Dopaminergic modulation of adenylate cyclase stimulation by vasoactive intestinal peptide in anterior pituitary.

Onali, Pierluigi; Schwartz, Joan P.; Costa, E.

doi:10.1073/pnas.78.10.6531

Cited by 105 publications

(45 citation statements)

References 30 publications

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“…It was demonstrated that dopamine both inhibits adenylate cyclase activity and reduces the intracellular content of cyclic AMP in pituitary cells (De Camilli et al 1979;Onali et al 1981;Enjalbert & Bockaert, 1983). In the experiments designed to test the role of cyclic AMP in mediating the changes in Rb+ efflux induced by dopamine, cells were exposed to the adenylate cyclase activator forskolin.…”

Section: Discussionmentioning

confidence: 99%

“…The intracellular mechanism involved in inhibiting both basal and stimulus-evoked hormone release is still not entirely known. Various groups of investigators have independently provided evidence that dopamine and dopaminergic agonists acting on D2 dopamine receptors can inhibit adenylate cyclase activity (De Camilli, Macconi & Spada, 1979;Onali, Schwartz & Costa, 1981;Weiss, Sebben, Garcia-Sainz, Bockaert, 1985). Recently we have found that dopamine was able to prevent both basal and neurotensin-stimulated Ca2+ influx into pituitary cells by stimulating a D2 receptor which appears to be uncoupled to adenylate cyclase (Memo, Carboni, Trabucchi, Carruba & Spano, 1985;Memo, Castelletti, Missale, Valerio, Carruba & Spano, 1986 a).…”

Section: Introductionmentioning

confidence: 99%

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Potassium channels involved in the transduction mechanism of dopamine D2 receptors in rat lactotrophs.

Castelletti

Memo

Missale

et al. 1989

The Journal of Physiology

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SUMMARY1. Radioactive rubidium (86Rb+) efflux was used to measure potassium (K+) permeability in a study designed to assess both the presence and the sensitivity to ions and drugs of the K+ channels in the plasma membrane of rat lactotrophs.2. Rb+ efflux from Rb+-pre-loaded lactotrophs into nominally calcium-free solution containing 5 mm-K+ was linear from 1 to 60 s, with a calculated rate of about 0-1 %/s. Raising K+ concentrations to depolarize the cells stimulated the Rb+ efflux (0-2 %/s), which was already significant after 1 s of exposure of the cells to 100 mM-K+. This component of Rb+ efflux has been designated component V (sensitive to voltage and Ca2+ independent).3. Addition of Ca2+ to 5 mM-K+ solution had no effect on resting Rb+ efflux (0-1 %/s), but did further stimulate Rb+ efflux into K+-rich solutions. This component, which has been designated component C, was completely inhibited by 0 5 mM-cadmium. These data fit the view that the increase in intracellular Ca2+ concentration during depolarization opens certain (Ca2+-activated) K+ channels.4. K+ efflux was differently affected by K+ channel blockers. Tetraethylammonium (TEA) inhibited both V and C components while 4-aminopyridine (4-AP) inhibited the component V without modifying the C component of Rb+ efflux.5. Dopamine appears to affect both types of Rb+ efflux components. Dopamine increased the efflux of Rb+ in a nominally Ca2+-free medium containing 5 mM-K+ (component V). This effect was statistically significant 15 s after exposure of the cells to 10 nM-dopamine. Increasing the concentrations of K+ to gradually depolarize the cells enhanced the rate of increase of Rb+ efflux induced by dopamine, being evident in the initial 2-5 s of incubations. Dopamine also increased Rb+ efflux in a 5 mM-K+ solution containing 1 mM-Ca2+ (component C). This effect was rapid (2-5 s) and inhibited by 0 5 mM-cadmium. The combined action of dopamine on both component C and V caused the cells to be less sensitive to depolarizing concentrations of K+. The increase in Rb+ efflux and the enhancement of prolactin release induced by high concentrations of K+ were, indeed, prevented by exposure of the cells to 10 nMdopamine.6. The effects of dopamine on either component V or component C were pharmacologically characterized as D2 receptor mediated, being mimicked by L. CASTELLETTI AND OTHERS selective D2 receptor agonists (quinpirole and RU 24213) and stereospecifically blocked by the D2 receptor antagonist sulpiride.7. The increase in Rb+ efflux induced by dopamine in a calcium-free medium (component V) was unaffected by treatment of the cells with the adenylate cyclase activator forskolin, but the same treatment caused the cells to be resistant to the effects of dopamine on component C.8. The kinetic and pharmacological data here reported suggest that lactotrophs contain at least two classes of K+ channels that participate in the regulation of K+ fluxes in both resting and stimulated conditions. Dopamine appears to promote opening of both types of K+ channels by inte...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Potassium channels involved in the transduction mechanism of dopamine D2 receptors in rat lactotrophs.

