STIMULATION OF ANTERIOR PITUITARY ADENYL CYCLASE ACTIVITY AND ADENOSINE 3′:5′-CYCLIC PHOSPHATE BY HYPOTHALAMIC EXTRACT AND PROSTAGLANDIN E
            <sub>1</sub>

Zor, U.; Kaneko, Takeshi; Schneider, Herman; McCann, Samuel M.; Lowe, Irene P.; Bloom, Gail; Borland, Barbara; Field, James B.

doi:10.1073/pnas.63.3.918

Cited by 91 publications

(22 citation statements)

References 18 publications

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“…Thus, we hypothesized that cAMP is an important chemical mediator, which, when present, dramatically increases the ability of sEHIs to reduce pain. Given that intracellular cAMP is increased by inflammation and is itself painful (17)(18)(19)(20), in the following experiments we used healthy rats without inflammation or neuropathy and monitored acute pain-related behavior measured as withdrawal responses to thermal and mechanical stimuli.…”

Section: Resultsmentioning

confidence: 99%

Analgesia mediated by soluble epoxide hydrolase inhibitors is dependent on cAMP

Inceoglu

Wagner

Schebb

et al. 2011

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

124

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Pain is a major health concern even though numerous analgesic agents are available. Side effects and lack of wide-spectrum efficacy of current drugs justify efforts to better understand pain mechanisms. Stabilization of natural epoxy-fatty acids (EFAs) through inhibition of the soluble epoxide hydrolase (sEH) reduces pain. However, in the absence of an underlying painful state, inhibition of sEH is ineffective. Surprisingly, a pain-mediating second messenger, cAMP, interacts with natural EFAs and regulates the analgesic activity of sEH inhibitors. Concurrent inhibition of sEH and phosphodiesterase (PDE) dramatically reduced acute pain in rodents. Our findings demonstrate a mechanism of action of cAMP and EFAs in the pathophysiology of pain. Furthermore, we demonstrate that inhibition of various PDE isozymes, including PDE4, lead to significant increases in EFA levels through a mechanism independent of sEH, suggesting that the efficacy of commercial PDE inhibitors could result in part from increasing EFAs. The cross-talk between the two major pathways-one mediated by cAMP and the other by EFAs-paves the way to new approaches to understand and control pain.nociception | antinociceptive | epoxyeicosatrienoic acid

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Section: Resultsmentioning

confidence: 99%

Analgesia mediated by soluble epoxide hydrolase inhibitors is dependent on cAMP

Inceoglu

Wagner

Schebb

et al. 2011

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

124

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“…Recently, a stimulatory effect of the N6-monobutyryl derivative and of various other derivatives of cAMI on the release of both LH and FSH from rat anterior pituitaries in vitro has been observed (G. Chavancy and F. Labrie, unpublished). Moreover, crude hypothalamic extracts stimulate adenohypophyseal adenylate cyclase activity and concomitant release of LH (20,21). However, definitive proof of the role of the adenylate cyclase system as mediator of the action of LH-releasing hormone/FSH-releasing hormone could be obtained only by measurements of adenohypophyseal adenylate cyclase activity or cAMP concentrations under the influence of the purified or synthetic neurohormone.…”

mentioning

confidence: 99%

Stimulation of Adenosine 3′:5′-Cyclic Monophosphate Accumulation in Anterior Pituitary Gland In Vitro by Synthetic Luteinizing Hormone-Releasing Hormone

