Inositol Phospholipid Metabolism During and Following Synaptic Activation: Role of Adenosine

Rubio, Rafael; Bencherif, Merouane; Berne, Robert M.

doi:10.1111/j.1471-4159.1989.tb02524.x

Cited by 17 publications

(8 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The possibility that adenosine prevents the effect of lithium by decreasing calcium entry in a magnesium-like manner seems unlikely since an increase in magnesium concentration in the bath did not modify the effect of lithium on neuromuscular transmission. Evidence that adenosine inhibits phosphoinositide metabolism in nerve cells has recently been produced (Petcoff & Cooper, 1987;Kendall & Hill, 1988;Rubio et al, 1989). It is worth noting that the adenosine receptor involved in the inhibition of phosphoinositide metabolism (Petcoff & Cooper, 1987;Kendall & Hill, 1988) has an agonist profile more similar to the agonist profile of the adenosine receptor mediating inhibition of neurotransmitter release (Ribeiro & Sebastiio, 1986), than to the agonist profiles of the adenosine receptors involved in inhibition or in stimulation of adenylate cyclase .…”

Section: Discussionmentioning

confidence: 99%

Interactions between adenosine and phorbol esters or lithium at the frog neuromuscular junction

Sebastião¹,

Ribeiro²

1990

British J Pharmacology

View full text Add to dashboard Cite

1 Interactions between the effects of adenosine or 2-chloro-adenosine (CADO) and the effects of substances that interfere with the phosphoinositides/protein kinase C transducing system or with the adenylate cyclase transducing system, on endplate potentials (e.p.ps), were investigated. The preparation used was the innervated sartorius muscle of the frog in which twitches had been prevented with high magnesium concentrations.2 The activator of protein kinase C, 4f,-phorbol-12,13-diacetate (PDAc) 7 The results suggest that the phosphoinositides/protein kinase C transducing system, but not the adenylate cyclase transducing system, might be involved in the inhibitory effect of adenosine on neuromuscular transmission.

show abstract

Section: Discussionmentioning

confidence: 99%

Interactions between adenosine and phorbol esters or lithium at the frog neuromuscular junction

Sebastião¹,

Ribeiro²

1990

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Since adenosine plays a physiologically significant role in the heart to dilate the coronary arteries (18), it may play a similar role to dilate the hypophysial portal vessels, thereby increasing anterior pituitary blood flow. Additional studies are necessary to determine the stimuli that release adenosine in the pituitary and its physiological or pathological significance in vivo.…”

Section: Discussionmentioning

confidence: 99%

Adenosine acts by A ₁ receptors to stimulate release of prolactin from anterior-pituitaries in vitro

Kimura²,

Walczewska

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Adenosine has been identified in the anterior pituitary gland and is secreted from cultured folliculostellate (FS) cells. To determine whether adenosine controls the secretion of anterior pituitary hormones in vitro, adenosine was incubated with anterior pituitaries. It stimulated prolactin (PRL) release at the lowest concentration used (10 ؊10 M); the stimulation peaked at 10 ؊8 M with a threefold increase in release and declined to minimal stimulation at 10 ؊4 and 10 ؊3M. Follicle-stimulating hormone release was maximally inhibited at 10 ؊8 M, whereas luteinizing hormone release was not significantly inhibited. Two selective A 1 adenosine receptor antagonists (10 ؊7 or 10 ؊5 M) had no effect on basal PRL release, but either antagonist completely blocked the response to the most effective concentration of adenosine (10 ؊8 M). In contrast, a highly specific A 2 receptor antagonist (10 ؊7 or 10 ؊5 M) had no effect on basal PRL release or the stimulation of PRL release induced by adenosine (10 ؊8 M). We conclude that adenosine acts to stimulate PRL release in vitro by activating A 1 receptors. Since the A 1 receptors decrease intracellularfree calcium, this would decrease the activation of nitric oxide synthase in the FS cells, resulting in decreased release of nitric oxide (NO). NO inhibits PRL release by activating guanylate cyclase that synthesizes cGMP from GTP; cGMP concentrations increase in the lactotrophs leading to inhibition of PRL release. In the case of adenosine, NO release from the FS cells decreases, resulting in decreased concentrations of NO in the lactotrophs, consequent decreased cGMP formation, and resultant increased PRL release. In 1989 Gonzalez et al.(1) presented evidence for a substance of pituitary origin that acts as a trophic agent for hypothalamic dopaminergic neurons. Their findings included the observation that implantation of anterior pituitaries into the brain of rats increased secretory activity of hypothalamic dopaminergic neurons. The secretion of dopamine by dispersed hypothalamic cells in culture was later found to be increased by coincubation with pituitary cells (J. C. Porter, unpublished observations) or by inclusion of pituitary extract in the medium (2). This substance was named pituitary cytotrophic factor (3). Cytotrophic factor produced a dose-and time-related increase in dopamine release as well as the quantity of tryosine hydroxylase mRNA and the enzyme itself. Cytotrophic factor was subsequently identified as adenosine by Porter et al. (4). They hypothesized that adenosine secreted by pituitary cells reached the hypothalamus by retrograde blood flow in the pituitary stalk vasculature (5), where it increased the secretory activity of dopaminergic neurons.Adenosine was secreted by folliculostellate (FS) cells cloned from a pituitary tumor (J. C. Porter, unpublished observations). Therefore, it is plausible that adenosine secreted by such cells may affect the secretion of other pituitary cells. To test this possibility, we conducted studies on the effect of ade...

