Adenosine A1 receptors inhibit both adenylate cyclase activity and TRH-activated Ca2+ channels by a pertussis toxin-sensitive mechanism in GH3 cells

Cooper, Dermot M.F.; Boyajian, Christine L.; Petcoff, Douglas W.; Schlegel, Werner

doi:10.1016/0898-6568(89)90023-5

Cited by 20 publications

(19 citation statements)

References 40 publications

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“…The involvement of A, adenosine receptors was further confirmed by the present results. In agreement with numerous studies indicating that A, receptors are coupled to G-proteins sensitive to PTX (Dolphin and Pestwich, 1985;Stiles, 1986;Cooper et al, 1989) the pretreatment of striatal astrocytes with the toxin was shown indeed to abolish selectively the potentiating effect of 2-chloroadenosine while it did not alter the q-adrenergicevoked production of 3H-inositol phosphates. This suggests that both types of receptors are coupled to different transduction systems (G-proteins) and effecters, the a,-adrenoceptors probably being linked to phospholipase C via a G-protein insensitive to PTX while the adenosine receptors are coupled to another effector regulated by a G-protein sensitive to this toxin (Fig.…”

Section: Discussionsupporting

confidence: 70%

2-Chloroadenosine potentiates the alpha 1-adrenergic activation of phospholipase C through a mechanism involving arachidonic acid and glutamate in striatal astrocytes

et al. 1992

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In cultured striatal astrocytes, 2-chloroadenosine, an adenosine analog resistant to adenosine deaminase, although inactive alone, markedly potentiated the activation of phospholipase C induced by methoxamine, an alpha 1-adrenergic agonist. This effect was suppressed by antagonists of either A1 adenosine or alpha 1-adrenergic receptors. An influx of calcium and two distinct G-proteins are involved in this phenomenon since the potentiating effect of 2-chloradenosine was suppressed in the absence of external calcium or when cells were pretreated with pertussis toxin. In addition, arachidonic acid is likely involved in this potentiating effect. This was shown first by examining the effects of inhibitors of phospholipase A2 or arachidonic metabolism, then by examining the action of arachidonic acid on the production of inositol phosphates in either the presence or absence of methoxamine, and finally by measuring the release of arachidonic acid. The sequential activation of phospholipase C and of protein kinase C is required for the 2-chloroadenosine-induced activation of phospholipase A2 since 2-chloroadenosine markedly stimulated phospholipase C activity in the absence of methoxamine when protein kinase C was activated by a diacylglycerol analog. Finally, the enhancing effect of 2- chloroadenosine on the methoxamine-evoked response seems to result from an inhibition of glutamate reuptake into astrocytes by arachidonic acid. Indeed, the potentiating effect of 2-chloroadenosine was suppressed when external glutamate was removed enzymatically and mimicked by either selective inhibitors of the glutamate reuptake process or direct application of glutamate.

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Section: Discussionsupporting

confidence: 70%

2-Chloroadenosine potentiates the alpha 1-adrenergic activation of phospholipase C through a mechanism involving arachidonic acid and glutamate in striatal astrocytes

et al. 1992

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“…Moreover, p-opioid receptors, stably expressed in GH3 cells, seem to be coupled to L-type calcium channels in a second messenger-independent manner (Piros et al, 1995). Adenosine inhibits calcium currents in GH3 cells via A1Rs, but the mechanism is not well known (Cooper et al, 1989;Mollard et al, 1991). In this article we demonstrate that adenosine inhibits operation of L-type calcium channels in GH4 cells by a mechanism that does not involve phosphatidylinositol hydrolysis.…”

mentioning

confidence: 75%

“…All these effects were mediated by A1Rs, and the G~proteinsinvolved in signaling were pertussis-sensitive, i.e., they were of the inhibitory type (Cooper et al, 1989). The experiments reported by Delahunty et al (1988) pointed out that the time response for adenosine action on cAMP and inositol phosphate production was different.…”

Section: Figmentioning

confidence: 91%

“…In GH3 cells the role of adenosine in inhibiting vasoactive intestinal peptide-induced increase of cAMP content, prolactin release, and thyrotropin-induced accumulation of either inositol phosphates or calcium mobilization has been demonstrated (Delahunty et al, 1988;Cooper et al, 1989). All these effects were mediated by A1Rs, and the G~proteinsinvolved in signaling were pertussis-sensitive, i.e., they were of the inhibitory type (Cooper et al, 1989).…”