Borgeat

Chavancy

Dupont

et al. 1972

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

183

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A near-maximal dose (20 ng/ml) of synthetic luteinizing hormone(LH)-releasing hormone/follicle-stimulating hormone(FSH)-releasing hormone added to incubated anterior pituitary tissue of male rats leads to concomitant increases of intracellular concentrations of adenosine 3': 5'-monophosphate and of release of both LH and FSH. The stimulatory effect of LH-releasing hormone/ FSH-releasing hormone is observed after a lag period of about 90 min and is progressive at later time intervals; a 3-fold stimulation of cAMP accumulation over control is seen after 210 min of incubation. Half-maximal stimulation of cAMP accumulation is observed between 0.1 and 1.0 ng/ml (0.1-1 nM) of LH-releasing hormone/FSH-releasing hormone. In the presence of 10 mM theophylline, the stimulatory effect of LH-releasing hormone/FSH-releasing hormone on cAMP accumulation is similar to that observed in the absence of the inhibitor of cyclic nucleotide phosphodiesterase, indicating that the releasing hormone exerts its effect by specific activation of adenylate cyclase in LH-and FSH-secreting cells rather than by inhibition of cyclic nucleotide phosphodiesterase. Since the release of growth hormone, thyrotropin, prolactin, and adrenocorticotropic hormone is not affected by LH-releasing hormone/FSH-releasing hormone, and since cAMP stimulates the release of all six adenohypophyseal hormones. the observed changes of cAMP concentrations indicate specific stimulation of adenylate cyclase activity in LHand FSH-secreting cells of the adenohypophysis.Secretion of luteinizing hormone (LH) and of follicle-stimulating hormone (FSH) by the anterior pituitary gland is controlled by a neurohormone released from the hypothalamic area and carried to its specific adenohypophyseal site of action by a portal blood system (1-4). Recently, after more than 10 years of research in many laboratories, this neurohormone was isolated from porcine (5-7) and ovine (8) hypothalami and characterized as a decapeptide having the following structure: (pyro)Glu-His-Try-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2 (9-11). Since this peptide stimulates the release of both LH and FSH under various experimental conditions (4-8, 10-13), it has been called the LH-releasing hormone/FSH-releasing hormone (4, 5, 7) or the gonadotropin-releasing factor (12). The availability of synthetic LH-releasing hormone/FSHreleasing hormone (14-16) and of its analogs is of obvious importance for studies of the mechanism of action of this neurohormone in the adenohypophysis.There was suggestive evidence for a role of adenosine 3': 5'-cyclic monophosphate (cAMP) as a mediator of the action of LH-releasing hormone/FSH-releasing hormone. These studies pertained to reported stimulatory effects of N6,2'.-Odibutyryl cAMP and theophylline (17) (20, 21). However, definitive proof of the role of the adenylate cyclase system as mediator of the action of LH-releasing hormone/FSH-releasing hormone could be obtained only by measurements of adenohypophyseal adenylate cyclase activity or cAMP concentrations under the inf...

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“…While there is a general agreement that PGE increases pituitary cyclic AMP production [3,4,7,16] reports differ as to the effect of PGE on LH release. Makino [7] and Ratner et al [16] found increased LH release when PGE was added to incubated pituitaries, but other workers failed to find any increase in LH release after short [ 171 or long incubation periods with PGE ([ 181 and present results fig.1).…”

Section: Discussionmentioning

confidence: 99%

“…Crude hypothalamic extract containing LH-releasing activity was reported to stimulate adenylate cyclase and to increase the cyclic AMP level in the pituitary gland [3] . Recently it was found that synthetic LH-RH increased adenylate cyclase activity [4] cyclic AMP level and concomitantly stimulated LH release [S-8] .…”

Section: Introductionmentioning

confidence: 99%

Pituitary cyclic AMP production and mechanism of luteinizing hormone release

et al. 1975

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STIMULATION OF ANTERIOR PITUITARY ADENYL CYCLASE ACTIVITY AND ADENOSINE 3′:5′-CYCLIC PHOSPHATE BY HYPOTHALAMIC EXTRACT AND PROSTAGLANDIN E ₁

Cited by 91 publications

References 18 publications

Analgesia mediated by soluble epoxide hydrolase inhibitors is dependent on cAMP

Analgesia mediated by soluble epoxide hydrolase inhibitors is dependent on cAMP

Stimulation of Adenosine 3′:5′-Cyclic Monophosphate Accumulation in Anterior Pituitary Gland In Vitro by Synthetic Luteinizing Hormone-Releasing Hormone

Pituitary cyclic AMP production and mechanism of luteinizing hormone release

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STIMULATION OF ANTERIOR PITUITARY ADENYL CYCLASE ACTIVITY AND ADENOSINE 3′:5′-CYCLIC PHOSPHATE BY HYPOTHALAMIC EXTRACT AND PROSTAGLANDIN E 1

Cited by 91 publications

References 18 publications

Analgesia mediated by soluble epoxide hydrolase inhibitors is dependent on cAMP

Analgesia mediated by soluble epoxide hydrolase inhibitors is dependent on cAMP

Stimulation of Adenosine 3′:5′-Cyclic Monophosphate Accumulation in Anterior Pituitary Gland In Vitro by Synthetic Luteinizing Hormone-Releasing Hormone

Pituitary cyclic AMP production and mechanism of luteinizing hormone release

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Product

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STIMULATION OF ANTERIOR PITUITARY ADENYL CYCLASE ACTIVITY AND ADENOSINE 3′:5′-CYCLIC PHOSPHATE BY HYPOTHALAMIC EXTRACT AND PROSTAGLANDIN E ₁