Castelletti

Memo

Missale

et al. 1989

The Journal of Physiology

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“…This latter difference may be due to differential coupling to adenylate cyclase for the GPCRs studied and consequent downstream actions on PKA. For example, the D2 and CB1 receptors, which activate G i/o -type G proteins, have been found to be negatively coupled to adenylyl cyclase (Howlett 1984;Howlett and Fleming 1984;Onali et al 1981)-reducing cAMP levels-whereas the G s -activating adenosine A2 receptor is positively coupled to adenylyl cyclase (van Calker et al 1979). Consistent with these findings, both CB1 and D2 effects on I Ca were mimicked by PKA inhibitor Rp-cAMPS, and the D2 effect occluded by PKA activator Sp-cAMPS (Stella and Thoreson 2000), whereas the A2 effect was occluded by RpcAMPS (Stella et al 2002).…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Cannabinoid Receptor Activation Differentially Modulates Ion Channels in Photoreceptors of the Tiger Salamander

Straiker

Sullivan

2003

Journal of Neurophysiology

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Staiker, Alex and Jane M. Sullivan. Cannabinoid receptor activation differentially modulates ion channels in photoreceptors of the tiger salamander. J Neurophysiol 89: 2647-2654, 2003; 10.1152/jn.00268.2002. Cannabinoid CB1 receptors have been detected in retinas of numerous species, with prominent labeling in photoreceptor terminals of the chick and monkey. CB1 labeling is well-conserved across species, suggesting that CB1 receptors might also be present in photoreceptors of the tiger salamander. Synaptic transmission in vertebrate photoreceptors is mediated by L-type calcium currents-currents that are modulated by CB1 receptors in bipolar cells of the tiger salamander. Presence of CB1 receptors in photoreceptor terminals would therefore be consistent with presynaptic modulation of synaptic transmission, a role seen for cannabinoids in other parts of the brain. Here we report immunohistochemical and electrophysiological evidence for the presence of functional CB1 receptors in rod and cone photoreceptors of the tiger salamander. The cannabinoid receptor agonist WIN 55212-2 enhances calcium currents of rod photoreceptors by 39% but decreases calcium currents of large single cones by 50%. In addition, WIN 55212-2 suppresses potassium currents of rods and large single cones by 44 and 48%, respectively. Thus functional CB1 receptors, present in the terminals of rod and cone photoreceptors, differentially modulate calcium and potassium currents in rods and large single cones. CB1 receptors are therefore well positioned to modulate neurotransmitter release at the first synapse of the visual system. I N T R O D U C T I O NCannabinoid CB1 receptors have been detected in the retinas of numerous species, including salamander, goldfish, chick, rat, mouse, monkey, and human (Straiker et al. 1999a,b;Yazulla et al. 1999) with a well-conserved pattern of staining that is particularly intense in both synaptic layers. In species for which double labeling has been performed-chick and monkey-outer plexiform layer staining is found to localize to photoreceptor terminals. CB1 is a member of the Gi/o-type G-protein-coupled receptor family and mediates a wide range of effects on ion channels, including voltage-dependent calcium and potassium channels (Deadwyler et al. 1995;Mackie and Hille 1992;Mackie et al. 1995;Mu et al. 1999). Retinal cannabinoid receptor activation has been shown to inhibit dopamine release in the guinea pig (Schlicker et al. 1996), to inhibit a delayed rectifier K ϩ current in ON cone bipolar cells of the goldfish (Yazulla et al. 2000), and to inhibit L-type calcium currents in bipolar cells of the tiger salamander (Straiker et al. 1999a). Three recent reports have described G-protein-coupled receptor-dependent modulation of ion channel function in photoreceptors of the tiger salamander by dopamine, adenosine, and somatostatin (Akopian et al. 2000;Stella and Thoreson 2000;Stella et al. 2002). These studies find that the calcium currents (I Ca ) of rods and large single cones respond differentially to activation ...

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“…Several lines of evidence indicate that the stimulatory effect of VIP on PRL release is mediated by cAMP. VIP has been shown to increase cAMP accumulation in intact pituitary cells 111, 21] and to stimulate adenylate cyclase activity in anterior pituitary membrane [18]. Moreover, it has been demonstrated that in pituitary tumor cells as well as in brain VIP stimulates the accumulation of cAMP in a Ca2+-dependent manner [2,9].…”

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confidence: 99%

A Mechanism Additional to Cyclic AMP Accumulation for Vasoactive Intestinal Peptide-Induced Prolactin Release

et al. 1990

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Vasoactive intestinal peptide (VIP) is a prolactin (PRL)-releasing factor which has been proposed to exert its secreting property by activating the adenylate cyclase enzyme. The present study shows that the omission of external Ca²⁺ did not affect the ability of VIP to induce PRL release while it completely abolished the VIP stimulatory effect on adenylate cyclase. We found that VIP (500 nM) stimulated PRL secretion in a time-dependent manner reaching a plateau at 3 min. This pattern was not changed when Ca²⁺ was omitted from the incubation medium. When tested at different concentrations, VIP stimulated PRL release with EC₅₀ values of 1.3 nM in the presence of Ca²⁺ and 30 nM in the absence of Ca²⁺. On the other hand, Ca²⁺ removal completely suppressed the VIP-induced cAMP formation. VIP (200 nM) was also found to activate Ca²⁺ influx into pituitary cells. The increase in Ca²⁺ permeability showed a peak at 5 s and remained significantly higher than control values until 1 min. In conclusion, in an experimental condition where Ca²⁺ was omitted from the medium, VIP was found to induce PRL release without stimulating cAMP production. This cAMP-independent PRL release was blocked by preincubation of the cells with 1 µg/ml pertussis toxin. An additional mechanism other than adenylate cyclase activation or Ca²⁺ entry is proposed to sustain VIP-induced PRL release.

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Dopaminergic modulation of adenylate cyclase stimulation by vasoactive intestinal peptide in anterior pituitary.

Abstract: ABSTRACT

Cited by 105 publications

References 30 publications

Potassium channels involved in the transduction mechanism of dopamine D2 receptors in rat lactotrophs.

Potassium channels involved in the transduction mechanism of dopamine D2 receptors in rat lactotrophs.

Cannabinoid Receptor Activation Differentially Modulates Ion Channels in Photoreceptors of the Tiger Salamander

A Mechanism Additional to Cyclic AMP Accumulation for Vasoactive Intestinal Peptide-Induced Prolactin Release

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