Section: Figmentioning

confidence: 99%

“…GH4 cells are clonal isolates of GH3 cells, selected for high prolactin production; however, they still produce significant amounts of growth hormone (Tashjian, 1979). The presence of A1Rs in these cells has been shown by different authors by means of pharmacological experiments analyzing the effect of adenosine on hormone release, calcium mobilization, inositol phosphate hydrolysis, and/or cyclic AMP (cAMP) production (Dorflinger and Schonbrunn, 1985;Delahunty et al, 1988;Cooper et al, 1989;Mollard et al, 1991).…”

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confidence: 99%

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Regulation of L‐Type Calcium Channels in GH₄ Cells via A₁ Adenosine Receptors

Zapata

Navarro

Canela

et al. 1997

Journal of Neurochemistry

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Identification of A1 adenosine receptors (A1 Ps) in a tumor cell line derived from rat pituitary (GH4 ce~is) was performed by ligand binding and immunological experiments. Subsequently, the involvement of A1Rs in the regulation of calcium conductance was studied in these cells. The agonist N 6-(R) -(2-phenylisopropyl) adenosine (R-PIA) did not modify the intracellular calcium basal levels, whereas it inhibited the increase produced by 15mM KCI depolarization. The antagonist 1 ,3-dipropyl-8-cyclopentylxanthine led to the opening of voltage-dependent cell surface calcium channels in the absence of exogenous KCI. The channels were of the L type because the effect was abolished by calciseptine and by verapamil. These results suggest that endogenous adenosine exerts a tonic inhibitory effect on calcium transport. This was confirmed by the high adenosine concentration found in cell supernatants (up to 1 pM) and by the calcium mobilization produced by exogenously added adenosine deaminase. In depolarizing conditions, the calcium peak in the presence of adenosine deaminase was reduced when cells were preincubated with R-PIA, thus suggesting that A 1R activation regulates the intensity of depolarization. These results demonstrate that adenosine is an important regulator of the physiological state of pituitary tumor cells by modulating, in an autocrine manner, the activity of Ltype voltage-dependent calcium channels.

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Serotoninergic innervation of the locust mandiblar closer muscle modulates contractions through the elevation of cyclic adenosine monophosphate

Baines

Tyrer

Downer

1990

J of Comparative Neurology

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The mandibular closer muscles of the locust receive innervation that is immunoreactive for the putative transmitter 5-hydroxytryptamine (5-HT). Cobalt-labelling suggests that the origin of this innervation is a group of cells located anteriorly in the suboesophageal ganglion. Bath application of 5-HT while the muscles are active produces marked changes in the contractions, increasing their amplitude, rate of contraction, and rate of relaxation. Incubation of isolated muscles with 5-HT shows that this amine elevates the levels of the cyclic nucleotide cyclic adenosine monophosphate (cAMP). In addition compounds that artificially elevate the levels of cAMP in the muscle--3-isobutyl-1-methylxanthine (IBMX), forskolin, and the cAMP analogue 8-(4-chlorophenylthio) cAMP--mimic the actions of 5-HT, whereas a potent inhibitor of insect adenylate cyclase, adenosine, considerably delays the onset of the effects produced by 5-HT. The effects observed with 5-HT in the mandibular muscle are similar to those of octopamine in the locust extensor tibiae muscle, and it is possible that this is an analogous modulatory system.

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Adenosine A1 receptors inhibit both adenylate cyclase activity and TRH-activated Ca2+ channels by a pertussis toxin-sensitive mechanism in GH3 cells

Cited by 20 publications

References 40 publications

2-Chloroadenosine potentiates the alpha 1-adrenergic activation of phospholipase C through a mechanism involving arachidonic acid and glutamate in striatal astrocytes

2-Chloroadenosine potentiates the alpha 1-adrenergic activation of phospholipase C through a mechanism involving arachidonic acid and glutamate in striatal astrocytes

Regulation of L‐Type Calcium Channels in GH₄ Cells via A₁ Adenosine Receptors

Serotoninergic innervation of the locust mandiblar closer muscle modulates contractions through the elevation of cyclic adenosine monophosphate

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Adenosine A1 receptors inhibit both adenylate cyclase activity and TRH-activated Ca2+ channels by a pertussis toxin-sensitive mechanism in GH3 cells

Cited by 20 publications

References 40 publications

2-Chloroadenosine potentiates the alpha 1-adrenergic activation of phospholipase C through a mechanism involving arachidonic acid and glutamate in striatal astrocytes

2-Chloroadenosine potentiates the alpha 1-adrenergic activation of phospholipase C through a mechanism involving arachidonic acid and glutamate in striatal astrocytes

Regulation of L‐Type Calcium Channels in GH4 Cells via A1 Adenosine Receptors

Serotoninergic innervation of the locust mandiblar closer muscle modulates contractions through the elevation of cyclic adenosine monophosphate

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Regulation of L‐Type Calcium Channels in GH₄ Cells via A₁ Adenosine Receptors