show abstract

“…Studies on isolated sympathetic ganglia demonstrated that endogenously released adenosine may inhibit postsynaptic stimulation and [ 3 H]myoinositol release (8). Other data have suggested that adenosine receptors that modulate membrane phosphoinositide hydrolysis do not interfere with the generation of cyclic adenosine monophosphate (cAMP) in cerebral cortex slices (9).…”

Section: Introductionmentioning

confidence: 99%

“…The activation of purinergic receptors may also modify the capacity for inositol triphosphate synthesis in different types of experimental preparations (7,8). Studies on isolated sympathetic ganglia demonstrated that endogenously released adenosine may inhibit postsynaptic stimulation and [ 3 H]myoinositol release (8).…”

Section: Introductionmentioning

confidence: 99%

Possible involvement of A1 receptors in the inhibition of gonadotropin secretion induced by adenosine in rat hemipituitaries in vitro

Picanço-Diniz

Valênça

Favaretto

et al. 1999

Braz J Med Biol Res

View full text Add to dashboard Cite

We investigated the participation of A 1 or A 2 receptors in the gonadotrope and their role in the regulation of LH and FSH secretion in adult rat hemipituitary preparations, using adenosine analogues. A dosedependent inhibition of LH and FSH secretion was observed after the administration of graded doses of the R-isomer of phenylisopropyladenosine (R-PIA; 1 nM, 10 nM, 100 nM, 1 µM and 10 µM). The effect of R-PIA (10 nM) was blocked by the addition of 8-cyclopentyltheophylline (CPT), a selective A 1 adenosine receptor antagonist, at the dose of 1 µM. The addition of an A 2 receptor-specific agonist, 5-Nmethylcarboxamidoadenosine (MECA), at the doses of 1 nM to 1 µM had no significant effect on LH or FSH secretion, suggesting the absence of this receptor subtype in the gonadotrope. However, a sharp inhibition of the basal secretion of these gonadotropins was observed after the administration of 10 µM MECA. This effect mimicked the inhibition induced by R-PIA, supporting the hypothesis of the presence of A 1 receptors in the gonadotrope. R-PIA (1 nM to 1 µM) also inhibited the secretion of LH and FSH induced by phospholipase C (0.5 IU/ml) in a dose-dependent manner. These results suggest the presence of A 1 receptors and the absence of A 2 receptors in the gonadotrope. It is possible that the inhibition of LH and FSH secretion resulting from the activation of A 1 receptors may have occurred independently of the increase in membrane phosphoinositide synthesis.

show abstract

Inositol Phospholipid Metabolism During and Following Synaptic Activation: Role of Adenosine

Cited by 17 publications

References 35 publications

Interactions between adenosine and phorbol esters or lithium at the frog neuromuscular junction

Interactions between adenosine and phorbol esters or lithium at the frog neuromuscular junction

Adenosine acts by A ₁ receptors to stimulate release of prolactin from anterior-pituitaries in vitro

Possible involvement of A1 receptors in the inhibition of gonadotropin secretion induced by adenosine in rat hemipituitaries in vitro

Contact Info

Product

Resources

About

Inositol Phospholipid Metabolism During and Following Synaptic Activation: Role of Adenosine

Cited by 17 publications

References 35 publications

Interactions between adenosine and phorbol esters or lithium at the frog neuromuscular junction

Interactions between adenosine and phorbol esters or lithium at the frog neuromuscular junction

Adenosine acts by A 1 receptors to stimulate release of prolactin from anterior-pituitaries in vitro

Possible involvement of A1 receptors in the inhibition of gonadotropin secretion induced by adenosine in rat hemipituitaries in vitro

Contact Info

Product

Resources

About

Adenosine acts by A ₁ receptors to stimulate release of prolactin from anterior-pituitaries in vitro