomelanocortin Gene Expression in AtT‐20 Pituitary Corticotroph Cells

Ion Channels and Signaling in the Pituitary Gland

A‐type potassium current modulated by A1 adenosine receptor in frog melanotrophs.

Contact Info

Product

Resources

About